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THIS  BOOK  WAS  DONATED 


Digitized  by  the  Internet  Archive 

in  2007  with  funding  from 

IVIicrosoft  Corporation 


http://www.archive.org/details/diseasesofdigestOObilliala 


DISEASES  OF 
THE   DIGESTIVE  SYSTEM 


MOBERN  CLINICAL   MEDICINE 


DISEASES 


OF  THE 


DIGESTIVE   SYSTEM 


n 


\^ 


EDITED  BY 

FRANK    BILLINGS,    M.D. 


PBOPESSOR  OF  MEDICINE,    UNIVEBSITY   OF  CHICAGO,    AND   PKOFESSOB  OF 
MEDICINE  AND  DEAN  OF   FACULTY,    BUSH   MEDICAL  COLLEGE 


AN  AUTHORIZED  TRANSLATION  FROM  "DIE  DEUTSCHE  KLINIK' 
UNDER  THE  GENERAL  EDITORIAL  SUPERVISION  OF 

JULIUS    L.    SALINGER,    M.D. 


WITH  FORTY-FIVE  ILLUSTRATIONS  IN  THE  TEXT 


NEW    YORK    AND    LONDON 
D.    APPLETON     AND    COMPANY 

1910 


VKJX^VCrO 


C^OPYKIOHT,   1906,  1909,  1910,  BY 

D.   APPLKTOxV    AND   COMPANY 


PRINTKU   AT  THE  APPLETON   PK£SS 
NEW    YORK,    U.    8.    A. 


s\o 


INTRODUCTION 


The  advances  of  chemistry  in  the  last  few  decades  have  placed  the 
diagnosis  and  treatment  of  Digestive  Diseases  upon  a  firm  foundation. 
Much  that  was  formerly  purely  theoretical  and  based  upon  hypothesis  has 
now  become  almost  absolute  knowledge.  The  study  of  metabolism  has 
lifted  the  veil  of  mystery  from  much  that  was  obscure.  In  the  investiga- 
tion of  diseases  of  digestion,  in  which  physiology,  chemistry,  and  pathology 
are  so  intimately  connected,  the  practitioner  has  received  valuable  aid  in 
relieving  suffering  humanity.  In  practice,  perhaps  the  greatest  benefits 
may  be  conveyed  by  the  correction  of  even  the  most  insignificant  alimentary 
errors. 

In  no  organ  of  the  abdominal  cavity,  and  perhaps  of  the  entire  body,  are 
the  functions  so  manifold  and  diverse  as  in  the  pancreas.  Text-books  dating 
back  a  few  decades  scarcely  mentioned  the  name  of  the  organ,  not  to  speak 
of  a  reference  to  its  diseases.  Thanks  to  the  labors  of  investigators  quite  a 
literature  is  to-day  extant,  and  the  search-light  of  diagnosis  is  beginning 
to  be  thrown  upon  maladies  of  this  important  digestive  organ. 

This  volume  treats  not  only  of  these  subjects,  but  a  new  study  has  been 
opened,  or,  more  properly,  revived;  namely,  the  investigation  of  the  feces. 
What  the  examination  of  the  sputum  is  to  disease  of  the  lungs,  what  the 
examination  of  the  urine  is  to  disease  of  the  kidney  and  to  disorders  of 
metabolism,  what  the  analysis  of  the  gastric  contents  is  to  the  diagnosis 
of  disease  of  the  stomach,  the  macroscopic,  microscopic,  bacteriologic  and 
chemical  investigation  of  the  feces  is  to  disease  of  the  intestines. 

Abdominal  surgery  has  aided  much  in  the  elucidation  of  many  of  these 
problems,  and  although  we  have  reached  but  the  first  step  of  the  ladder 
in  the  ascent  of  the  tree  of  knowledge,  much  has  been  learned  and  still 
more  may  be  expected.- 


%     '>^^    "*^^ 


INTRODUCTION  TO  THE  SECOND  EDITION 


'V}iK  need  for  a  second  edition  of  this  volume  in  a  brief  space  of  time 
is  an  evidence  not  only  of  the  appreciation,  but  also  of  the  necessity  for 
the  study  of  diseases  of  the  digestive  tract.  It  is  with  a  certain  degree  of 
satisfaction  that  we  are  able  to  state  that  the  material  contained  in  this 
book  is  so  abreast  of  the  times  that  but  very  few  changes  could  be  made 
in  tlie  new  edition.  Some  recent  points  have  been  added  in  symptom- 
atology and  in  treatment.  It  is  to  be  hoped  that  future  editions  will  meet 
with  the  same  favorable  reception  as  that  accorded  to  the  original  volume. 

Julius  L.  Salinger. 


EDITOK'S    PREFACE 


To-day  diseases  of  the  Digestive  Tract  stand  in  the  forefront  of  sub- 
jects which  interest  the  practitioner  and  the  surgeon. 

Many  of  the  diseases  included  in  this  volume  lie  on  the  borderland  of 
medicine  and  surgery. 

This  volume  includes  articles  from  many  of  the  most  eminent  men  of 
Europe,  specialists  in  internal  medicine  and  in  diseases  of  the  digestive 
tract. 

The  subjects  are  treated  very  fully  and  at  the  same  time  in  a  concise 
and  practical  manner.  The  modern  methods  of  examination,  including 
physical  and  chemical  measures,  are  clearly  set  forth,  which  will  enable 
the  practitioner  to  apply  them  with  the  same  ease  that  he  may  make  a 
physical  examination  of  the  chest  and  a  chemical  and  microscopic  uran- 
alysis. 

The  diagnosis  of  the  various  diseases  is  fully  discussed  and  the  treat- 
ment, including  the  dietary,  is  satisfactorily  full  and  complete.  Indeed,  the 
subjects  are  so  fully  treated  that  the  editor  found  it  inexpedient  to  add  to 
or  to  modify  the:  text  to  any  important  extent. 

The  translator  has  done  the  work  well,  with  the  result  that  the  text 

is  smooth  and  interestingly  readable. 

Frank  Billings. 
100  State  Street,  Chicago. 


LIST  OF  CONTRIBUTIONS 


Stenosis  of  the  Esophagus.     By  Th.  Rosenheim,  Berlin. 

The  History  and  Clinical  Indications  of  Gastric  Lavage.     By  W.  Fleiner,  Heidel- 
berg. 

Functional  Diseases  of  the  Stomach.     By  H.  Leo,  Bonn. 

The  Diagnostic  and  Therapeutic  Significance  of  Secrdory  Disturbances  of  the  Stomach. 
By  H.  Strauss,  Berlin. 

Diagnosis  and  Treatment  of  Gastric  DUaiaiion.     By  F.  Riegel,  Giessen. 

Gastric  Ulcer  and  Gastric  Hemorrhage.     By  C.  A.  Ewald,  Berlin. 

Gastric  and  Intestinal  Cardnomata.     By  J.  Boas,  Berlin. 

Displacements  of  the  Abdominal  Viscera  and  of  the  Heart.     By  F.  HirschfelDj 
Berlin. 

Symptomatology  of  the  Diseases  of  the  Pancreas.     By  L.  Oser,  Vienna. 

Jaundice  and  Hepatic  Insufficiency.     By  O.  Minkowski,  Cologne. 

Chronic  Inflammation  of  the  Liver.     By  E.  Stadelmann,  Berlin. 

Neoplasms  of  the  Liver  and  Biliary  Passages.     By  Fr.  Kraus,  Graz. 

Echinococcus  of  the  Liver.     By  E.  Stadelmann,  Berlin. 

Gall-stones.     By  E.  Neusser,  Vienna. 

Acute  Diffuse  Peritonitis,  Appendicitis,  and  Perityphlitis: 

I.     Diffuse  and  Circumscribed  Peritonitis.     By  O.  Vierordt,  Heidelberg. 
II.     Chronic  Perityphlitis.     By  J.  Boas,  Berlin. 

Examination  of  the  Feces.     By  J.  Strasburger,  Bonn. 

Diarrhea,  Intestinal  Catarrh,  and  Intestinal  Tuberculosis.     By  W.  Fleiner,  Heidel- 
berg. 

Constipation  and  Hemorrhoids.     By  J.  Boas,  Berlin.  < 

Mucous  Colic  and  Membranous  Intestinal  Catarrh.     By  G.  Hoppe-Seyler,  Kiel. 

Intestinal  Constriction  and  Intestinal  Occlu^n.     By  H.  Nothnagel,  Vienna. 


CONTENTS 


DISEASES  OF  THE  ESOPHAGUS   AND  OF  THE  STOMACH 

PAGE 

Stenosis  of  the  Esophagus 1 

Etiology 1 

Symptoms 2 

Diagnosis 10 

Treatment 19 

The  History  and  Clinical  Indications  of  Gastric  Lavage      ...  32 

The  History  of  Gastric  Lavage 32 

The  Clinical  Employment  of  Gastric  Lavage 46 

Functional  Diseases  of  the  Stomach 63 

To  Test  the  Function  of  the  Stomach 63 

Examination  of  the  Gastric  Contents 66 

Dyspepsia 69 

Neuroses  of  the  Stomach 70 

The  Diagnostic  and  Therapeutic  Significance  of  Secretory  Disturb- 
ances OF  the  Stomach 87 

Gastric  Secretions 88 

Subacidity  (Apepsia  Gastrica) 94 

Hyperacidity              103 

Hypersecretion 113 

Supplement 119 

Diagnosis  and  Treatment  of  Gastric  Dilatation 122 

Clinical  Forms 122 

Pathology 131 

Symptomatology 132 

Differential  Diagnosis 143 

Course  of  the  Disease 144 

Diagnosis 146 

Prognosis  and  Treatment 149 

Gastric  Ulcer  and  Gastric  Hemorrhage 159 

Etiology 159 

Pathological  Anatomy 163 

Symptoms 168 

Diagnosis 188 

Prognosis 199 

Treatment 201 

Literature 216 


xii  CONTENTS 

PAGE 

Gastric  and  Intestinal  Cabcinomata 221 

i:tiolof:j- 222 

t'hoiiiical  and  Microscopical  Investigation  of  the  Gastric  Contents      .        .  230 

(lastric  Carcinoma 234 

Carcinoma  of  the  Intestines 240 

Treatment  of  Carcinomata  of  the  Stomach  and  of  the  Intestines        .        .  251 

Displacements  of  the  Abdominal  Viscera  and  of  the  Heart  .       .       .  263 

Displacement  of  the  Stomach.     (Gastroptosis) 265 

Displacement  of  the  Kidneys — Wandering  Kindey — Nephroptosis        .        .  281 

Displacement  of  the  Liver — Wandering  Liver  (Hepatoptosis)        .        ,        .  290 

Displacement  of  the  Spleen — Wandering  Spleen 292 

Displacement  of  the  Colon  (Coloptosis) 294 

Displacement  of  the  Heart — Wandering  Heart,  Cor  Mobile           .        .        .  295 

DISEASES  OF  THE   PANCREAS 

Symptomatology  of  the  Diseases  of  the  Pancreas 303 

History 303 

Atiatomy  and  Physiology 304 

Symptoms 306 


DISEASES  OF  THE   LIVER  AND   BILIARY  PASSAGES 

Jaundice  and  Hepatic  Insufficiency 325 

Jaundice 325 

Hepatic  Insufficiency 340 

Acute  Yellow  Atrophy 342 

Chronic  Inflammation  of  the  Liver 361 

A.  The  Various  Forms  of  Chronic  Hepatic  Inflammation     ....  363 

B.  Cirrhosis    Hepatis — Laennec's    Cirrhosis — Granular    Atrophy     of     the 

Liver 371 

C.  Hypertrophic  Hepatic  Cirrhosis 385 

D.  Biliarj-  Hepatic  Cirrhosis 388 

E.  Syphilis  of  the  Liver 389 

Literature 393 

Neoplasms  of  the  Liver  and  Biliary  Passages 396 

1.  Neoplasms  of  the  Gall-bladder 397 

2.  Obstructions  of  the  Common  Gall-duct  by  Tumors 406 

3.  Neoplasms  of  the  Liver 438 

IvCHiNococcus  OF  the  Liver 454 

A.    I'.chiuococcus  Cysticus 455 

H.    Kchinococcus  Multilocularis  Seu  Alveolaris 460 

Gall-stones 454 

Symptomatologj' 464 

Prognosis 503 

Treatment 504 

Etiology 50§ 


CONTENTS  xiii 
DISEASES  OF  THE   INTESTINES 

PAGE 

Acute  Diffuse  Peritonitis,  Appendicitis,  and  Perityphlitis  .       .       .  513 

I.  Diffuse  and  Circumscribed  Peritonitis 513 

Acute  Diffuse  Peritonitis 513 

Circumscribed  Acute  Peritonitis  with  Particular  Reference   to  Peri- 
typhlitis         540 

Circumscribed  Peritonitis,  Particularly  Perityphlitis      ....  564 

II.  Chronic  Perityphlitis 573 

Etiology 574 

Anatomical  and  Histological  Changes 575 

Chnical  Picture 578 

I.     Residual  Perityphlitis 578 

II.     Chronic  Relapsing  Perityphlitis 581 

Complications 588 

Diagnosis  and  Differential  Diagnosis 589 

Prognosis 595 

Treatment 597 

Examination  op  the  Feces 605 

Test  Diet 607 

Test  for  Occult  Blood 633 

Diarrhea,  Intestinal  Catarrh,  and  Intestinal  Tuberculosis         .       .  635 

I.     Diarrhea 635 

Intestinal  Bacteria 637 

Etiology 644 

Symptoms 647 

Diagnosis 650 

II.  Intestinal  Catarrh 654 

Acute  Intestinal  Catarrh 654 

Chronic  Intestinal  Catarrh 668 

III.  Intestinal  Tuberculosis 687 

Pathology 689 

Symptoms         .        .        -        ,        , 691 

Diagnosis 697 

Treatment 698 

Constipation  and  Hemorrhoids      .       .       . 704 

Constipation 704 

Etiology  of  Habitual  Constipation 705 

Etiology  of  Hemorrhoids 708 

Symptoms  of  Habitual  Constipation 709 

Symptoms  of  Hemorrhoids 711 

Diagnosis  of  Habitual  Constipation 713 

Diagnosis  of  Hemorrhoids •  715 

Treatment  of  Habitual  Constipation 716 

Treatment  of  Hemorrhoids      .    , 730 

Mucous  Colic  and  Membranous  Intestinal  Catarrh          ....  735 

Etiology  and  Pathogenesis 736 

Pathologic  Anatomy 738 

Symptoms  and  Course 739 


xiv  CONTENTS 

PAOB 

Prognosis 746 

Diagnosis 746 

Treatment 747 

Intestinal  Constriction  and  Intestinal  Occlusion 751 

I.     Intestinal  Constriction 751 

Symptomatology 751 

Etiology 754 

Prognosis 762 

Treatment ' 763 

II.     Intestinal  Occlusion 765 

Pathology 765 

Symptoms 767 

Diagnosis 775 

Treatment 780 

INDEX  OF  AUTHORS 787 

INDEX  OF  SUBJECTS 797 


LIST  OF  ILLUSTRATIONS 

{FOUR  IN  COLORS) 

"**•  PAGB 

1.  The  Sippy  Dilator 25 

2.  Terminal  piece  of  a  soft  stomach  tube 49 

3.  Terminal  piece  of  a  soft  stomach  tube  with  lateral  and  central  openings.  49 

4.  Terminal  piece  of  a  soft  stomach  tube  with  a  central  and  numerous  lateral 

openings 50 

5  and  6.     Terminal  piece  of  soft  tubes  with  rounded  openings       ....  50 

7.  Complete  apparatus  for  washing  the  stomach.     (After  Kussmaul)          .        .  53 

8.  Hard  rubber  ring  on  which  to  bite,  drawn  over  the  sound        ....  54 

9.  Inserted  piece  of  hard  rubber  with  cock 55 

10.  Case  of  gastric  dilatation  with  low  position  of  the  stomach  in  a  woman 

aged  59 148 

11.  Normal  position  of  the  stomach 268 

12.  Gastroptosis  of  the  first  degree 269 

13.  Gastroptosis  of  the  second  degree 270 

14.  Gastroptosis  of  the  third  degree 271 

15.  Constriction  of  right  lobe  of  liver  and  pylorus 272 

16.  Displacement  of  the  liver 291 

17.  Displacement  of  the  liver 292 

18.  Pericardium  with  vessels.     (After  Henke) 295 

19.  Frontal  section  through  the  trunk 297 

20.  Constriction  of  the  cecum 556 

21.  Temperature  curve  in  perityphlitic  exudate 592 

22.  A  fragment  of  a  grain  from  bread.     (Magnified  250  times)       .        .        .        .611 

23.  Potato  cells.     (Magnified  250  times) 612 

24.  Fragment  of  peas.     (Magnified  250  times) 612 

25.  (Colored). — Carrot  cells  with  crystals  of  carrotin.     (Magnified  250  times)     .  613 

26.  A  portion  of  a  leaf  of  lettuce.     (Magnified  250  times) 613 

27.  Two  stippled  vessels  in  juxtaposition.     (Magnified  250  times)         .        ,        .  613 

28.  Elongated  cells  from  stalks  of  asparagus.     (Magnified  250  times)   .        .        .  614 

29.  Spores  from  truffles  in  an  ascus.     (Magnified  250  times) 614 

30.  Mildew  spores  of  wheat.     (Magnified  250  times) 614 

31.  Spores  of  lycopodium  clavatum.     (Magnified  250  times) 614 

32.  Stone  cells  (core)  from  the  pulp  of  pears.     (Magnified  250  times)  .        .        .615 

33.  Elastic  fibers.     (Magnified  250  times) 615 

34.  Connective  tissue.     (Magnified  250  times) 616 

35.  Muscle  fibers  in  various  stages  of  digestion.     (Magnified  250  times)       .        .  617 

36.  Fermentation  tubes  with  contents.     (One-fifth  natural  size)    .        .        .        .621 

37.  Soap  crystals  and  soap  granules.     (Magnified  500  times)          ....  623 

38.  Same  as  Fig.  37,  but  after  heating  with  dilute  sulphuric  acid.     (Magnified 

500  times) 624 

39.  (Colored).     Normal  feces  from  a  test  diet.     (Combination  picture)         .        .  627 


xvi  LIST  OF  ILLUSTRATIONS 

KIO.  PAGE 

40.  (Colored).     Pathologic  constituents  in  feces  after  a  test  meal.     (Combina- 

tion picture) 628 

41.  Connective  tissue  from  the  feces.     (Natural  size) 629 

42.  Mucus  from  the  feces.     (Natural  size) 630 

43.  Mucus  with  isolated  disintegrated  epithelia.     (Magnified  250  times)       .        .  630 

44.  Same  after  thorough  admixture  with  dilute  acetic  acid.     (Magnified    250 

times) 631 

45.  (Colored).     Mucus  with  numerous  red  blood-corpuscles  in  process  of   de- 

struction,   together   with    crystals   of   triple    phosphates.     (Magnified 

250  times) 632 


DISEASES  OF  THE   ESOPHAGUS  AND   OF 
THE  STOMACH 


STENOSIS  OF  THE  ESOPHAGUS 

By  TH.   ROSENHEIM,  Berun 

ETIOLOGY 

Diseases  of  the  esophagus  are,  as  a  rule,  infrequent.  Almost  invaria- 
bly, however,  they  are  of  great  importance,  as  an  essential  function  of 
the  organ  is  rapidly  influenced,  and  because  these  processes  occur  in  the 
immediate  vicinity  of  the  most  vital  organs,  so  that  a  dangerous  trans- 
mission of  the  disease  may  readily  take  place.  As  the  organ  in  question 
is  one  of  the  least  sensitive  ones,  pain  in  disease  of  the  esophagus  is  rare. 
In  the  main,  there  is  but  one  symptom:  disturbance  of  deglutition.  This 
occurs  in  varying  degrees  of  intensity  in  all  esophageal  affections,  yet  the 
severity  of  the  causal  process  has  no  decisive  influence  upon  the  degree; 
for  the  hindrance  in  deglutition  may  be  slight  in  carcinoma,  and,  on  the 
contrary,  it  may  be  high-graded  in  small  erosions,  or  in  derangement  of 
innervation.  The  basis  for  most  disturbances  of  deglutition  is  a  stenosis 
of  the  lumen,  which  may  arise  from  manifold  causes,  and  to  which  this 
article  will  be  exclusively  devoted.  The  majority  of  diseases  occurring 
in  the  esophagus  must  be  more  or  less  considered;  this  will  broaden  our 
theme  to  a  great  extent,  but  we  shall  confine  ourselves  well  within  the 
required  limits  if  we  emphasize  only  the  most  important  features  from  a 
diagnostic  and  therapeutic  standpoint.  The  researches  of  the  last  few 
years,  and  especially  since  the  introduction  of  esophagoscopy,  have  revealed 
much  that  is  new  and  important. 

The  most  frequent  and,  practically,  the  most  significant  cause  of  steno- 
sis of  the  esophagus  is  cancer;  other  diseases  are  rarely  mentioned,  at  most, 
here  and  there,  stricture  due  to  swallowing  of  caustics.  But  the  forms 
of  stenosis  are  by  no  means  exhausted  with  this,  and  the  spastic  stenoses, 
particularly,  call  for  more  thorough  consideration  than  was  formerly  de- 
voted to  them.  Disturbances  in  innervation  play  an  important  part  in  the 
origin  of  derangement  of  deglutition.  Yet  it  is  often  extraordinarily  diffi- 
cult accurately  to  measure  the  part  which  they  play  in  the  causation  of 
the  symptoms  of  the  disease,  as  they  rarely  occur  alone,  but  usually  are 
combined  with  other  pathologico-anatomical  changes  in  the  esophagus  or 
adjacent  organs.     We  must,  however,  always  endeavor  to  analyze  as  accu- 

1 


2  STENOSIS  OF  THE  ESOPHAGUS 

rately  as  possible  the  genesis  of  the  difficulty  in  swallowing,  as  this  is  of 
decisive  importance  in  the  therapy. 

In  reviewing  the  morbid  processes  in  the  esophagus  which  come  into 
question  under  the  picture  of  stenosis,  the  enormous  amount  of  material 
may  be  divided  into  two  groups:  In  the  first  group  we  are  dealing  with 
abnormal  ju'ocesses  which  have  their  seat  in  the  organ  itself,  i.  e.,  they  arise 
directly  from  the  organ,  and  thus  narrow  its  lumen;  in  the  second  group 
we  consider  the  cases  in  which  stenosis  is  due  to  compression.  Here  may 
be  mentioned  tumors  of  the  mediastinum,  of  the  vertebral  column,  goiter 
or  enlarged  lymph-glands,  aortic  aneurysm,  peri-esophageal  abscesses,  and, 
finally,  filled  diverticula  which  produce  stenosis  by  pressure. 

To  the  first  group  belong:  (a)  neoplastic  stenoses;  (b)  inflammatory 
and  cicatricial  stenoses;  (c)  spastic  stenoses;  (d)  hereditary  stenoses,  and, 
lastly,  (e.)  the  obstruction  to  the  propulsion  of  the  ingesta  which  may  be 
produced  by  the  esophagus,  in  which  sense  foreign  bodies  that  have  been 
swallowed,  polypi  with  long  pedicles,  and  aphthous  stomatitis  may  act. 

SYMPTOMS 

Let  us  now  describe  the  subjective  and  objective  symptoms  of  stenosis 
of  the  esophagus  in  the  various  forms  of  the  disease  which  are  to  be  here 
considered,  and  let  us  observe  the  differences  in  the  manifestations  pre- 
sented by  the  several  types.  For  this  purpose  it  is  best  to  analyze  the 
symptoms  of  cancer  of  the  esophagus,  the  affection  that  most  frequently 
causes  stenosis  of  the  esophagus.  How  frequent  carcinoma  is  can  be  defi- 
nitely seen  from  statistics  which  show  that  about  60  per  cent,  of  all  diseases 
of  the  esophagus  are  of  a  malignant  nature,  according  to  other  compila- 
tions even  90  per  cent. ;  but  from  my  own  experience  I  think  the  latter 
figure  somewhat  too  high.  It  may  be  remarked  in  passing  that  cancer 
of  the  esophagus  occurs  in  different  countries  with  variable  frequency.  For 
example,  in  Moscow  unquestionably  the  cases  are  more  numerous  than  in 
Berlin. 

DifficuJty  or  an  impediment  in  deglutition,  therefore  dysphagia,  is  the 
most  constant  symptom  of  cancer  of  the  esophagus.  It  is  usually  the  first, 
also,  which  makes  the  patient  anxious,  and  leads  him  to  consult  a  physician. 
The  disturbance  in  swallowing  appears  gradually  as  mild  pressure,  some- 
times behind  the  corpus  sterni  and  behind  the  larynx,  sometimes  in  front 
of  the  stomach  and  noted  upon  swallowing  solid  food;  later,  solid  masses, 
even  if  well  masticated,  pass  only  with  the  greatest  difficulty  or  only  simul- 
taneously with  fluid;  often  they  are  arrested;  then  comes  a  stage  in  which 
watery,  pappy  food  can  be  forced  into  the  stomach  only  with  effort;  it  must 
be  swallowed  in  small  portions,  slowly  and  carefully;  finally,  the  passage 
is  entirely  occluded,  transitorily  or  permanently,  so  that  the  patient  faces 
starvation.      Besides  this  gradual,  insidious,  progressive  development  of 


SYMPTOMS  3 

dysphagia,  which  is  the  usual  course,  we  observe  in  some  cases  in  the  midst 
of  the  best  of  health  and  without  prodromes  a  sudden  and  decided  impedi- 
ment to  deglutition.  At  other  times,  decided  variation  in  the  degree  of 
passability  of  the  esophagus  may  be  noted.  On  some  days  the  patient 
can  apparently  swallow  anything,  on  other  days  there  is  an  obstacle. 
Doubtless  the  condition  of  the  nervous  system  here  plays  an  important 
role,  for  I  have  repeatedly  observed  this  in  very  nervous  patients  with 
carcinoma  of  the  esophagus.  With  a  prolonged  course  of  the  affection, 
amelioration  may  come  by  the  purulent  softening  and  ichorous  decomposi- 
tion of  prominent  cancer  proliferations;  the  patient  again  becomes  hope- 
ful, but  this  improvement  is  only  the  precursor  of  the  final  catastrophe. 

The  following  fact  is  also  remarkable:  The  patients  complain  of  in- 
creasing difficulty  in  deglutition,  so  that  even  fluids  fail  to  pass,  or  only 
with  great  effort,  but,  in  this  condition  it  is  always  possible  to  pass  esopha- 
geal bougies  into  the  stomach.  This  disproportion  between  the  natural 
power  of  deglutition  and  the  results  of  probing  is  found  in  all  the  varied 
affections  of  the  esophagus,  but  chiefly  in  compression  of  the  organ  and 
in  neuroses;  occasionally,  however,  it  is  also  observed  in  flat  carcinomata 
situated  in  the  wall  of  the  organ  and  not  distributed  in  annular  form,  since 
these  offer  no  marked  resistance  to  the  sound,  which  readily  passes  them, 
and  they  disturb  the  active  deglutition  only  in  a  reflex  manner.  Thus 
spasms  are  caused  especially  at  the  upper  portion  of  the  diseased  area,  but 
they  may  also  occur  in  normal  portions  of  the  canal.  For  example,  as  not  in- 
frequent complications,  we  may  have  spasms  behind  the  larynx,  provided  the 
tumor  is  situated  in  the  cardia,  and,  in  addition  to  this,  very  disagreeable 
sensations  of  constriction  are  felt  at  the  boundary  line  between  the  pharynx 
and  esophagus,  and  these  necessitate  continued  efforts  at  swallowing  on 
the  part  of  the  patient ;  this  forms  a  very  usual  complication  in  the  various 
diseases  of  the  esophagus,  and  particularly  in  carcinoma,  immaterial  what 
its  situation.  The  reports  of  the  patient  as  to  the  region  in  which  he  feels 
constriction  and  pressure  are  often  inaccurate  and  misleading.  Frequently 
he  will  state  that  the  bolus  is  arrested  in  the  neck,  while  the  cancer  is 
situated  in  the  cardia,  or  vice  versa;  the  distress  is  sometimes  localized  in 
the  epigastrium,  when  the  neoplasm  has  developed  in  the  upper  half  of 
the  esophagus.  Therefore,  the  origin  of  disturbances  of  deglutition  is 
the  combination  of  a  series  of  factors.  At  one  time,  mechanical  obstruc- 
tion such  as  is  presented  by  the  infiltration  of  the  wall  of  the  esophagus 
plays  an  important  role;  at  another,  we  observe  increased  sensitiveness  of 
the  nerves  of  the  muscular  apparatus  which,  as  soon  as  the  food  reaches 
the  inflamed  area,  readily  show  abnormal  reaction.  This  reaction  is  the 
result  of  irritation,  and  is  usually  manifest  as  a  spasm  at  the  seat  of  the 
affection  or  in  distant  areas.  Added  to  this  are  disturbances  due  to  inflam- 
matory processes  in  the  mucous  membrane  of  the  areas  surrounding  the 
cancer,  alone  or  in  combination  with  an  atonic-ectatic  condition  of  the  organ 


4  STENOSIS  OF  THE  ESOPHAGUS 

above  the  neoplasm.  In  regard  to  the  last  point,  it  must  be  remembered 
that  hypertrophy,  and  also  dilatation,  may  develop  above  the  stenosed  area, 
that  the  latter,  however,  only  rarely  is  decided,  as  a  prolonged  and  perma- 
nent stagnation  of  food  does  not  readily  take  place.  On  the  contrary,  w^hen 
the  bolus  is  arrested,  it  is  usually  soon  regurgitated.  This  regurgitation 
naturally  occurs  the  more  promptly  the  greater  the  disproportion  between 
the  narrowness  of  the  stricture  and  the  consistency  of  the  food,  as  well 
as  between  the  local  sensitiveness  and  irritability  of  the  food.  As  a  rule, 
regurgitation  occurs  immediately  after  swallowing,  or  from  a  few  minutes 
to  a  quarter  of  an  hour  after,  rarely  later.  When  delayed,  however,  dilata- 
tion is  usually  present.  In  this  case,  if  the  esophageal  sound  be  used,  masses 
of  food  may  be  brought  up  in  which  the  absence  of  peptonization  shows 
clearly  that  they  have  never  reached  the  stomach.  It  is  obvious  that 
processes  of  decomposition  must  arise  when  the  food  remains  for  a  long 
time  in  the  esophagus;  consequently  the  patients  not  rarely  complain  of  a 
fetid  odor  from  the  mouth.  But  these  processes  may  occur  in  an  advanced 
stage  of  the  disease  even  without  a  decided  retention  of  food  owing  to  the 
decomposition  of  the  cancer,  and  thus  give  rise  to  offensive  breath. 

Besides  food,  and  even  independently  of  its  introduction,  a  foamy, 
mucoid  fluid  having  a  fetid  odor,  is  often  ejected,  and  not  rarely  shows 
traces  of  blood.  This  is  the  product  of  the  inflammatory  process  which 
accompanies  cancer  of  the  esophagus,  and  which  sometimes  also  extends 
to  the  pharynx  and  larynx.  The  combined  effect  of  these  irritative  factors 
is  cough,  which  often  increases  to  extremely  severe  paroxysms  which  natur- 
ally distress  the  patient ;  added  to  this  is  the  fact  that  bronchitis  and  tuber- 
culous changes  in  the  lungs  commonly  coexist  with  cancer. 

Apart  from  the  unpleasant  sensation  of  pressure  mechanically  caused 
by  the  arrest  of  the  bolus,  the  affection  may  he  painless  for  a  long  time 
or  even  permanently,  for  the  esophagus  is  one  of  the  least  sensitive  organs, 
and  in  this  malady  only  an  implication  of  the  mediastinum,  the  pleura, 
and  the  pericardium,  the  compression  of  important  nerve  plexuses  in  the 
vicinity,  the  implication  of  the  vertebral  column  and  the  spinal  cord,  will 
be  productive  of  pain.  Then  boring,  burning,  lancinating  pains  set  in  which 
accompany  the  act  of  deglutition  or  follow  it,  but  may  come  on  independ- 
ently of  the  introduction  of  food,  particularly  at  night.  The  pains  are 
felt  in  the  intercostal  spaces,  between  the  shoulder  blades,  in  the  epigas- 
trium, in  tlie  throat  and  head ;  for  example,  frequently  in  the  ear  and  in  the 
extremities.  It  is  obvious  that  by  the  metastatic  distribution,  and  by  the 
further  growth  of  the  cancer,  manifold  symptoms  may  be  produced.  I 
shall  here  mention,  for  example,  vasomotor  and  trophic  disturbances  in  the 
nails;  also  the  occurrence  of  inequality  of  the  pupils;  almost  always  the  left 
pupil  is  contracted.  Paralysis  of  the  recurrent  laryngeal  nerve,  above  all, 
deserves  special  mention.  Unilateral  paralysis  of  the  vocal  cord  is  a  quite 
coniniou  symptom.     As  this  may  not  cause  any  change  in  voice  production, 


SYMPTOMS  5 

it  can  be  detected  only  by  a  laryngeal  examination,  and  thus  is  frequently 
overlooked.  Often,  however,  it  is  an  early  symptom,  and  may  even  be 
present  when  as  yet  the  stenosis  is  scarcely  obvious. 

Dyspnea  and  attacks  of  pain  resembling  angina  pectoris  arise  in  the 
course  of  the  disease  either  because  the  neoplasm  posteriorly  presses  imme- 
diately upon  the  trachea,  or  upon  both  recurrent  laryngeal  nerves,  or  impli- 
cates the  posterior  plate  of  cricoid  cartilage  and  its  surroundings,  in  which 
case  the  nerve  and  the  muscular  substance  of  the  dilators  of  the  vocal  cords 
are  directly  destroyed. 

Perforation  of  the  esophageal  wall  may  take  place  without  producing 
special  symptoms,  and  this  is  true  even  if  the  formation  of  a  fistula  between 
the  esophagus  and  the  trachea  or  the  bronchi  has  already  occurred,  provided 
that  the  opening  is  small  and  the  esophageal  stricture  slight,  so  that  food 
may  pass  the  organ  without  being  arrested ;  otherwise,  severe  paroxysms  of 
cough  and  marked  dyspnea  upon  the  ingestion  of  food  are  the  character- 
istic signs  of  this  last-named  complication.  The  paroxysms  of  cough  cause 
the  ejection  of  mucus  stained  with  blood  simultaneously  with  particles  of 
food  which  have  found  their  way  into  the  respiratory  apparatus;  sooner  or 
later,  upon  continued  nutrition  by  the  mouth,  pneumonia  or  pulmonary 
gangrene  occurs.  If  the  fistulous  passage  is  very  narrow,  and  the  stricture 
still  relatively  permeable,  it  is  sometimes  noted  that  thin  fluids  cause  parox- 
ysms of  cough,  while  more  compact  food  passes  with  ease. 

Decided  spontaneous  hemorrhages  from  cancerous  ulcers  in  the  esophagus 
which  cause  hematemesis  are  rare  symptoms  of  carcinoma.  More  frequent 
are  fatal  internal  hemorrhages  due  to  the  erosion  of  a  vessel  with  the  ad- 
vance of  the  process. 

Concerning  the  difficulties  on  the  part  of  the  gastrointestinal  canal 
and  the  general  condition:  At  the  onset  of  the  affection  the  patients  usu- 
ally have  a  good  appetite,  and  in  some  pitiable  cases  this  continues  until 
death.  In  the  further  course  of  the  disease,  as  a  rule,  hunger  becomes  less 
pressing,  while  burning  thirst  almost  invariably  persists.  Stubborn  con- 
stipation is  common.  In  advanced  cases,  after  the  food  has  reached  the 
stomach,  it  sometimes  produces  a  continuous  dull  pain  in  the  epigastrium, 
not  rarely  accompanied  by  eructations  and  nausea.  These  dyspeptic  sjonp- 
toms  have  no  direct  significance  in  cancer  of  the  esophagus.  They  are 
to  be  attributed  to  secondary  inflammatory  atrophic  processes  in  the  mucous 
membrane  of  the  stomach  which  are  sooner  or  later  added,  and  the  more 
rapidly,  the  closer  the  cancer  lies  to  the  stomach,  and  the  sooner  it  impli- 
cates this  organ. 

It  is  obvious  that  inanition  and  cachexia  will  early  develop  in  the 
clinical  picture,  according  to  the  nature  of  the  disturbances  which  the 
affection  produces.  At  first  the  loss  in  strength  is  parallel  with  the  dura- 
tion of  the  disease  and  the  degree  of  obstruction  to  deglutition.  If  it  is 
possible  to  diminish,  or  even  to  remove,  the  latter,  although  only  tem- 


6  STENOSIS  OF  THE  ESOPHAGUS 

porarily,  the  patients,  as  a  rule,  rapidly  recover  and  increase  in  weight. 
Exceptionally  carcinoma  of  the  esophagus,  without  any  functional  disturb- 
ance, causes  extreme  debility  by  a  deleterious  and  toxic  influence  upon 
proteid  metabolism. 

Examination  of  the  patient  in  the  various  stages  of  the  affection  fur- 
nishes results  which  are  further  modified  according  to  the  seat  of  the  diffi- 
culty and  the  complications.  Inspection  and  palpation  frequently  permit 
us  to  recognize  enlargement  of  the  lymph-glands  in  the  supraclavicular  and 
cervical  regions;  but  the  utilization  of  this  finding  necessitates  caution, 
since  quite  marked  enlargement  of  the  glands  is  also  found  in  scrofulo- 
tuberculous  individuals,  a  moderate  enlargement  not  infrequently  in  syphi- 
lis and  catarrhal  affections  of  the  organs  of  the  throat;  it  may  even  he 
present  without  a  recognizable  disease.  If  the  cancer  is  situated  in  the 
upper  portion  of  the  esophagus  it  may  be  externally  palpated  as  a  tumor 
beside  the  trachea  and  the  larynx,  and  if  it  attack  the  cricoid  plate  or  the 
pharynx  it  may  even  be  seen  by  the  laryngoscope. 

When  the  cancer  is  deeply  located,  and  cannot  be  thus  recognized,  we 
must  investigate  by  means  of  the  sound.  We  should  first  determine  that 
no  disease  is  present  which  contraindicates  the  use  of  the  sound,  and  then 
attempt  to  pass  the  stricture  with  a  thick  instrument  (10  to  12  mm.  in 
diameter).  After  it  is  within  the  esophagus  it  should  be  slowly  and  care- 
fully forced ;  if  resistance  is  met  with,  it  must  be  overcome  by  gentle  means, 
but  boring  should  be  avoided;  upon  withdrawal  the  length  of  the  narrow 
portion  from  the  teeth  should  be  carefully  noted.  It  will  frequently  hap- 
pen that  the  figures  gained  in  this  manner  will  vary  several  centimeters 
upon  different  days — this  is  explained  by  the  fact  that  the  sound  enters 
to  a  different  depth,  or  the  point  is  embedded  in  the  stricture — ^nevertheless, 
in  spite  of  these  variations,  they  enable  us  to  locate  the  constriction,  but 
give  us  no  idea  of  its  extent.  The  resistance  that  the  sound  meets  may 
be  in  the  upper,  in  the  middle,  or  in  the  lower  part  of  the  malignant 
neoplasm.  It  is  a  valuable  diagnostic  aid  carefully  to  examine  the  fenester 
of  the  sound.  In  this  we  frequently  find  remains  of  food,  blood,  pus, 
mucus,  and  sometimes  even  shreds  of  tissue  which  under  the  microscope 
permit  the  exact  recognition  of  the  disease.  If  it  be  impossible  to  recog- 
nize the  characteristic  cancer  cell  nests  in  the  investigation  of  the  fresh 
preparation,  then  the  suspicious  portion  may  be  examined  by  the  stroma 
preparation  of  sections  after  hardening  in  alcohol,  or,  a  more  rapid  process, 
the  frozen  section  with  the  microtome  and  its  staining  (for  example,  with 
picro-carmin). 

Alter  the  presence  of  a  stenosis  has  been  determined  by  means  of  a 
thick  sound,  we  should  attempt  to  pass  through  the  narrow  passage  with 
more  slender  instruments;  frequently  it  will  be  impossible  to  reach  the 
stoniacli  with  the  finest  instruments,  although  pappy  and,  occasionally,  even 
solid  food  still  pass  the  stricture.     The  explanation  of  this  is  either  that 


SYMPTOMS  7 

the  point  of  the  sound  is  caught  in  a  diverticulum  above  the  narrowed  area, 
or  the  canal  of  the  stricture  is  not  straight  but  follows  an  irregular,  spiral 
course.  On  the  other  hand,  the  patients  may  complain  of  difficulty  in 
swallowing  food  in  a  certain  area  of  the  esophagus,  yet  the  largest  sound 
finds  no  resistance  in  its  entire  course  to  the  stomach ;  in  cases  of  beginning 
cancer  formation,  particularly,  the  results  of  examination  may  he  negative. 
Here  the  latter  course  must  explain  the  case,  or,  if  an  early  diagnosis  is 
desired,  we  must  investigate  by  means  of  the  esophagoscope.  The  nar- 
rowed area  which  has  been  revealed  by  the  sound,  even  in  advanced  cases, 
may  be  entirely  unrecognizable  if  extensive  ulceration  and  rapid  destruc- 
tion have  occurred;  but  here  also  the  esophagoscope  gives  the  desired 
information. 

The  esophagoscopic  pictures  show  great  variations,  which  certainly  de- 
pend upon  the  stage  of  development  of  the  neoplasm,  and,  above  all,  the 
nature  of  the  growth.  The  picture  which  presents  itself  is  entirely  differ- 
ent when  cauliflower-like  proliferations  enter  into  the  lumen,  or,  on  the 
contrary,  when  only  an  induration  of  the  wall  has  occurred,  when  ulcer 
formation  has  taken  place,  when  the  mucous  membrane  is  still  retained, 
when  the  narrowing  is  very  decided,  or  when  it  is  very  slight. 

The  cancerous  protuberances  which  narrow  the  space,  if  accurately 
investigated,  cannot  be  confounded  with  anything  else;  there  is  no  process 
in  the  esophagus  except  carcinoma  that  runs  its  course  with  the  formation 
of  these  prominent,  whitish-grey  to  greyish  or  dirty  greyish-yellow  nodules 
permeated  by  punctiform  hemorrhages.  The  finding  of  a  prominence  cov- 
ered with  mucous  membrane,  however,  may  be  of  varying  significance. 

Even  in  advanced  cases  of  carcinoma  the  stenosis  is  generally  not  due 
to  cancerous  masses  which  have  proliferated  into  the  lumen,  but  is  due 
to  infiltration,  and  this,  viewed  from  above,  presents  itself  as  a  swelling 
or  a  round  tumor  about  the  size  of  a  cherry  with  well-retained  mucous 
membrane,  while  ulceration  or  splitting  of  the  surface  cannot  be  detected 
because  it  occurs  only  toward  the  inner  wall,  therefore,  arises  in  the  lumen 
of  the  stricture.  Frequently,  above  these  protuberances  the  mucous  mem- 
brane appears  paler  than  normal,  sometimes  more  yellow  or,  cyanotically, 
bluish-red,  occasionally  even  loosened  and  markedly  reddened.  Worthy  of 
note  are  the  epithelial  thickenings  in  different  forms  (streaks,  flakes,  etc.), 
which  resemble  leukoplakia  of  the  tongue,  and  are  found  in  the  immediate 
surroundings  of  the  morbid  focus.  At  other  times  whitish,  papillary  ex- 
crescences, resembling  pointed  condylomata,  or  papillae  consisting  of  several 
whitish  papillary  proliferations,  are  met  with  in  front  of  the  narrowed  area, 
frequently  situated  upon  a  perfectly  normal  mucous  membrane.  These 
last  mentioned  changes  are  not  pathognomonic  of  carcinoma;  we  also  meet 
with  them  in  other  conditions. 

Not  rarely  the  wall  is  deeply  infiltrated  only  in  the  cancerous  mass; 
then  the  formation  of  the  above-mentioned  one-sided  protuberance  does 


8  STENOSIS  OF  THE  ESOPHAGUS 

not  occur,  but  frequently  there  is  an  annular  narrowing,  with  increasing 
constriction  downward.  We  can  then  pass  the  tube  as  far  as  this  rigid 
area,  but  no  farther,  and  we  descry  from  above  a  funnel-shaped  passage 
with  mucous  membrane  folds  converging  downward.  Sometimes  the  en- 
trance into  the  stricture  may  be  distinctly  perceived,  even  in  the  deepest 
area,  occasionally,  however,  the  folds  so  overlap  that  ttlis  is  impossible. 

A  similar  picture  is  sometimes  presented  to  us  by  strictures  due  to 
caustics,  and  the  previously  mentioned  protuberances  with  well-retained 
mucous  membrane  may  also  be  produced  by  the  bulging  of  the  wall  of  the 
esophagus  in  consequence  of  compression  from  without.  Therefore,  the 
proof  of  ulceration  or  of  a  cauliflower-like  proliferation  entering  into  the 
lumen  is  of  the  greatest  importance.  Sometimes  it  is  possible  to  recognize 
the  line  of  demarcation  where  the  healthy  mucous  membrane  terminates, 
having  an  eroded  appearance,  or  the  transition  to  the  ulcerating  part,  the 
surface  of  which  can  no  longer  be  recognized,  betrays  itself  here  and  there 
by  free,  floating  shreds  of  mucous  membrane.  We  may  distinguish  the 
ulcerated  portion  by  the  dirty,  greyish-yellow,  purulent  coating  under  which 
and  beside  which  the  greyish-red,  uneven  cancer  surface  can  sometimes  only 
be  brought  to  view  by  cleansing,  and  which  is  characterized  by  its  tendency 
to  continuous  capillary  hemorrhages.  Sometimes  after  the  introduction  of 
the  tube,  blood  oozes  continuously  from  the  ulcerated  surface,  and,  in  spite 
of  careful  cleansing  with  cotton,  nothing  more  can  be  seen.  In  other  cases 
foaming,  muco-purulent,  bloody  fluid  becomes  visible,  and  with  every  ex- 
piration is  forced  up  through  the  narrow  passage  with  a  gurgling  murmur. 
If  we  are  certain  that  no  injury  has  been  done  with  the  esophagoscope  at 
the  point  of  lesion,  the  expulsion  of  hemorrhagico-purulent  secretions  from 
the  stenosis  confirms  the  diagnosis  of  carcinoma. 

The  pulsating  motion  of  the  esophagus,  which  is  synchronous  with  the 
dilatation  of  the  aorta,  disturbs  the  investigation,  particularly  if  the  focus 
of  the  disease  be  situated  at  the  point  of  bifurcation.  But,  with  some  prac- 
tice, we  become  accustomed  to  this  rhythmic  motion  of  the  picture.  The 
respiratory  displacement  of  the  organ,  by  which  its  walls  approximate  one 
another  in  expiration,  scarcely  interferes,  provided  breathing  is  not  too 
deep  and  rapid ;  it  is  absent,  or  almost  so,  when  the  cancer  has  infiltrated 
the  walls  of  the  organ;  it  may,  therefore,  be  absent  upon  one  side  or  in 
the  entire  circumference.  On  the  other  hand,  there  may  be  a  disagreeable 
disturbance  due  to  severe  cough,  which,  in  spite  of  cocain  and  morphin,  is 
a  common  consequence  of  the  existing  laryngitis  or  trachitis.  It  is  impor- 
tant that  the  patients  be  examined  upon  an  empty  stomach.  If  the  field 
of  vision  is  obscured  by  remains  of  food,  such  as  portions  of  milk,  particles 
of  ojjpf  and  the  like  upon  the  mucous  membrane,  and  particularly  over  the 
narrowed  areas  of  the  rough  cancerous  surface,  mistakes  are  readily  made ; 
in  other  cases  it  is  easily  possible  to  mistake  these  whitish  masses  for  cancer. 

A   single  inspection  will  not  always  suffice  for  us  to  recognize  thq 


SYMPTOMS  9 

carcinoma.  In  cases  in  which  the  diagnosis  is  uncertain,  small  particles 
of  tissue  may  be  extracted  and  later  microscopically  examined,  but  great 
care  is  necessary  in  this  procedure. 

The  esophagoscope  should  never  he  used  immediately  after  sounding 
with  a  rigid  tube.  If  the  sound  has  been  introduced  into  the  esophagus 
to  determine  a  stricture  and  to  measure  its  distance  from  the  teeth,  even 
with  careful  manipulation  the  field  of  vision  may  be  obscured  with  blood. 
It  is  well,  therefore,  to  wait  a  few  hours. 

The  results  furnished  by  auscultation  of  the  esophagus  are  in  the  main 
meager.  If  the  patient  takes  fluid,  swallow  by  swallow,  he  himself  will 
frequently  notice,  as  do  those  about  him,  a  gurgling  sound  which  is  some- 
times heard  for  a  few  seconds  and  is  produced  at  the  narrowed  area  by 
the  checking  and  regurgitation  of  the  fluid  stream.  By  auscultation  at 
the  previously  designated  area,  these  deglutition  murmurs  give  us  diagnostic 
points  of  support,  which,  although  not  absolute  proof,  are  nevertheless 
auxiliary,  particularly  in  those  cases  in  which,  for  example,  upon  suspicion 
of  aneurysm,  it  is  unwise  to  introduce  instruments  into  the  esophagus.  No 
importance  is  to  be  attached  to  the  rarity  of  the  murmur  in  question  (press- 
ing-through murmur)  or  its  absence;  if  it  be  present,  however,  and  conspicu- 
ously prolonged,  an  impediment  in  the  upper  portion  of  the  esophagus  is 
indicated.  //,  however,  the  pressing-through  murmur  is  invariably  absent, 
simultaneously  with  the  first  sounds — an  occasional  absence  is  without  im- 
portance— this  is  in  favor  of  a  pathologic  process  which  limits  the  muscula- 
ture in  its  function  at  the  cardia,  and  which,  according  to  experience,  is, 
as  a  rule,  of  a  carcinomatous  nature;  for  only  very  exceptionally  are  both 
murmurs  absent  under  normal  conditions.  Rarely  does  the  esophageal 
bougie,  even  when  it  does  not  pass  into  the  stomach,  fill  itself  with  fluid  or 
pappy  or  compact  remains  of  food  which  must  have  lodged  in  that  portion 
above  the  carcinoma ;  they  betray  their  origin  by  the  absence  of  hydrochloric 
acid,  pepsin,  bile,  and  peptone,  and  by  their  alkaline  or  neutral  reaction, 
which,  however,  may  occasionally  be  acid,  and  is  then  due  to  organic  fer- 
mentative acids. 

The  gastric  function  must  suffer  sooner  or  later,  and  earliest  if  the 
cancer  be  situated  in  the  vicinity  of  the  cardia.  The  hydrochloric  acid 
secretion  is  therefore  not  rarely  found  to  be  absent.  The  urine  is  scant 
owing  to  the  limited  ingestion  of  fluid,  and,  in  advanced  stages,  frequently 
shows  the  products  of  proteid  decomposition  (indican)  and  those  of  patho- 
logic albumin  decomposition  (acetone,  aceto-acetic  acid,  oxybutyric  acid). 
Examination  of  the  larynx,  lungs  and  pleura  should  never  be  neglected. 
This  often  gives  valuable  aid  in  judging  our  cases. 


10  STENOSIS  OF  THE  ESOPHAGUS 

,  DIAGNOSIS 

The  most  important  point  in  the  diagnosis  of  carcinoma  of  the 
esophagus  is  the  recognition  of  a  stenosis  of  the  esophagus.  //  we  deter- 
mine this  by  the  aid  of  the  bougie  in  a  previously  healthy  person,  between 
the  ages  of  forty  and  seventy,  the  affection  having  arisen  without  a  recog- 
nizable cause,  and  steadily  increased  from  weeks  to  months,  nothing  is  more 
likely  than  that  we  are  dealing  with  a  carcinoma  of  the  esophagus.  Yet  a 
stenosis  that  has  developed  in  this  way,  and  under  these  conditions,  may 
occasionally  be  of  a  non-malignant  nature,  and  on  account  of  the  impor- 
tance of  this  point  for  the  patient,  this  possibility  should  first  be  excluded. 
It  must  be  borne  in  mind  that  the  history  and  the  subjective  symptoms, 
as  well  as  most  of  the  objective  symptoms,  may  lead  us  astray.  It  some- 
times liappens,  for  I  have  myself  observed  and  described  such  cases,  that 
in  benign  dilatations  and  with  the  formation  of  a  diverticulum  as  well 
as  in  spasm  of  the  esophagus  and  atony,  dysphagia  may  begin  without 
assignal)le  cause,  and  increase  in  a  few  months  to  a  threatening  degree, 
rapidly  undermining  the  strength.  On  the  other  hand,  in  consequence  of 
tlie  chronic  nature  of  disease  of  the  esophagus,  we  must  by  no  means  per- 
mit ourselves  to  give  a  relatively  favorable  prognosis,  and  to  exclude  car- 
cinoma. I  have  seen  patients  in  whom  difficulty  in  deglutition  had  existed 
from  four  to  ten  years  prior  to  death,  and  due  to  carcinoma  at  the  seat 
of  the  obstruction.  These  cases  may  be  explained  by  the  hypothesis  that 
the  cancer  formed  secondarily  upon  a  base  which  had  long  been  in  a  state 
of  irritation,  and  had  been  well  prepared.  We  know  that  ulcers  due  to 
a  variety  of  causes  (to  tuberculosis,  to  caustics,  or  to  digestive  processes) 
in  cicatrices,  in  inflammatory,  irritative  areas,  therefore,  wherever  me- 
chanical obstruction  causes  local  irritation,  prepare  a  soil  suitable  for  the 
formation  of  cancer. 

A  second  factor  in  the  history,  which  can  only  be  applied  after  thor- 
ough investigation,  is  the  age  of  the  patient.  It  is  true  cancer  usually 
develops  at  an  advanced  age;  but  I  have  seen  a  number  of  cases  of  cancer 
of  the  esophagus  in  persons  between  30  and  40  years  of  age,  and  hardly 
a  year  passes  in  which  I  do  not  see  at  least  one  case  in  early  youth. 

Another  point  which  may  mislead  us  is  the  cachexia.  This  is  mani- 
fest in  all  diseases  of  the  esophagus,  provided  they  form  a  hindrance  to 
the  ingestion  of  food;  in  nervous  disturbances  and  in  dilatation  of  the 
esophagus,  it  may  even  be  excessive. 

It  must  l)e  remembered  that  a  steady  increase  of  dysphagia  for  months, 
or  oven  for  years,  occurs  in  various  affections  of  the  esophagus,  namely, 
in  simple  inflammatory  processes,  in  dilatation,  and  in  diverticulum.  A 
conspicuous  change  in  the  power  of  swallowing  is  present  in  nervous  dvi- 
fiirlxinrrs  of  the  esophagus;  but  nervous  influences  may  also  occasionally 
appear  in  carcinoma. 


DIAGNOSIS  11 

Resistance  to  the  passage  of  the  esophageal  sound  is  objective  proof 
of  importance  in  diagnosis,  but  this  does  not  demonstrate  with  absolute 
certainty  that  there  is  an  anatomical  obstruction.  Spasm  may  arrest  the 
bougie,  and  it  may  be  impossible  to  overcome  this  either  by  prolonged  wait- 
ing or  by  attempts  at  swallowing  on  the  part  of  the  patient  (see  below).  More 
important  is  the  recognition  of  an  admixture  of  blood,  of  pus,  or  of  the 
products  of  decomposition  which  have  lodged  in  the  opening  of  the  tube 
during  probing,  but  it  must  be  borne  in  mind  that  ulcerative  processes 
and  decomposition  may  be  present  in  dilated  portions  of  the  organ  with- 
out the  presence  of  a  carcinoma.  Only  when  we  are  fortunate  enough 
to  find  shreds  of  tissue,  which  unquestionably  demonstrate  the  carcinom- 
atous character  of  the  affection,  is  this  positive  result  a  decisive  proof; 
and  this  can  only  occur  in  exceptional  cases;  in  the  early  stages  of  the 
disease  when  the  diagnosis  is  still  doubtful  it  rarely  happens. 

A  positive  and  early  diagnosis  may  be  made  most  frequently  by  the 
esophagoscope.  The  esophagoscopic  picture  is  generally  the  determining 
factor;  in  the  majority  of  cases  it  may  be  readily  obtained;  in  a  minority 
this  is  unsatisfactory,  1.  e.  it  does  not  give  a  positive  result;  and  this  may 
be  readily  understood  when  we  consider  the  fact  that  we  are  able  to  inspect 
only  the  upper  border  of  the  diseased  area,  and  the  later  course  of  the 
affection  and  the  consideration  of  all  its  accompanjdng  circumstances  can 
alone  clear  the  situation. 

From  this  it  is  evident  that  the  positive  determination  of  the  character 
of  a  constriction  of  the  esophagus  is  by  no  means  easy.  Although  the  ma- 
lignant form  predominates,  many  others  must  be  considered  which  furnish 
a  similar  symptom-picture,  and  well  deserve  the  interest  of  the  physician. 
We  should,  therefore,  avoid  making  a  positive  diagnosis  of  cancer  of  the 
esophagus,  as  is  very  commonly  done,  without  certain  indications  such 
as  dysphagia  and  resistance  upon  probing.  Based  on  these  criteria,  no 
positive  diagnosis  is  possible,  and,  when  we  consider  how  much  is  at  stake 
for  the  patient,  we  should  be  somewhat  more  thorough  in  our  differential 
diagnosis  and  more  cautious  in  our  prognosis. 

We  shall  now  describe  the  other  manifold  processes  which  cause  obstruc- 
tion to  the  passage  of  food,  and,  therefore,  present  the  picture  of  stenosis 
of  the  esophagus.  These  are  to  be  minutely  discussed,  and  are  best  con- 
sidered according  to  the  classification  given  above.  As  benign  neoplasms 
(myoma,  fibroma,  and  cysts)  are  great  rarities,  and  scarcely  ever  give 
rise  to  clinical  symptoms,  we  may  at  once  direct  our  attention  to  the  second 
group  of  stenoses,  those  which  originate  from  inflammatory  ulcerative 
processes. 

Stenoses  of  the  lumen  of  the  esophagus  due  to  the  action  of  caustics 
stand  first  in  practical  importance.  These,  as  is  well  known,  are  not  rare, 
and  in  regard  to  the  symptoms  it  is  immaterial  whether  acids,  alkalies. 


12  STENOSIS  OF  THE  ESOPHAGUS 

or  other  chemical  agents,  which  have  been  swallowed  either  for  purposes 
of  poisoning  or  by  accident,  produce  alterations  in  the  mucous  membrane. 
We  sliall  not  describe  the  stage  of  the  acute,  florid,  inflammatory  process  and 
tlie  phenomena  to  be  attributed  to  this.  We  are  more  interested  in  the 
conditions  which  result  in  the  course  of  weeks  and  months  in  consequence 
of  infiltrations  of  the  wall,  formation  of  cicatrices,  and  narrowing  of  the 
lumen.  The  strictures  which  originate  in  this  manner,  if  very  narrow, 
annular  or  tubular,  are  limited  to  certain  areas  of  the  esophagus,  and  this 
is  generally  the  upper  portion,  the  region  of  the  bifurcation,  and  the  area 
of  the  foramen  oesophageum.  If  we  are  dealing  with  long,  tubular  strict- 
ures, their  centers  are  at  these  points,  whence  they  distribute  themselves 
upward  or  downward  or  in  both  directions.  There  may  be  strictures  at 
several  points  of  the  esophagus,  and  by  the  coalescence  of  several,  the  con- 
striction becomes  extensive,  and  finally  total. 

The  diflieulties  in  deglutition  are  not  specially  characteristic.  They 
are  permanent,  and  vary  in  intensity  according  to  the  degree  of  the  con- 
striction and  the  local  irritation,  as  is  true  of  all  stenoses.  An  aid  in 
diagnosis  is  the  circumstance  that  from  the  history  alone  the  nature  of  the 
difiease  may  he  determined  with  some  degree  of  certainty.  But  the  anatomic 
condition  of  the  organ  caused  by  caustic  we  can  only  ascertain  by  an  exact 
investigation,  and  here  our  first  question  is:  Are  we  dealing  with  one  or 
more  strictures?  In  this  respect,  the  reports  of  the  patient  regarding  the 
act  of  deglutition  permit  some  deductions.  However,  this  information 
must  be  utilized  with  necessary  reserve,  as  it  is  frequently  shown  to  be 
erroneous.  Moreover,  we  desire  to  know:  Are  inflammatory,  ulcerative 
processes  still  present  in  the  mucous  membrane,  or  has  definite  cicatriza- 
tion occurred  in  all  parts?  Is  dilatation  present?  Finally,  the  question 
must  be  answered  whether  carcinoma  has  developed  in  consequence  of  the 
changes  which  are  to  be  here  considered.  Information  in  regard  to  all 
these  points  is  given  us  by  the  sound  and  the  esophagoscope.  Soft  tubes, 
firm  English  and  French  bougies,  also  the  metallic  spirals  which  I  prefer- 
ably employ  when  it  is  necessary  to  find  a  passage,  may  be  repeatedly  used 
in  order  to  acquaint  ourselves  with  the  situation  and  to  enable  us  to  form 
a  correct  opinion.  The  esophagoscope  gives  us  accurate  knowledge;  strict- 
ures due  to  caustics  form  very  characteristic  pictures.  In  the  neck  and  in 
tlie  suprabifurcating  area  of  the  esophagus  frequently  striated,  elongated, 
and  flaky  white  cicatrices  are  outlined  sharply  against  the  rose-red  mucous 
iiKiubraue ;  the  nearer  the  stricture  the  more  numerous  the  cicatrices  upon 
the  mucous  membrane.  The  ring  form,  or  the  beginning  of  an  annular 
stricture,  manifests  itself  either  as  a  cicatricial  funnel  at  the  apex  of  which 
a  more  or  less  circular  or  oval  lumen  is  noted,  or  it  resembles  the  portio 
vaginalis,  from  the  fact  that  the  region  of  the  esophagus  above  it  is  dilated, 
and  with  the  tube  is  uniformly  forced  downward  above  the  invaginating 
stricture.     Only  with  a  very  superficial  cicatricial  formation  does  the  nar- 


DIAGNOSIS  13 

rowed  area,  whose  lumen  is  often  eccentrically  layered  from  contraction  of 
the  cicatrix  and  frequently  resembles  a  folded  diaphragm,  still  show  respira- 
tory movement  and  radial  folds;  the  deeper  the  effect  of  the  caustic,  the 
more  rigid  and  immotile  is  the  area  of  the  stricture.  The  whole  portion 
looks  like  a  canal  partly  or  entirely  covered  with  white  cicatricial  tissue. 
At  other  times  the  mucous  membrane  up  to  the  point  of  stricture  is  a  deep, 
dark  red,  and  shows  a  tendency  to  bleed  readily;  in  the  earlier  stages  of 
the  disease,  and  even  later,  or  as  the  result  of  improper  treatment,  we  find 
ulcerative  areas  between  the  cicatrices. 

If  the  caustic  action  has  been  slight,  the  secondary  cicatricial  formation 
may  be  of  little  extent,  and  after  the  acute  symptoms  have  passed  away  no 
difficulty  in  deglutition  remains;  but  in  several  cases  of  this  kind  I  have 
observed  that  10  to  20  years  later  difficulties  in  deglutition  may  reappear, 
particularly  if  the  food  is  very  coarse;  larger,  poorly  masticated  particles 
may  be  arrested.  Thus,  in  adults,  I  have  twice  been  obliged  to  extract 
coarse  pieces  of  meat,  about  the  size  of  a  thumb- joint,  which  were  arrested 
in  the  upper  third  of  the  esophagus.  In  both  cases  slight  corrosive  strict- 
ures were  present  which  had  been  formed  in  earliest  childhood.  Up  to 
that  time  the  patients  had  ingested  their  food  without  any  difficulty,  and 
scarcely  remembered  the  early  disease  of  the  esophagus.  In  both  instances, 
the  esophagoscope  revealed  a  marked  injection  in  that  portion  of  the  esopha- 
gus in  which  the  bolus  was  arrested.  Only  in  one  of  the  patients  was  there 
a  distinct  cicatrix.     With  care  further  consequences  were  averted. 

Stenoses  due  to  other  ulcerative  processes  are  very  rarely  multiple. 
Mostly  limited  to  a  portion  of  the  wall,  the  contracting  cicatrix  draws  the 
corresponding  portion  of  the  retained  mucous  membrane  toward  it,  and 
thus  the  stenoses  cause  diverticuli  and  valve  formation.  It  may  then  hap- 
pen that  if  the  bougie  is  caught  in  the  narrowing,  it  may  appear  of  great 
extent,  while,  at  other  times,  quite  a  large  tube  may  be  passed  with  ease. 
The  differentiation  of  cicatricial  strictures  according  to  the  nature  of  the 
ulcerative  processes  to  which  they  are  due  is  very  difficult,  and  even  impos- 
sible except  in  the  ease  of  the  ulcer  due  to  caustics.  We  consider  chiefly 
syphilitic,  tuberculous,  peptic,  and  diphtheritic  ulcerations.  In  doubtful 
cases  the  presence  of  syphilis  and  tuberculosis  will  aid  in  the  diagnosis; 
peptic  ulcers  occur  only  in  the  lower  third  of  the  esophagus,  and  there  are 
usually  accompanying  symptoms  which  point  to  gastric  ulcer.  I  treated 
successfully  a  case  of  stricture  of  the  esophagus  following  scarlatinal  diph- 
theria. Naturally  here  also  the  preceding  disease  is  a  guide  to  the  diag- 
nosis. In  conclusion  we  must  consider  cicatricial  constrictions  which  have 
their  origin  in  peri-esophageal  processes  which  start  from  the  lymph-glands, 
secondarily  producing  ulceration  of  the  esophagus,  which,  in  case  healing 
occurs,  results  in  stenosis  of  the  lumen. 

The  finer  differentiation  of  cicatricial  strictures  according  to  their  gen- 
esis is  not  of  practical  importance.     It  is,  however,  always  an  advantage 


14  STENOSIS  OF  THE  ESOPHAGUS 

to  obtain  a  clear  picture  of  the  anatomic  condition  by  aid  of  the  esophago- 
scope,  and  thus  determine  whether  or  not  florid  inflammatory  processes  are 
present,  and  whether  carcinoma,  especially,  can  be  excluded. 

Of  great  import  is  the  recognition  of  stenosis  due  to  spasm  of  the 
esophagus.  By  the  pathologic  contraction  of  a  layer  of  the  annular  fibers 
of  the  musculature,  a  segment  of  the  esophagus  becomes  impermeable,  or 
can  only  be  passed  with  difficulty.  The  obstruction  to  deglutition  resulting 
from  this  is  of  varying  duration  and  intensity,  and  occasionally  is  also 
accompanied  by  painful  sensations.  The  spasm  may  be  transitory  or  per- 
manent; sometimes  the  affection  persists  uninterruptedly  for  weeks  or 
months  or  even  for  years,  occasionally  it  is  intermittent,  and  at  other  times 
only  occurs  after  a  definite  irritation  from  food.  In  many  cases  this 
esophagismus  accompanies  hysteria  and  neurasthenia,  epilepsy,  chorea,  and 
tetanus;  it  is  an  invariable  and  most  important  symptom  of  hydrophobia. 
Occasionally  it  is  one  of  the  manifestations  of  disease  of  the  central  nervous 
s}steni ;  very  frequently  it  is  reflex.  Thus,  a  spasm  may  prevent  the  ingress 
of  our  instrument,  even  of  a  soft  tube;  foreign  bodies,  coarse  food,  irrita- 
tive fluids,  anything  that  produces  decided  retching,  may  give  rise  to  stub- 
born spasm.  Above  all,  spasm  is  frequently  a  concomitant  symptom  of 
other  diseases  of  the  esophagus.  Every  anatomical  process  in  the  esophagus 
may  be  accompanied  by  spasm.  Diseases  of  other  organs  may  produce  the 
spasm ;  affections  of  the  pharynx  and  larynx,  of  the  stomach  and  intestine, 
of  the  male  and  female  genital  organs,  may  be  its  etiologic  basis,  and 
trauma,  which  directly  affects  the  head  of  the  thorax,  may  cause  reflex 
spasm.  The  appearance  of  spasm  in  certain  intoxications  (from  bella- 
donna, from  strychnin,  from  sausage,  etc.),  following  refrigeration  with 
or  without  rheumatic  affection  of  the  joints  and  muscles,  and  with  or  with- 
out catarrhal  affections  of  the  larynx  and  pharynx,  is  worthy  of  mention. 

This  neurosis  shows  itself  chiefly  by  dysphagia.  The  nature  of  the 
difficulty  in  deglutition  is  often  not  characteristic;  the  symptoms  are  the 
same  as  those  complained  of  by  patients  with  stenosis  of  the  esophagus 
from  other  causes.  Occasionally  the  spasm  is  accompanied  by  dull  pressure 
in  the  chest,  by  a  painful  feeling  of  constriction,  by  lancinating  or  burning 
pains  in  the  neighborhood  of  the  esophagus,  for  example,  in  the  shoulder 
or  tlie  neck,  or  it  follows  these  symptoms.  Spasm  of  the  muscles  of  the 
pharynx,  of  the  larynx,  of  the  trunk,  and  of  the  extremity  may  coexist  and 
alternate  with  esophagospasm,  particularly  in  those  cases  in  which  a  gen- 
eral neuiosis  is  the  foundation  of  the  affection.  The  degree  of  hindrance 
in  deglutition  varies  greatly.  Only  rarely  is  the  esophagus  absolutely, 
or  almost  wholly,  impermeable  for  a  long  time;  in  these  eases  severe  inani- 
tion may  result,  and  the  patient  finally  perish  from  the  neurosis.  This 
(lyspliaiiia  may  appear  in  dissimilar  forms.  Sometimes  the  patients  ex- 
j»erience  only  the  sensation  of  an  arrest  of  the  food,  and  by  the  aid  of  a 


DIAGNOSIS  15 

few  deep  inspirations,  or  by  swallowing  some  fluid,  the  bolus  finally  reaches 
the  stomach;  or  the  first  food  is  regurgitated  while  that  subsequently 
taken  passes  without  difficulty.  In  some  cases  the  spasm  shows  itself  only 
upon  abnormal  irritation,  for  example,  during  probing  or  when  certain 
foods  are  taken,  usually  coarse  food  or  solid  food  in  general ;  but  we  some- 
times meet  a  patient  who  finds  fluids  more  difficult  to  swallow  than  solid 
food.  Occasionally  the  spasm  occurs  only  at  certain  times  of  the  day,  or 
during  the  course  of  prolonged  meals. 

In  spite  of  the  fact  that  some  of  these  disturbances  we  have  mentioned 
certainly  arise  only  under  the  influence  of  a  derangement  of  innervation, 
positive  proof  that  we  are  dealing  only  with  a  nervous  affection  can  never 
be  attained  in  the  given  case  by  the  history  and  the  subjective  observation 
of  the  patient.  The  diagnosis  of  spasm  is  rarely  easy.  The  most  useful 
points  of  support  for  the  recognition  of  the  neurosis  from  the  subjective 
and  objective  symptoms  will  now  be  briefly  described. 

The  sudden  appearance  of  difficulty  in  deglutition,  particularly  of  fluid 
food,  indicates  the  presence  of  spasm,  and  still  more  so  the  intermittence 
of  the  attacks,  which  may  be  quite  irregular  or  be  produced  by  very  definite 
influences,  partly  nervous,  the  intensity  and  duration  of  which  vary.  Dif- 
ferences in  the  degree  of  permeability  of  the  esophagus  is  a  conspicuous 
symptom  favoring  spasm ;  the  first  food  may  be  arrested,  the  succeeding  may 
pass,  or,  the  first  masses  of  food  may  pass  readily,  and  then,  without  assign- 
able cause,  a  sudden  stoppage  occurs.  More  important  is  a  variation  in  the 
seat  of  the  constriction,  so  that,  for  example,  on  one  day  the  upper,  and 
upon  another  day  the  lower,  third  of  the  esophagus  becomes  impermeable. 
But  this  is  a  very  rare  symptom,  and  is  only  found  as  an  accompaniment 
of  severe  nervous  affections.  An  absolute  diagnosis  of  this  condition  can 
only  be  made  by  means  of  the  bougie  and  the  esophagoscope.  The  first 
sounding  should  take  place  with  a  rigid  instrument,  as  this  will  more  cer- 
tainly pass  the  axis  of  the  organ  than  a  soft  one,  which  is  easily  bent.  If 
we  probe  during  a  time  when  the  difficulty  in  deglutition  exists,  a  resist- 
ance must  be  objectively  noted.  After  a  short  pause,  or  on  moderate 
pressure,  it  may  disappear,  for  there  are  many  mild  forms  of  spasm,  but 
it  must  positively  be  present.  It  is  worthy  of  note  that  the  resistance  may 
be  caused  to  disappear  by  probing,  by  means  of  which  we  force  the  patient 
repeatedly  to  swallow  very  rapidly,  and  this  brings  about  a  more  decided 
innervation  of  the  longitudinal  muscles  of  the  esophagus,  therefore,  the 
dilators,  and  thus  we  overcome  at  least  moderate  grades  of  spasm.  More- 
over, probing  may  reveal  a  variation  in  the  degree  of  permeability  and  in 
the  seat  of  the  constriction  which  is  often  of  decisive  import. 

By  means  of  the  esophagoscope  we  are  enabled  to  recognize  other  esopha- 
geal diseases,  and  positively  to  diagnosticate  spasm;  for  this,  as  a  rule, 
usually  gives  a  characteristic  picture, — sharply  rising  folds  of  mucous  mem- 
brane which  converge  toward  a  point  in  the  middle  of  the  lumen  and  form 


16  STENOSIS  OF  THE  ESOPHAGUS 

a  rosette-like,  more  or  less  rigid  closure.  The  lumen,  if  it  can  be  recognized 
at  all,  is  narrow.  Only  upon  deep  inspiration  or  on  coughing  are  fluids 
(mucus,  gastric  contents)  and  air  regurgitated  through  the  narrow  open- 
ing, not  rarely  accompanied  by  a  hissing  or  gurgling  murmur.  The  mucous 
membrane  of  the  contracted  portion  of  the  esophagus  shows  abnormal,  in- 
tense reddening.  Occasionally  the  mucosa  is  found  eroded,  particularly 
in  the  region  where  regurgitation  or  stagnation  has  occurred. 

If  an  examination  be  made  during  a  time  free  from  attacks,  all  the 
previously  mentioned  criteria  may  be  absent,  but  a  negative  finding,  in 
particular,  is  of  diagnostic  value.  The  determination  of  the  previously 
mentioned  causes  of  spasm  is  an  important  aid:  The  proof  of  another 
affection  of  the  esophagus  coexisting,  the  recognition  of  a  local  affection 
of  which  the  spasm  of  the  esophagus  may  he  the  reflex  symptom.  Above 
all,  we  must  consider  the  status  of  the  nervous  system;  but  even  if  dis- 
ease of  this  region  be  unquestionably  present,  it  does  not  permit  a  con- 
clusion regarding  the  character  of  a  coincident  difficulty  in  deglutition. 
This  must  be  borne  in  mind  if  we  would  avoid  falling  into  gross  error. 
Inversely,  we  should  observe  that  in  true  spasm  also  the  difficulty  in 
deglutition  may  progressively  increase,  that  extreme  cachexia  may  also 
develop,  and  that  more  or  less  complete  impermeability  of  the  esophagus 
may  persist  stubbornly  for  months  and  years. 

Congenital  stenoses  of  the  esophagus,  from  the  onset,  either  make  life 
impossible,  or  they  manifest  themselves  by  a  difficulty  in  deglutition  which 
appears  in  early  youth;  it  must  be  remarked  here  that  congenital  dilatation 
of  the  organ  (anterior  stomach)  may  give  rise  to  symptoms  similar  to  those 
of  stenosis.  If  it  is  possible  to  demonstrate  that  considerable  masses  of 
food  are  retained  in  the  esophagus,  this  is  proof  that  dilatation  at  least 
is  present;  whether  beneath  this  a  constriction  also  exists  can  only  be 
determined  by  the  sound  and  the  esophagoscope. 

Occlusion  stenoses,  to  the  description  of  which  we  now  turn,  are  due 
to  impaction  by  foreign  bodies  which  are  arrested  in  the  esophagus;  they 
occlude  the  passage  more  or  less  completely,  irritate  the  mucous  membrane, 
and  eventually  may  produce  phlegmons  and  perforation.  Even  very  small 
objects,  for  example,  small  fish  bones,  by  giving  rise  to  local  irritation  and 
spasm,  may  cause  pain  and  symptoms  of  stenosis;  and,  even  if  the  foreign 
body  is  not  arrested  but  reaches  the  stomach,  erosions  and  fissures  which 
it  produces  in  the  mucous  membrane  may  cause  the  same  symptoms.  On 
the  contrary,  it  will  be  observed  that  not  only  small  but  also  comparatively 
large  foreign  bodies,  for  example,  a  plate  of  false  teeth,  may  be  arrested 
in  the  esophagus  without  giving  rise  to  decided  subjective,  or  even  marhed 
objective,  symptoms.  For  example,  as  I  myself  have  seen,  a  plate  of  false 
teeth  larger  than  a  silver  half-dollar  may  be  arrested  in  the  upper  third 


DIAGNOSIS  17 

of  the  esophagus  below  the  larynx,  and  lie  with  its  convex  surface  in  the 
concavity  of  the  anterior  wall  of  the  esophagus,  so  that  the  organ  gapes, 
and  thus  not  only  food  but  thick  bougies  may  pass  the  large  foreign  body 
without  difficulty.  In  this  case,  it  had  been  supposed  that  the  plate  of 
false  teeth  was  no  longer  in  the  esophagus,  and  the  symptoms  still  present 
had  been  referred  to  lacerations  in  the  mucous  membrane;  the  true  state 
of  affairs  was  revealed  by  the  esophagoscope. 

Foreign  bodies,  almost  without  exception,  are  arrested  in  the  upper, 
narrower  parts  of  the  esophagus;  when  they  are  found  in  the  lower  por- 
tions they  have  usually  been  forced  down  by  instruments.  With  a  pre- 
viously existing  stenosis  even  a  small  foreign  body,  for  instance,  a  fruit 
kernel,  may  bring  about  complete  obstruction  of  the  esophagus,  and  abso- 
lute impermeability  arises  when  a  spastic  process  of  the  musculature  holds 
a  small  foreign  body. 

If  foreign  bodies  have  been  swallowed,  the  patient  is  generally  aware 
of  it,  and  reports  the  circumstance;  where  no  history  can  be  utilized,  the 
acute  appearance  of  stenosis  at  once  leads  us  to  think  of  obstruction;  but 
also  when  the  stenosis  is  due  to  foreign  bodies,  the  variation  in  permeahility 
occasionally  favors  this  hypothesis.  Temporarily  the  closure  is  complete, 
then  the  foreign  body,  in  consequence  of  a  paroxysm  of  coughing,  or  by 
retching,  changes  its  position,  and  food  now  passes,  perhaps  also  a  bougie. 
But  the  sensation  of  a  foreign  body  being  lodged  in  the  esophagus  mostly 
remains,  and  after  a  short  time  difficulty  in  deglutition  again  becomes 
noticeable. 

The  examination  with  the  bougie  in  doubtful  cases  will  scarcely  show 
the  nature  of  the  obstruction.  By  the  introduction  of  instruments,  we 
are  at  most  only  able  to  determine  that  a  mechanical  obstruction  is  present, 
and  this  is  not  even  certain  in  all  cases;  for  the  probe  may  pass  alongside 
of  the  foreign  body  through  the  lumen  of  the  esophagus.  On  the  other 
hand,  esophagoscopy  always  enables  us  to  make  a  positive  diagnosis.  By 
the  aid  of  the  eye  we  can  extract  the  foreign  body,  or  force  it  down,  and 
readily  cure  any  existing  lesions  in  the  mucous  membrane  by  cauterization. 

The  stenoses  due  to  compression  of  the  esophagus  are  of  the  greatest 
practical  importance.  Any  tumor  formation  in  the  neighborhood  of  the 
organ  may  sooner  or  later  lead  to  compression  of  the  tube.  The  esophagus 
is  naturally  motile,  and  may  deviate.  If,  however,  it  is  completely  sur- 
rounded, or  only  adherent  on  one  side,  symptoms  of  stenosis  appear. 
Goiter  itself  most  readily  causes  difficulty  in  respiration,  but  rarely  dis- 
turbs the  function  of  deglutition;  this  will  occur  if  it  be  very  large,  or  if 
it  surround  the  esophagus  with  greatly  developed  processes,  or  show  ma- 
lignant degeneration.  Carcinoma  of  the  larynx  or  of  the  vertebral  column 
often  interferes  with  the  act  of  deglutition,  and  very  early. 

In  the  thoracic  cavity,  as  well  as  in  the  neck,  the  esophagus  may  deviate 


Ig  STENOSIS  OF  THE  ESOPHAGUS 

from  compression.  Cancer  of  the  lung,  of  the  pleura,  or  of  the  vertebral 
column  must  first  proliferate  into  the  peri-esophageal  tissue  before  produc- 
ing marked  dysphagia.  Enlargement  of  the  tracheobronchial  or  mediastinal 
lymph-glands  from  cancer,  tuberculosis,  or  syphilis  more  frequently  dis- 
turbs the  act  of  deglutition;  as  the  result  of  purulent  liquefaction  of  the 
glands,  broncho-esophageal  fistula  may  form,  and  later,  upon  cicatrization, 
true  stenosis  or  traction  diverticulum  may  develop.  A  massive  pericarditis 
or  a  cor  bovinum  scarcely  ever  produces  dysphagia,  and  only  exceptionally 
will  tlie  pressure  of  an  aortic  aneurysm  narrow  the  lumen  of  the  esophagus. 
Tbese  patients  more  frequently  complain  of  constriction  and  difficulty  of 
respiration  upon  swallowing  than  of  actual  difficulty  in  forcing  their  food 
downward.  The  disturbances  in  deglutition  from  the  presence  of  a 
diverticulum  of  the  esophagus  are  due  to  various  causes,  and  compression  of 
the  organ  by  the  filled  sac  is  only  one  of  the  most  important,  but,  neverthe- 
less, must  be  taken  into  consideration.  The  filled  diverticulum  may  un- 
questionably completely  occlude  the  passage  into  the  stomach.  If  it  is 
empty,  food  as  well  as  the  sound  will  often  pass.  This  variation  in  the 
jHTineability  has  a  certain  diagnostic  importance. 

The  dili'erentiation  between  compression  stenosis  and  other  forms  of 
narrowing  of  the  esophagus  is  frequently  not  easy.  Of  utmost  consequence 
here  is  the  differentiation  of  compression  of  the  esophagus  hy  disease  of 
the  neighboring  organs  from  cancer  of  the  esophagus.  In  the  esophagoscope 
the  picture  of  compression  stenosis  may  resemble  that  which  we  observe 
where  there  are  infiltrating  tumors  of  the  organ.  From  one  side  a  tumor 
with  smooth,  reddened  mucous  membrane  protrudes  into  the  lumen,  and 
does  not  change  its  position  upon  respiration.  The  lumen  of  the  organ 
deviates  toward  the  side  and  is  recognized  as  a  small  semilunar  space,  or 
it  shows  a  funnel  shape  gradually  tapering  downward.  This  finding  is 
not  uniform ;  it  may  also  occasionally  be  noticed  in  carcinoma.  For  the 
diagnosis  of  compression  stenosis  the  e.Tamination  of  the  thorax  often  reveals 
exact  grounds  of  support;  a  retardation  of  one-half  of  the  thorax  upon 
respiration,  the  conspicuous  appearance  of  veins  upon  the  skin  of  the  chest, 
dulness  or  abnormal  pulsations,  are  important  factors;  expectoration,  par- 
ticularly if  hemorrhagic,  true  hemoptysis,  the  signs  of  infiltration  of  the 
lung,  exudation  into  the  pleura,  painful  points  upon  the  vertebral  column, 
all  aid  us  in  the  recognition  of  the  underlying  condition.  Finally,  in 
stenosis  of  the  lumen  by  compression,  the  nature  of  the  dysphagia  and  the 
results  of  probing  may  be  characteristic.  Occasionally,  a  crass  disproportion 
may  be  determined  between  the  results  of  probing  and  the  ability  to  swal- 
hiw.  Such  a  disproportion  is  also  found  in  atony  and  paralysis  of  the 
esophagus,  in  tumors  developing  in  the  walls  of  the  organ,  occasionally  also 
when  foreign  bodies  are  present,  and  in  hyperesthetic  conditions,  but  in 
(omprossion  this  symptom  is  of  special  import.  While  with  atony  and 
paralysis  of  the  esophagus  the  sound  invariably  passes  unarrested  into  the 


TREATMENT  19 

stomach,  in  compression  we  note  resistance  whenever  the  instrument  is 
passed;  this  is  usually  slight,  and  may  be  overcome  with  comparative  ease 
by  the  use  of  moderate  force;  even  a  very  thick  tube  may  pass  under  these 
circumstances,  while  the  patient  is  scarcely  able  to  swallow  thin  fluid.  The 
muscles  lack  the  power  to  do  what  the  pressure  of  the  hand  which  guides 
the  sound  can  achieve.  Moreover,  it  is  noteworthy  that  in  these  cases  of 
compression  forced  proHng,  provided  an  aneurysm  is  not  present,  is  not 
dangerous  and  is  well  home;  traces  of  blood  are  scarcely  ever  noted  upon 
the  bougie  or  in  the  fenestra  of  the  tube,  which,  without  exception,  is  always 
the  case  in  carcinoma  if  the  esophagus  be  energetically  sounded.  Where 
such  a  result  of  probing  is  combined  with  the  esophagoscopic  finding 
sketched  above,  carcinoma  of  the  esophagus  may  be  certainly  excluded,  for 
with  a  carcinomatous  infiltration  of  the  esophagus  producing  a  prominent 
tumor,  such  as  we  have  described  above,  the  lumen  of  the  organ  must,  under 
all  circumstances,  be  decidedly  narrowed,  and  we  find  it  is  impossible  to 
pass  a  thick  sound. 

The  differentiation  from  one  another  of  the  various  kinds  of  stenosis 
which  we  have  here  separately  analyzed  is  of  the  utmost  practical  value; 
it  is  naturally  not  always  possible  to  make  an  exact  diagnosis,  but  much  is 
already  gained  if  we  are  able  positively  to  exclude  carcinoma. 

If  it  be  doubtful  whether  cancer  is  present  or  not,  and  in  my  opinion 
this  is  frequently  the  case,  in  the  interest  of  the  patient  all  possibilities 
should  be  carefully  investigated  and  treatment  be  directed  accordingly. 
Thus,  in  the  last  few  years,  I  have  been  able  by  energetic  iodin  treatment 
to  keep  alive  two  cases  of  suspected  carcinoma  of  the  esophagus,  because 
I  made  a  correct  diagnosis  of  compression  stenosis  of  the  esophagus,  and 
was  right  in  assuming  syphilitic  enlargement  of  the  glands  to  be  the  cause 
of  the  obstruction. 

In  many  cases,  even  by  the  aid  of  the  esophagoscope,  it  is  impossible 
absolutely  to  define  the  difficulty,  but  this  must  not  prevent  us  from  mak- 
ing every  effort  to  clear  the  complicated  situation.  Certainly  the  great 
majority  of  cases  of  stenosis  of  the  esophagus  are  incurable,  but,  in  the 
minority  in  which  the  affection  is  recognized,  therapeutic  success  is  possible, 
and,  even  if  we  do  not  cure  the  others,  we  can  benefit  them  by  treatment, 
and,  by  the  clear  insight  which  we  have  obtained  of  the  character  of  the 
disturbance,  can  bring  about  a  decided  amelioration. 

TREATMENT 

In  the  treatment  of  all  stenoses  of  the  esophagus  some  general  thera- 
peutic rules  are  operative  concerning  hygiene  and  dietetics.  As  the  total 
intake  of  food  is  frequently  lessened  on  account  of  the  difficulty  of  degluti- 
tion, such  patients  emaciate,  even  in  cases  in  which  there  is  no  malignant 
process.     Accordingly  a  leading  and  important  object  of  treatment  is  to 


20  STENOSIS  OF  THE  ESOPHAGUS 

produce  a  favorable  influence  upon  nutrition.  Nourishment  should  always 
be  plentiful,  and,  under  some  circumstances,  it  should  be  calculated  to  in- 
crease flesh.  It  need  scarcely  be  mentioned  that  in  the  solution  of  this 
problem  great,  frequently  insurmountable,  difficulties  are  opposed,  yet  even 
here  much  may  be  attained  by  the  proper  choice  of  food,  and  by  the  utiliza- 
tion of  all  auxiliary  methods  for  artificial  nutrition.  We  should  make  it 
a  rule  that  the  patients  take  only  such  food  as  we  know  will  pass  easily 
through  the  narrow  space;  for  it  is  possible  to  take  sufficient  food  even 
though  it  be  in  the  thinnest  of  fluids.  Trials  with  coarser  food,  in  many 
cases,  only  increase  the  local  irritation,  and  thereby  make  it  more  difficult 
to  swallow  liquid  food.  Large  particles  may  he  arrested,  and  thus  render 
the  stenosis  completely  impermeable;  connective  tissue  shreds,  in  particu- 
lar, which  adhere  to  particles  of  fat  and  meat,  obstruct  with  extraordinary 
ease  a  lumen  which  is  already  narrowed.  For  this  reason  we  must  exercise 
the  greatest  care  to  have  the  particles  of  meat,  vegetable,  etc.,  as  small  as 
possible,  and  where  we  are  not  certain  that  the  patient  masticates  the  food 
thoroughly  with  his  teeth,  these,  so  far  as  permitted,  should  only  be  given 
in  a  crushed  form.  That  foods  with  skin,  stems,  kernels,  and  husks  are 
forbidden  is  self-evident,  but  even  highly  seasoned  or  spiced  food  (mustard, 
etc. ) ,  concentrated  alcohol,  or  very  acid  foods,  are  to  be  avoided  on  account 
of  their  irritative  effect.  The  same  is  true  of  extremes  of  temperature. 
Lukewarm  or  slightly  cooled  fluids  are  easiest  to  swallow,  and  this  does 
not  contradict  the  fact  that  occasionally,  where  there  is  marked  congestion 
and  swelling,  ice  may  be  well  borne;  food  of  a  low  temperature  is  not 
suitable  for  prolonged  use,  as  it  unfavorably  influences  gastric  activity. 

Naturally,  the  food  in  its  composition  should  contain  all  the  important 
nutritive  elements,  and  as  we  are  able  to  administer  not  only  salts  and  carbo- 
hydrates but  even  fats  and  proteids  (the  latter,  for  example,  in  the  form 
of  artificial  foods)  in  a  form  soluble  in  water,  it  is  quite  possible  to  nourish 
the  patient  sufficiently  in  those  cases  in  which  only  a  thin  fluid  passes.  I 
attach  especial  importance  to  the  administration  of  fat  in  the  form  of  melted 
l)iitter,  or  olive  oil,  or  cream.  Apart  from  the  high  combustion  value  by 
wliich  it  is  distinguished  above  all  other  food,  it  is  particularly  advisable 
because  it  makes  the  bolus  soft  and  slippery,  and  because,  adhering  to 
the  mucous  membrane,  it  protects  the  same,  thus  diminishing  the  irrita- 
bility of  the  inflamed  parts;  sometimes  it  will  trickle  through  a  stricture 
when  even  water  is  regurgitated. 

The  arrangement  of  meals  and  the  manner  in  which  they  are  eaten  is 
of  vital  importance.  All  over-exertion  of  the  diseased  organ  should  be 
avoided.  The  patients  are  therefore  advised  to  swallow  slowly,  with  pauses 
hctwecn;  where  compact  food  is  taken,  the  ingestion  of  thin  fluid  after  each 
l)itc  will  facilitate  its  passage.  Each  meal,  therefore,  should  consume  a 
comparatively  long  time,  even  when  only  small  amounts  of  food  are  eaten, 
but  tliis  does  not  matter;  such  patients  should  be  encouraged  to  eat  very 


TREATMENT  21 

often.  That  mental  rest  and  bodily  relaxation  are  beneficial  here  is  true, 
all  the  more  so  as  unfavorable  nervous  influences  very  readily  aggravate 
the  disturbance  in  swallowing,  even  in  those  cases  in  which  a  carcinoma 
is  present.  The  avoidance  of  all  unnecessary  exertion  is  absolutely  essen- 
tial for  the  purpose  we  have  in  view,  namely,  to  improve  the  nutrition. 
Not  rarely  we  observe  that  with  complete  rest  in  bed  the  power  of  swallow- 
ing improves.  It  need  hardly  be  mentioned  that  everything  that  stimu- 
lates the  appetite  and  increases  the  power  of  assimilation  (fresh  air, 
massage,  wine,  etc.)  will  aid  in  the  treatment. 

Further  curative  measures  in  patients  with  stenosis  of  the  esophagus 
depend  upon  the  nature  of  the  underlying  process.  Let  us  first  consider 
the  treatment  in  the  cases  which  are  in  the  majority,  in  carcinoma.  The 
object  in  cancer  is  this,  to  maintain  the  patient  in  such  a  condition  that 
he  is  able  to  ingest  fluid  or  pappy  food  readily,  or,  at  least,  without  decided 
difficulty.  We  attempt  to  keep  the  stenosis  from  becoming  impermeable, 
but  it  is  not  our  aim  to  extend  our  therapeutic  endeavors  beyond  the  limit 
just  mentioned,  and  to  bring  about  greater  ease  in  swallowing  more  com- 
pact food  no  matter  at  what  cost.  If  it  is  clear  to  us  to  what  the  dysphagia 
in  cancer  of  the  esophagus  is  due,  the  two  possibilities  which  are  present 
here,  and  to  which  I  have  already  called  attention,  will,  above  all  else, 
prevent  this.  In  the  first  place  the  disturbances  in  deglutition  are  pro- 
duced by  a  mechanical  obstruction,  by  infiltration  of  the  walls,  or  by  the 
proliferating  neoplasm.  The  second  factor  of  no  less  consequence  is  the 
damage  to  the  nervous  and  muscular  apparatus  of  the  esophagus,  which, 
in  some  of  the  cases,  is  in  an  extremely  irritable  condition,  and  reacts 
abnormally  as  soon  as  food  reaches  the  ulcerated,  inflamed  area.  This 
reaction  frequently  manifests  itself  as  spasm,  during  which  not  a  drop 
of  fluid  will  pass  the  stricture,  yet  the  same  patient,  after  a  preceding 
hypodermic  injection  of  morphin,  may  readily  swallow  solid  food.  At  other 
times  atonic  conditions  react  unfavorably  upon  deglutition  in  that  portion 
above  the  cancer,  and  even  in  the  areas  in  which  there  is  no  dilatation. 
From  hyperesthesia  of  the  inflamed  parts,  by  over-exertion,  etc.,  irregularity 
and  weakness  of  function  may  arise  and  lead  to  an  interruption,  or,  at  least, 
to  a  disturbance  of  peristalsis  which  manifests  itself  by  an  unfavorable 
influence  on  the  muscles,  sometimes  the  longitudinal,  at  other  times  the 
annular,  the  final  result,  however,  being  the  same,  namely,  a  disturbance 
of  deglutition. 

If  we  observe  these  points,  we  must  distinguish  the  treatment  of  me- 
chanical obstruction  from  that  of  irritative  conditions  and  atony.  The 
former  is  a  very  unsuitable  point  toward  which  to  direct  our  treatment; 
in  general  more  harm  is  done  here  than  good,  yet  all  the  more  must  we 
attempt  to  relieve  the  local  irritation  and  weakness.  Besides  a  bland  diet, 
we  must  prohibit  any  food  that  does  not  pass  easily,  anything  that  may 


22  STENOSIS  OF  THE  ESOPHAGUS 

cause  regurgitation,  and  must  consider  an  anesthetic  process.  Morphin 
administered  internally  is  often  beneficial;  the  objections  to  its  prolonged 
use  (becoming  accustomed  to  the  poison,  and  loss  of  appetite)  are  naturally 
not  slight.  Morphin  may  be  administered  alone,  or  in  combination  with 
eocain  or  antipyrin  or  menthol  in  the  form  of  compressed  tablets,  which 
are  slowly  dissolved  in  the  mouth;  I  use  these  very  frequently  in  high- 
seated  carcinomata  which  are  near  the  larynx  and  pharynx,  or  which  attack 
these  organs  (for  example,  morphin  muriate  0.0025,  eocain  0.0025,  anti- 
pyrin 0.1,  sacch.  0.3.  M.  f.  tabl.  compr.  dos.  30;  one  tablet  several  times 
daih',  immediately  before  eating). 

Where  morphin  fails  of  success,  I  resort  to  local  anesthesia.  With  the 
aid  of  the  esophageal  syringe  devised  by  me  (a  simple  syringe  with  a 
capacity  of  about  3  grams,  and  to  which  a  fine  tube  of  about  25  to  35  cm. 
in  length  is  attached)  I  inject,  reaching  the  point  of  the  affection,  a  three 
to  five  per  cent,  eucain  solution,  at  first  twice  daily,  later  less  frequently: 
doses  of  from  2  to  3  grams  of  the  solution  per  day  are  well  borne  and  do 
not  give  rise  to  symptoms  of  intoxication.  There  are  also  cases  in  which 
cauterization  of  the  hyperesthetic  inflamed  mucous  membrane  with  a  1-3 
j)er  cent,  silver  nitrate  solution  may  prove  beneficial.  The  improvement 
is  sometimes  remarkable,  even  though,  for  the  most  part,  only  transitory; 
but,  nevertheless,  this  process  assists  materially  in  attaining  the  object 
sketched  above,  namely,  the  retention  of  the  patient's  ability  to  swallow 
fluid  and  pappy  food.  The  process  of  injection  is  quite  simple,  and  may 
be  employed  by  any  physician;  it  can  never  do  harm,  but  only  good.  The 
same  may  be  said  of  mild  measures  to  combat  atonic  and  ectatic  conditions 
— here,  above  all,  mild  lavage  of  the  esophagus  with  the  same  instrument 
which  we  employ  for  the  stomach  is  advisable  and  readily  carried  out; 
mucous  masses,  obstructing  coagula,  remains  of  food,  foreign  bodies,  products 
of  decomposition,  etc.,  are  thus  removed,  and,  simultaneously,  this  cleans- 
ing process  acts  also  as  a  kind  of  massage,  and  has  a  tonic  effect  upon 
the  muscle. 

All  of  these  auxiliary  measures  are  more  worthy  of  trial  in  the  treat- 
ment of  (lie  carcinoma  than  probing,  by  which  the  mechanical  obstruction 
whicli  causes  the  disturbance  is  increased.  In  my  experience  the  majority 
of  all  malignant  neoplasms  are  unsuitable  for  treatment  by  the  sound, 
and  only  in  a  few  cases  have  I  been  convinced  of  an  improvement  in  degluti- 
tion  by  this  process.  So  long  as  the  patients  are  able  to  swallow  fluid  and 
pnppi/  food,  I  avoid  every  process  which  dilates  mechanically.  In  such 
cases  we  must  be  content  with  the  existing  condition,  for  the  probability 
of  attaining  anything  more  satisfactory  by  sounding  is  very  slight.  If  the 
ability  to  swallow  is  markedly  disturbed,  so  that  deglutition  of  thin  fluids 
is  only  accomplished  with  extreme  difficulty,  if  anesthetics  do  not  relieve 
the  condition,  if  lavage  simultaneously  is  without  result,  we  can  no  longer 
refrain  from  dilating  the  stricture.     It  must  be  borne  in  mind  that  sound- 


TRK\TMENT  23 

ing  is  never  an  insignificant  procedure;  it  increases  the  irritability  of  the 
organ,  the  tendency  to  hemorrhage  and  ulceration,  and  adds  to  the  danger 
of  perforation. 

In  probing,  the  hollow,  fenestrated,  hard  rubber  instruments  may  be 
used  with  advantage  after  being  previously  softened  in  warm  water,  but, 
nevertheless,  by  bending  in  the  stricture,  or  even  before  they  reach  it,  these 
are  soon  worn  out.  Solid  bougies  of  the  same  material  with  a  button-shaped 
or  pointed  end  are  more  satisfactory,  although  they  are  not  much  more  dura- 
ble. I  have  for  years  frequently  employed  bougies  which  were  manufac- 
tured for  me  after  Crawcour's  method.  They  are  made  from  rolled  sheet 
metal,  cut  into  spirals,  the  flexible  part,  40  cm.  long,  making  up  the  coils ; 
they  terminate  in  a  button-like  attachment  about  1^  cm.  in  length,  the  upper 
part  consisting  of  a  solid  steel  handle  10  cm.  in  length.  They  are  very 
flexible,  find  their  way  into  the  stricture  even  if  it  is  excentrically  situated 
more  readily  than  other  sounds,  and  are  almost  indestructible  if  kept  clean 
(a  diluted  lysol  solution  and  subsequent  drying  by  heat  are  sufficient  for 
cleansing  purposes).  In  carcinoma  we  must  be  extremely  cautious  in  the 
passage  of  the  sound,  and  never  employ  the  slightest  degree  of  force.  The 
sound,  which  will  barely  pass,  is  allowed  to  remain  for  a  few  minutes;  it 
should  be  introduced  every  other  day,  not  oftener,  for  the  diseased  mass 
reacts  to  every  irritation,  bleeds  readily,  and  thus  edema  and  pain  are 
rapidly  produced.  Often  it  is  difficult  to  reach  the  narrow  canal  from  the 
dilated  portion  above  the  stenosis,  especially  as  this  passage  is  not  always 
straight;  portions  of  the  tumor  may  occlude  the  opening,  or  the  sound 
may  bend  and  be  pressed  against  the  wall  of  the  organ,  where  even  slight 
pressure  may  be  followed  by  the  most  serious  consequences.  If  the  open- 
ing into  the  canal  is  not  readily  found,  further  manipulation  should  be 
stopped  for  a  time;  if,  however,  we  succeed  in  passing  an  instrument  of 
considerable  size,  at  the  next  trial  we  should  try  most  carefully  to  pass  one 
a  size  larger.  If  we  succeed  in  this,  a  still  larger  one  may  later  be  used. 
In  the  main,  we  must  be  careful  to  use  no  force  in  this  method  of  treat- 
ment, but  should  rather  be  content  with  moderate  success,  and  avoid  too 
frequent  and  too  prolonged  soundings. 

It  will  not  rarely  surprise  us  that  although,  for  example,  No.  5  passes 
readily,  at  the  next  attempt  No.  2  can  hardly  be  passed  through  the  obstruc- 
tion; acute  swellings  have  appeared,  or  the  tumor,  in  consequence  of  irrita- 
tion, shows  a  more  pronounced  growth  into  the  lumen  of  the  canal.  On 
the  other  hand,  it  may  happen  that  the  narrow  passage  will  suddenly  become 
permeable  for  compact  food  and  thicker  bougies  owing  to  the  removal  of 
obstructions  by  ulcerative  decomposition  on  the  part  of  the  tumor  masses. 
If  it  is  impossible  to  introduce  a  bougie  in  the  usual  manner  through  the 
narrowed  esophagus,  the  attempt  may  be  made  with  the  patient  in  the 
recumbent  posture,  eventually  ivith  the  aid  of  the  esophagoscope;  instead 
of  working  in  the  dark  we  may  occasionally  find  the  entrance  to  the  canal 


24  STENOSIS  OF  THE  ESOPHAGUS 

immediately,  and  we  may  sometimes  succeed  in  cases  where  we  have  pre- 
viously failed.  For  this  purpose  I  employ  spiral  bougies  (see  above)  or 
l^nglish  bougies  with  a  solid  metallic  guiding  staff. 

For  dilatation  of  esophageal  stenosis,  still  other  instruments  have  been 
('mj)loyed.  Senator  was  the  first  to  introduce  laminaria  tents  of  varying 
thickness  into  the  carcinomatous  stricture  to  attain  a  dilatation  by  their 
gradual  swelling.  The  laminaria  tent  was  fastened  by  a  screw  to  a  thin, 
liexihle  bougie.  I  have  entirely  abandoned  this  method  in  the  treatment 
of  carcinoma;  but  the  idea  may  be  well  utilized  in  the  dilatation  of  other 
strictures  if  the  laminaria  tents  armed  with  a  silk  thread  under  the  direc- 
tion of  the  eye  and  by  the  aid  of  the  esophagoscope  are  introduced  into 
the  narrow  passage,  and  are  permitted  to  remain  from  three  to  ten  hours, 
perhaps  even  longer,  and  the  tents  are  then  drawn  up  by  the  silk  threads. 
Dilatation  may  thus  be  promoted  with  extraordinary  rapidity.  We  may 
soon  convince  ourselves  that  there  is  no  danger  in  this  process,  and  in  des- 
perate cases  I  have  obtained  from  it  excellent  results  (see  below). 

To  produce  a  slow  and  careful  dilatation,  Schreiber  advises  a  dilator 
consisting  of  an  ordinary,  thin,  non-fencstrated  stomach-tube,  at  the 
osopliagoal  end  of  which  a  rubber  tube  3  to  3  cm.  in  length  is  attached, 
which  again  terminates  in  a  smooth  firm  point.  At  the  opposite  end  of 
the  sound  there  is  a  metallic  attachment  which  is  connected  with  a  suitable 
syringe  having  a  capacity  of  from  10  to  30  c.c.  The  sound  is  introduced 
through  the  narrow  passage,  water  being  injected  into  the  sound  so  that 
the  rubber  piece  fills  and  expands.  The  tense,  elastic  balloon  we  now 
attempt  to  withdraw  through  the  narrow  passage.  This,  in  fact,  is  ex- 
tiemely  difficult,  but  with  great  care  quite  decided  pressure  is  exerted  upon 
the  internal  walls  of  the  stenosed  area.  This  process  I  very  rarely  employ 
in  carcinomatous  strictures,  as  they  are  generally  too  unyielding  to  respond 
to  the  pressure.  But  the  method  is  well  adapted  to  soft,  recent,  cicatricial 
tissue,  and  to  overcoming  spastically  stenosed  areas. 

[Professor  B.  AV.  Sippy,  of  Chicago,  has  invented  an  instrument  for 
the  dilatation  of  spasmodic  and  other  strictures  of  the  esophagus,  especially 
cardiosjiasm  (see  Fig.  1).  The  instrument  is  especially  applicable  in 
liyi)ertrophic  stenosis  of  the  cardia  due  to  long  standing  cardiospasm.  It 
has  been  successfully  employed  in  several  patients.  In  two  patients  under 
my  charge  the  result  was  notable.  In  one,  a  woman  with  long  standing 
(-anliospasm  and  apparent  hypertrophy  of  the  circular  fibers  due  to  the 
spasm  of  the  cardia.  and  with  considerable  dilatation  of  the  esophagus,  three 
applications  of  the  instrument  resulted  in  complete  relief.  Other  methods 
i ailed  after  a  trial  of  several  months.  The  instrument  is  applicable  in  cases 
of  organic  stricture,  but  should  then  be  used  with  extreme  caution. — Ed.] 

In  conclusion  I  must  mention  the  treatment  with  a  permanent  cannula 
\\hi(li  was  so  strongly  advised  in  foreign  countries,  was  tested  by  Leyden 
and  Kenvcrs,  and  has  been  of  late  especially  praised  by  Curschmann.     The 


TREATMENT 


25 


cannula  employed  for  this  purpose  is  best  manufactured  from  elastic  ma- 
terial, it  should  be  10  to  12  cm.  in  length,  and  have  at  its  point  a  width 


Fig.  1.— The  Sippy  Dilator. 

[The  dilator  consists  of  a  rubber  bag  3  inches  long  and  IJ  inches  wide  when  col- 
lapsed. At  an  upper  corner  of  the  bag  a  firm  piece  of  rubber  tubing  about  20  inches 
long  is  attached.  Another  piece  of  rubber  tubing  3  inches  long  is  secured  in  the  center 
of  the  inside  of  the  rubber  bag.  The  lower  end  of  this  piece  of  tubing  is  closed;  the 
upper  end  remains  open  and  is  secured  air  tight  in  the  wall  of  the  rubber  bag.  The  tip  of  a 
whalebone  bougie  introduced  into  this  compartment  guides  the  bag  into  the  seat  of  the 
stricture.  The  essential  feature  is  a  bag  made  of  thin  firm  cloth  which  encloses  the  rubber 
bag,  and  limits  accurately  the  degree  of  dilatation.  The  length  of  the  cloth  sac  should  be 
about  3  inches.  Its  width  determines  the  degree  of  dilatation.  In  dilating  strictures 
due  to  spasm  the  width  of  the  cloth  sac  should  be  about  6  or  7  cm.  for  adults. 
Smaller  sizes  must  be  constructed  for  children  and  for  dilating  strictures  due  to  malignant 
growths  and  cicatrix.  The  cloth  sac  must  be  uniform  in  width.  When  ready  to  introduce, 
a  rubber  condom  is  slipped  on  over  the  collapsed  dilator  and  tied  loosely  about  the  rubber 
tubing  and  bougie.  The  distance  of  the  stricture  from  the  teeth  is  measured  and  the  collapsed 
dilating  bag  guided  well  into  it. 

A  firm  rubber  bulb  such  as  accompanies  an  ordinary  Paquelin  cautery  may  be  used  as 
an  air-pump.  The  dilating  force  that  may  be  applied  directly  to  the  stricture  is  enormous, 
but  limited  accurately  by  the  size  of  the  cloth  sac. — Ed.] 


and  lumen  of  about  5  mm.  and  above  of  about  12  mm.  Such  a  cannula 
is  introduced  by  means  of  a  whalebone  stylet  with  two  ivory  buttons;  the 
lower  button  serves  as  an  obdurator.     The  upper  is  larger,  and  permits 


26  STENOSIS  OF  THE  ESOPHAGUS 

the  introduction  of  a  tube  which  is  held  by  means  of  a  silk  thread.  After 
the  stylet  has  been  withdrawn  the  thread  is  fastened  upon  the  cheek.  The 
advantage  of  this  process  is  that  nourishment,  either  fluid  or  pappy  food, 
may  he  introduced  in  quite  large  amounts  without  difficulty.  It  is  also 
said  to  prevent  the  decomposition  of  the  cancer,  as  the  food  does  not  come 
in  contact  with  the  tumor.  My  experience  with  the  use  of  permanent 
cannula^  is  not  particularly  favorable.  The  retention  of  the  silk  thread  in 
the  mouth  is  uncomfortable  to  the  patient;  if  it  is  drawn  through  the  nose, 
it  irritates  the  epiglottis  and  the  pharynx,  and  is  most  unpleasant  to  some 
patients,  for  example,  if  catarrh  of  the  larynx  or  of  the  pharynx,  which 
is  so  frequent,  is  present.  The  mechanical  irritation  of  the  carcinoma  is 
also  not  to  be  underestimated.  Encircling  of  the  tube  by  its  growth,  and 
clogging  of  the  same,  are  not  rare.  The  most  unpleasant  feature,  how- 
ever, is  this,  that  occasionally  in  withdrawing  the  cannula  the  thread  breaks, 
and  we  are  then  compelled  to  remove  it  with  the  esophagoscope,  and  this 
may  be  a  very  difficult  operation.  Above  all  it  must  be  remembered  that 
this  cannula  treatment  is  only  adapted  to  patients  in  whom  a  tube  of  from 
5  to  6  mm.  still  passes  the  obstruction.  There  are,  however,  patients  in 
whom  for  some  time  sufficient  nourishment  may  be  introduced  according 
to  the  method  I  have  first  described,  without  subjecting  them  to  particular 
discomfort.  The  methods  with  laminaria  tents  and  with  the  rubber  ball 
sound  presuppose  a  certain  permeability  of  the  stricture,  although  not  to 
the  extent  necessary  for  the  cannula,  but  this  is  evidently  one  of  the  reasons 
why  these  methods  have  not  been  more  frequently  resorted  to  in  the  treat- 
ment of  carcinoma. 

If  tlie  stricture  is  too  narrow,  so  that  probing  with  and  without  the 
esopliagoscopc  gives  no  results,  and  the  local  application  of  drugs  to  com- 
bat the  liyperosthesia  and  the  spasms  affords  no  material  relief,  when,  there- 
fore, the  condition  is  such  that,  in  spite  of  all  endeavors,  no  fluids,  or  only 
slight  amounts,  trickle  through  the  esophagus,  and  the  patients  rapidly 
emaciate,  in  my  opinion  the  time  has  arrived  for  surgical  interference. 
But  before  deciding  upon  this,  I  would  urgently  advise  the  simple  trial 
of  putting  the  patient  to  bed  for  a  few  days,  with  absolute  rest,  and  to 
nourish  liim  l)y  the  bowel,  entirely  refraining  from  the  introduction  of  food 
i)\  the  moutli.  Hunger  and  thirst  may  be  allayed  by  small  doses  of  cocain 
(0.02  per  dose,  two  or  three  times  daily),  and  the  mouth  and  pharynx  should 
be  frequently  rinsed  with  ice  water.  A  favorable  change  is  often  noted 
in  that  (ho  local  condition  improves  decidedly.  After  these  few  days  of 
rest,  the  passage  is  likely  to  be  decidedly  more  free  than  it  formerly  was, 
and  tlio  introduction  of  the  tube  or  the  injections  may  be  resumed  should 
tliis  a|)i)oar  advantageous;  sometimes  it  is  unnecessary,  for  we  find  that 
if  sucli  patients  nre  nourished  with  enemata  on  one  or  two  days  in  the  week 
they  are  able  to  swallow  quite  well  during  the  remaining  period,  particu- 
larly if  small  doses  of  morphin  are  simultaneously  administered.     In  this 


TREATMENT  27 

stage  of  the  disease  we  have  little  hope  of  long  averting  the  catastrophe, 
but  whether  in  this  crisis  gastrostomy  will  greatly  avail  appears  to  be  very 
questionable. 

In  my  opinion,  only  in  the  most  unfavorable  cases  is  the  production 
of  a  gastric  fistula  indicated.  This  operation  is,  in  truth,  for  me  the  ultima 
ratio,  notwithstanding  the  fact  that  the  operation,  through  the  successes  of 
prominent  surgeons,  has  become  a  relatively  safe  one,  and  that  the  fistula 
functionates  perfectly  for  a  long  time.  Gastrostomy  appears  to  be  abso- 
lutely indicated  when  hroncho-esophageal  fistulce  cause  the  continuous 
passage  of  food  into  the  wrong  channel,  when  imperfect  permeability  of 
the  esophagus  for  any  kind  of  food  exists,  and,  finally,  when  in  an  early 
stage  of  the  disease  impassibility  occurs  and  causes  a  rapid  loss  of  strength. 
In  well-advanced  cases,  with  decided  stenosis  of  the  lumen,  a  marked  pro- 
longation of  life,  a  noticeable  improvement  in  the  general  nutritive  con- 
dition, and  a  decided  amelioration  of  the  dysphagia  is  not  to  be  expected 
from  the  operation.  As  a  prophylactic  measure  there  is  not  the  slightest 
reason  for  early  operation  while  there  is  still  sufficient  permeability  of  the 
esophagus.  The  radical  treatment  of  cancer  of  the  esophagus  by  extirpa- 
tion could  only  come  into  question  with  high-seated  tumors ;  up  to  this  time 
not  a  single  case  of  recovery  has  been  reported.  This  is  partly  due  to 
the  great  difficulties  which  the  surgeon  must  combat,  but  partly  also  to  the 
fact  that  the  diagnosis  is  not  made  early  enough.  The  more  thorough  use 
of  the  esophagoscope  may,  perhaps,  be  productive  of  better  results  iir  the 
near  future. 

Of  other  symptomatic  treatment,  I  shall  only  mention  the  irrigation 
of  the  esophagus  with  disinfectant  solutions  (thymol  0.5-1000,  salicylic  acid 
1-1000,  silver  nitrate  1-1000,  etc.)  to  remove  the  symptoms  due  to  stagna- 
tion (fetid  odor,  eructations).  For  the  catarrh  ot  the  pharynx,  of  the 
larynx,  and  of  the  bronchi,  which  so  frequently  accompany  the  condition, 
I  employ  Ems  water,  morphin,  etc.;  the  salts  of  iodin,  also,  bring  about 
amelioration  by  thinning  the  tough  mucus.  The  many  neuralgic  pains  are 
relieved  by  our  reliable  antirheumatics. 

The  therapy  of  cicatricial  strictures  must  be  constructed  on  principles 
entirely  different  from  those  that  come  into  question  in  carcinoma.  Here 
there  is  a  possibility  of  preserving  life,  under  favorable  circumstances  of 
permanently  curing  the  local  lesion,  and  here  dilatation  of  the  stricture  is 
the  most  important  aim  of  the  treatment.  The  results  depend  very  much 
upon  the  methods  of  procedure.  We  shall  first  describe  the  simplest  process, 
that  of  sounding.  It  is  generally  admitted  that  slight  pressure  is  permissi- 
ble in  shoving  the  instrument  through  the  narrowed  cicatrized  area,  and 
that  it  may  be  permitted  to  remain  for  some  time  (from  three  to  fifteen 
minutes).  Daily  probing  is  not  always  advisable;  often  a  certain  amount 
of  forbearance  gives  better  results,  so  that  the  method  is  only  employed 


28  STENOSIS  OF  THE  ESOPHAGUS 

every  second  day.  If  we  are  dealing  with  an  excentrically  layered  canal, 
or  with  a  somewhat  circular  narrow  pass,  the  metallic  spiral  probes  such 
as  I  advised  many  years  ago,  appear  to  me  to  be  the  most  suitable  in- 
struments. If  the  way  into  the  stricture  may  be  found  more  easily,  it 
is  quite  immaterial  of  what  the  dilator  is  made.  Sounds  with  a  button  of 
whalebone,  or  English  or  French  bougies,  may  be  employed.  If  it  is  impos- 
sible to  attain  our  end  by  the  usual  sightless  method,  before  we  conclude 
upon  further  surgical  procedures  (esophagotomy,  gastrostomy)  we  should 
always  make  an  attempt  to  probe  with  the  aid  of  the  esophagoscope.  In 
apparently  quite  desperate  cases  I  have  at  last  succeeded  in  finding  the 
entrance  to  the  stricture,  and  in  passing  it  with  a  fine  instrument.  The 
process  is  laborious,  but  the  results  are  sometimes  brilliant.  For  dilatation 
with  the  esophagoscope,  I  am  partial  to  the  use  of  metallic  spiral  sounds, 
or  so-called  "  director  sounds,"  i.  e.,  narrow  bougies  of  impregnated  tissue 
which  terminate  in  a  quite  long  metal  staff  that  permits  of  firm  direction. 
Occasionally  I  have  also  employed  with  advantage  fine  lead  and  zinc  staffs 
to  direct  the  passage  through  the  obliterated  organ.  After  finding  the  way 
a  few  times  with  the  esophagoscope,  I  frequently  succeed  in  attaining  my 
purpose  upon  simple  probing  in  the  recumbent  posture  without  the  intro- 
duction of  the  esophageal  tube,  and  if  the  canal  has  been  at  all  dilated 
I  resume  the  trial  in  the  sitting  posture  with  the  ordinary  sound,  A 
number  of  little  artifices,  which  I  do  not  care  to  describe  here,  may  facili- 
tate this  process  in  difficult  cases. 

If  the  cicatricial  tissue  is  not  too  firm,  and  the  narrowed  pass  not  too 
long,  I  find  Schreiber's  sound,  cautiously  used  (see  above),  particularly 
useful  in  producing  dilatation  with  comparative  rapidity. 

The  treatment  of  cicatricial  strictures  by  bougies  should  be  begun  as 
early  as  possible.  Tliis  treatment  should  be  carried  out  every  day,  and 
should  be  continued  for  a  long  time,  for,  even  after  extensive  stretching, 
the  tendency  of  cicatricial  tissue  to  contract  continues.  Although  we  may 
attempt  decidedly  more  in  this  affection  of  the  organ  than  in  carcinoma, 
cautious  manipulation  is 'nevertheless  necessary,  and  it  must  be  home  in 
mind  that,  besides  cicatrices,  ulceration  may  also  be  present,  that  the 
nuieous  membrane  above  the  narrowing  is  frequently  irritated  and  in- 
flamed, so  that  here,  as  well  as  in  cancer,  the  disturbance  in  degluti- 
tion does  not  necessarily  depend  upon  the  mechanical  obstruction  alone, 
but  may  be  due  also  to  nervous  disturbance,  to  a  tendency  to  spasm, 
and  to  atony. 

There  are,  however,  cases  where  the  most  persistent  use  of  the  bougie, 
even  if  it  really  pass  through  the  constricted  area,  produces  no  noteworthy 
dilatation;  and  we  often  meet  with  cases  in  which  it  is  impossible  to  pass 
the  stricture  with  any  of  our  instruments.  In  difficult  cases  of  this  kind, 
and  sometimes  in  almost  desperate  situations,  an  attempt  must  be  made  to 
dilate  in  the  esophagoscope  with  sounds  or  by  the  introduction  of  laminaria 


TREATMENT  29 

tents  at  the  starting  point  of  the  stricture.  The  latter  process,  which 
Ebstein  has  advised  as  a  modification  of  the  earlier  Senator  method  (which 
see),  I  have  repeatedly  tested.  For  the  introduction  of  the  stylets  into 
the  stricture  I  employ  forceps  with  smooth,  concave,  internal  surfaces;  if 
the  entrance  to  the  stricture  is  extremely  small,  the  lower  end  of  the  tent 
is  pointed,  and  cautiously  pressed  into  the  narrow  canal.  During  this  treat- 
ment the  patient  must  be  very  carefully  watched.  At  first  the  tent  should 
be  allowed  to  remain  only  for  three  to  eight  hours,  provided  there  is  no 
pain  or  fever,  and  later,  for  a  longer  time.  Withdrawal  is  usually  easy 
by  the  aid  of  the  silk  thread.  In  elongated  strictures  the  process  with  the 
laminaria  tent  is  an  arduous  one,  and  gives  only  very  slow  results.  In  these 
cases  we  should  always  try  to  attain  our  end  by  the  introduction  of  long 
thin  bougies  by  the  aid  of  the  esophagoscope.  After  we  have  found  a 
passage,  according  to  v.  Hacker  and  Ebstein,  dilatation  may  be  facilitated 
under  some  circumstances  by  employing  drains  which  are  placed  over  a  thin 
metallic  introduction  rod  of  about  2  mm.  in  size;  if  the  staif  is  withdrawn 
the  tension  lessens,  the  drain  contracts,  and  thus  exerts  decided  pressure  upon 
the  wall,  particularly  if  it  is  allowed  to  remain  for  a  longer  time,  up  to 
24  hours.  In  my  own  experience  the  process  is  somewhat  painful  and  not 
absolutely  harmless;  even  with  close  watching  of  the  patient,  the  jerking 
back  of  the  rubber  may  occasionally  cause  a  laceration  in  the  wall  of  the 
organ. 

If  we  do  not  succeed  by  these  methods,  if  the  results  are  unsatisfactory 
in  that  deglutition  is  not  facilitated,  and  the  patient's  nutrition  now  suf- 
fers, gastrostomy  should  not  be  too  long  delayed.  By  producing  a  gastric 
fistula,  we  need  no  longer  be  anxious  about  the  nutrition,  we  may  influence 
favorably  the  irritation  and  inflammatory  condition  created  in  the  esophagus 
by  the  inactivity  of  the  organ,  and  may  devote  ourselves  to  the  object  of 
restoring  its  permeability.  For  this  time  is  often  necessary,  much  time. 
Besides,  there  is  the  added  advantage  that  through  the  wound  produced 
by  gastrostomy  we  may  attack  the  focus  of  the  disease  in  the  esophagus. 
Primarily  this  is  possible  by  means  of  bougies,  and  cases  have  been  reported 
where  dilatation  has  been  produced  from  below  at  a  point  which  could  not 
be  reached  by  sounding  through  the  mouth.  This  presupposes  that  the 
fistula  is  located  in  such  an  area  that  from  it  we  may  with  comparative  ease 
reach  the  cardia.  This,  unfortunately,  is  not  the  case  with  the  fistulas 
commonly  produced  by  Witzel's  method;  their  advantage  consists  in  their 
permitting  an  excellent  occlusion,  but  manipulation  with  sounds  from  the 
gastric  opening  is  exceedingly  difficult.  There  are  methods,  however,  which, 
even  under  these  circumstances,  may  be  quite  well  employed  for  dilatation. 
The  simple  experiment,  after  Socin,  with  silver  halls  which  are  fastened 
to  a  silk  thread  should  first  be  tried.  A  very  small  one  may  be  swallower? 
by  the  patient  in  the  evening,  and  we  are  sometimes  surprised  to  find  that 
in  the  course  of  the  night  it  has  found  its  way  into  the  stomach.     Various 


30  STENOSIS  OF  THE  ESOPHAGUS 

processes  have  been  devised  for  securing  through  the  fistula  the  silver  thread 
which  has  been  fastened  above  through  the  cheek.  The  stomach  may  be 
filled  with  water  or  soup,  and  these  fluids  are  then  permitted  rapidly  to 
ilow  off  through  the  tube :  not  rarely  the  thread  will  be  carried  with  them. 
Or  slightly  curved  instruments  (dressing  forceps)  must  be  introduced  into 
the  stomach  and  an  attempt  be  made  to  catch  the  thread  while  the  patient 
assumes  different  positions,  and  to  draw  it  into  the  fistulous  canal.  If  this 
is  successful  the  ends  of  the  silk  thread  are  fastened  together,  the  ring  is 
closed,  a  fine  rubber  drain  is  inserted  within  it,  and  an  effort  is  made  to 
draw  this  through  the  stricture.  Then  larger  drains  may  be  employed,  and 
the  stricture  be  thus  dilated.  But  we  must  not  be  too  hasty,  and  too  forci- 
ble pulling  upon  the  thread  must  be  avoided,  as  this  causes  great  tension 
in  the  narrow  pass,  and  the  danger  of  injury  is  not  inconsiderable. 

It  must  be  mentioned  that  esophagotomy  may  also  be  occasionally  em- 
ployed if  it  can  be  carried  out  helow  the  obstruction.  Nutrition  is  possible 
through  the  fistula,  and,  under  some  circumstances,  dilatation  may  be 
attempted  at  the  opening  in  the  neck.  Here,  however,  it  must  be  observed 
that  a  stricture  in  the  opening  at  the  neck  of  the  esophagus  may  be  diag- 
iiosticated  positively,  but  it  is  by  no  means  certain  that  there  are  not  also 
other  impermeable  ones  in  the  lower  part  of  the  organ.  Then  we  have 
to  deal  with  a  new  obstruction.  This  we  may  occasionally  remove  from 
the  wound  in  the  neck  by  probing,  or  cutting,  but  such  a  process  is  always 
])rotracted,  and,  in  the  meantime,  the  exhausted  patient  may  perish. 
Therefore  in  all  doubtful  and  difficult  cases  it  is  wise  to  assure  ourselves 
of  the  nutrition  by  the  production  of  a  gastric  fistula.  In  the  treatment 
of  compression  stenoses,  sounding  is  also  useful,  and  generally  still  more 
so  than  in  cicatricial  constriction,  for  we  may  manipulate  the  organ  to  a 
greater  extent,  the  mucous  membrane  being  everywhere  intact. 

We  are  soon  convinced  that  a  decided  improvement  in  deglutition  is 
not  to  be  brought  about  by  bougies;  but  if,  at  regular  intervals,  we  intro- 
duce sounds  with  fenestrated  openings  into  the  stomach  the  nutrition  of 
the  patient  may  be  carried  on  satisfactorily,  and  thus  inanition  be  prevented. 
This  is  all  that  we  can  really  accomplish  in  patients  with  compression 
stenosis,  if  the  treatment  does  not  diminish  the  size  of  the  tumor  which 
causes  compression  or  remove  it.  The  latter,  unfortunately,  is  only  excep- 
tionally possible;  for  example,  in  syphilitic  lymphomata  by  potassinm  iodid 
or  an  inunction  treatment,  in  diverticulum  by  cleansing  or  extirpation  of 
the  sac. 

In  spastic  contracture  of  the  esophagus,  soundings  may  occasionally 
1)0  of  use;  I  have  frequently  brought  about  a  lessened  tendency  to  spasm  at 
tlio  cardia  l)y  over-distention  of  the  esophageal  orifice  of  the  stomach,  for 
which  8ehreil)er's  rubber  balloon  sound  serves  the  ptirpose  best.  This  in- 
strnmonl  is  carefully  introduced  into  the  cardia,  perhaps  by  the  aid  of 
se\cial  attempts  at  deglutition,  or  by  local  anesthesia,  when  the  balloon  is 


TREATMENT  31 

distended,  and  pulled  through  the  cardia.  Above  all,  however,  we  must 
endeavor  to  ascertain  the  cause  of  the  spasm,  whether  inside  or  outside  of 
the  esophagus,  whether  produced  by  local  disease,  or  whether  the  general 
condition  produces  the  tendency  to  spasm.  The  etiological  therapy  which 
results  from  this  is  of  vital  importance,  but,  for  this  reason,  the  importance 
of  the  local  symptomatic  treatment  is  by  no  means  to  be  undervalued.  Be- 
sides sounding,  the  injection  of  remedies  that  produce  anesthesia  (eucain, 
3  per  cent.)  or  electricity  by  the  aid  of  a  simple  esophageal  electrode,  such 
as  I  have  proposed,  may  be  of  decided  benefit.  Where  the  spasm,  particu- 
larly at  the  cardia,  has  produced  secondary  changes  (dilatation,  inflamma- 
tion), the  resulting  conditions  are  naturally  to  be  also  considered  in 
treatment. 

In  conclusion,  a  few  remarks  may  be  in  order  concerning  the  treatment 
of  ohstruction  stenosis;  polypus  (an  extraordinarily  rare  occurrence)  should 
be  removed  surgically;  in  obstruction  due  to  masses  of  thrush,  irrigations 
and  the  use  of  borax  (3  per  cent,  solution,  a  tablespoonful  every  two  hours) 
internally,  are  very  serviceable.  When  foreign  bodies  are  lodged  in  the 
esophagus,  we  must  above  all  things  refrain  from  at  once  employing  the 
sound.  We  must  first  endeavor  to  remove  the  object  which  has  entered 
the  esophagus  by  the  mouth,  particularly  if  it  has  pointed  or  sharp  edges, 
for,  if  forced  downward,  these  may  give  rise  to  dangerous  symptoms  in  the 
stomach  and  in  the  intestines.  Smooth  bodies,  for  example,  coins,  even  if 
large,  are  not  very  dangerous  in  their  journey  through  the  digestive 
apparatus.  It  is,  however,  of  the  utmost  importance  that  (if  possible)  a 
foreign  body  be  speedily  removed,  provided  we  may  extract  it  under  the 
direction  of  the  eye.  Esophagoscopy  enables  us  to  achieve  this  in  many 
cases  by  a  bloodless  process,  where  formerly  an  operation  was  necessary; 
small  pointed  objects,  particularly,  are  thus  rapidly  removed  and  without 
danger.  Instead  of  the  manifold  instruments  which  were  formerly  neces- 
sary (coin  catchers,  hooks,  esophageal  probangs)  we  now,  in  most  cases 
when  employing  the  esophagoscope,  use  only  a  simple  forceps.  Combined 
with  this  an  instrument  constructed  according  to  the  principles  of  the 
Leroy  curette  may  sometimes  be  useful.  That  a  small  foreign  body  which 
causes  disturbance  of  deglutition  may  sometimes  be  removed  by  the  admin- 
istration of  an  emetic  must  be  also  mentioned.  Fissures  and  erosions  which 
subsequently  cause  difficulty  are  best  treated  by  the  application  of  caustic 
under  the  direction  of  the  eye,  provided  rest  of  the  organ  and  morphin 
do  not  bring  about  rapid  recovery. 

If  the  foreign  body  reaches  the  stomach,  the  old  efficacious  potato  treat- 
ment for  its  expulsion  per  anum  is  still  the  best  method:  For  three  or 
four  days  the  patient  is  given  daily  3  or  4  pounds  of  potatoes  prepared  in 
different  ways,  constipation  being  induced  by  the  administration  of  the 
tincture  of  opium;  then  the  bowel  is  cleansed  by  enemata  or  the  adminis- 
tration of  castor  oil, 
4 


THE    HISTORY   AND    CLINICAL    INDICATIONS 
OF   GASTRIC    LAVAGE 

By  W.   FLEINER,  Heidelberg 

At  the  turning  point  of  the  century  the  treatment  of  gastric  diseases 
has  reached  a  high  degree  of  development.  This  progress  has  taken  place 
upon  the  fruitful  soil  of  an  exact  method  of  diagnosis  based  upon  precise 
indications,  and  the  seed  was  the  ingenious  idea  of  Kussraaul  promulgated 
about  a  lifetime  ago :  Introduce  a  tube  into  the  stomach,  remove  the  ab- 
normal contents  by  washing,  and  treat  locally  the  diseased  gastric  mucous 
membrane. 

Up  to  the  middle  of  the  previous  century,  but  few  of  the  pathologic 
changes  of  the  stomach  could  be  recognized  with  certainty,  not  even  those 
for  which  pathologic  anatomy  had  already  furnished  an  explanation.  Our 
knowledge  of  functional  disturbances  of  the  stomach  Was  even  more  obscure. 
Digestive  disturbances  whose  organic  foundation  was  unrecognizable  were 
attributed,  according  to  the  views  of  the  time,  to  pathologic  processes  of 
the  stomach,  and  were  thus  treated. 

Naturally  empiric  treatment  of  an  assumed  affection  could  only  produce 
unsatisfactory  results — such  as  we  sometimes  attain  even  to-day  when  a 
greatly  eulogized  remedy  is  used  to  relieve  a  prominent  symptom  in  a 
clinical  case. 

The  modern  physician  who  has  been  trained  to  employ  his  therapeutics 
according  to  definite  indications  and  with  clear  ideas  possesses  also,  with- 
out effort  on  his  part,  an  advanced  technic  which  is  the  fruit  of  the  labor 
of  his  predecessors;  he  can  scarcely  realize  the  conditions  in  that  time  when 
modern  auxiliary  measures  did  not  exist,  yet  in  these  we  have  not  advanced 
to  the  fullest  extent.  And  he  will  correctly  measure  and  fully  appreciate 
the  value  of  his  inheritance  only  when  he  studies  its  historical  development 
and  considers  the  labor  that  has  brought  to  completion  so  great  a  work. 

THE   HISTORY  OF   GASTRIC   LAVAGE 

At  the  close  of  the  sixth  decade  of  the  preceding  century,  dilatation  of 

the  stomach,  particularly  that  advanced  form  developing  from  narrowing 

and  closure  of  the  pylorus,  was  reckoned  among  the  diseases  most  difficult 

to  treat.     "  Only  exceptionally,"  says  Kussmaul,  "  did  we  attain  any  results 

32 


THE  HISTORY  OF  GASTRIC  LAVAGE  33 

in  the  treatment  of  this  distressing  affection.  As  a  rule,  little  could  be 
done  to  ameliorate  the  sufferings,  and  nothing  to  cure." 

Cases  of  this  kind  were  looked  upon  as  hopeless,  and  for  this  reason 
were  not  welcomed  in  hospitals  and  clinics.  Thus  Kussmaul,  at  that  time 
Director  of  the  Freiburg  Medical  Clinic,  was  disinclined  to  admit  to  his 
Clinic,  which  was  then  greatly  overfilled,  a  country  girl,  Marie  Weiner,  from 
Heimbach,  aged  25,  who  sought  admittance  upon  April  15,  1867.  She 
had  been  suffering  from  a  gastric  affection  since  her  eleventh  year,  having 
an  extreme  dilatation  of  the  stomach  due  to  pyloric  ulcer,  hypertrophy  of 
the  pylorus,  and  chronic  catarrh  of  the  stomach ;  she  was  greatly  emaciated 
and  suffered  besides  from  peculiar  spasmodic  attacks  which  are  now  known 
and  dreaded  under  the  name  of  gastric  tetany;  however,  at  the  repeated 
urgent  entreaty  of  the  patient,  Kussmaul  relented  and  admitted  her  to 
the  Clinic. 

This  patient  suffered  almost  daily  from  gastric  pain  and  vomiting,  and 
passed  sleepless  nights  of  suffering  unless  relieved  by  the  administration 
of  morphin;  her  pitiful  condition  gave  Kussmaul  the  idea  of  employing 
the  stomach-pump.     His  considerations  and  reasons  were  as  follows: 

"  Quite  frequently,  when  I  observed  the  patient  in  the  miserable  pro- 
dromal stage  of  vomiting,  the  thought  had  occurred  to  me  that  I  might 
ameliorate  her  sufferings  by  the  employment  of  the  stomach-pump,  as  the 
removal  of  large  masses  of  decomposed  acid  gastric  contents  should  cause 
the  agonizing  burning  and  retching  at  once  to  cease.  The  introduction  of 
the  esophageal  sound  was  naturally  not  difficult,  for  where  a  gastric  dilata- 
tion has  existed  for  so  long  a  time  the  esophagus  also  is  usually  dilated. 
The  artificial  emptying  of  the  stomach  by  the  pump  could  be  no  more 
painful  or  distressing  than  her  condition  before  and  during  vomiting.  At 
all  events,  it  would  be  more  rapid  and  complete  than  the  natural  emptying 
of  the  stomach  by  the  act  of  vomiting,  with  its  prolonged  prodromal  stage 
of  nausea,  pain  and  retching.  Eepeatedly,  even  after  vomiting,  palpation 
and  percussion  revealed  that  the  stomach  still  contained  considerable  masses. 
This  condition  reminded  me  of  the  so-called  ischuria  paradoxa,  in  which 
large  amounts  of  urine  flow  daily  from  the  dilated  urinary  bladder  with- 
out its  actually  becoming  empty  and  without  reducing  its  circumference. 
By  means  of  the  pump  we  must  succeed  in  emptying  the  stomach  completely, 
and,  if  its  elastic  and  contractile  power  have  not  been  entirely  exhausted, 
perhaps  even  give  to  it  the  tone  to  contract  to  its  smallest  extent,  just  as 
the  catheter  occasionally  brings  about  recovery  in  ischuria  paradoxa. 

"  In  our  patient  the  gastric  dilatation  was  due  to  constriction  of  the 
pylorus.  At  the  autopsy  of  cases  of  extreme  gastric  dilatation  I  had  repeat- 
edly observed  that  the  stenosis  which  caused  them  would  still  permit  the 
passage  of  a  small  finger  from  the  stomach  into  the  duodenum,  although 
toward  the  end  of  life  there  had  appeared  to  be  complete  closure  of  the 
pylorus.     In  such  cases  I  had  occasionally  noted  at  the  bedside  through 


34        HISTORY  AND  CLINICAL  INDICATIONS  OF  GASTRIC  LAVAGE 

the  abdominal  covers  active  movement  in  the  stomach.  A  paresis  of  the 
gastric  musculature  might  be  present,  but  certainly  not  complete  paralysis. 
It  appeared  to  me  as  though  the  excessive  distention,  the  filling  and  over- 
loading of  the  stomach  itself,  produced  a  mechanical  action  which  increased 
the  constriction  of  the  pylorus  to  complete  closure,  and  this  condition  I 
hoped  to  remove  by  emptying  the  stomach  and  decreasing  its  size. 

"  Finally,  it  appeared  that  the  employment  of  the  stomach-pump  would 
permit  a  more  active  topical  treatment  of  the  diseased  gastric  mucous  mem- 
brane than  was  formerly  possible.  In  the  case  of  our  patient  this  organ 
had  for  years  been  continuously  irritated  by  extremely  acid  contents.  The 
retention,  stagnation,  and  decomposition  of  masses  of  food  in  the  stomach 
because  of  pyloric  stenosis  is  certainly  often  the  only  cause  of  the  catarrh 
of  the  mucous  membrane;  as,  for  example,  in  cases  in  which  originally 
tliere  was  but  an  ulcer  or  a  cicatrix  at  the  pylorus,  the  stomach  bedng  other- 
wise intact ;  in  all  other  cases  it  probably  maintains  and  increases  a  catarrh 
already  present.  This  is  probably  why  we  note  so  constantly,  in  constric- 
tion of  the  ])ylorus,  that  the  mucous  membrane  about  the  pylorus,  where 
the  gastric  contents  especially  accumulate,  shows  most  intense  disease.  The 
stomach-pump,  I  hoped,  would  not  only  make  it  possible  completely  to 
evacuate  these  acid,  irritating  masses,  but  would  also  permit  the  washing 
and  cleansing  of  the  diseased  mucous  membrane  which  had  been  irritated 
by  acid  and  alkaline  fluids,  as,  for  instance,  with  Vichy  water  or  with  an 
artificial  soda  solution." 

In  pursuance  of  these  considerations  Ku^smaul,  upon  July  22,  1867, 
for  the  first  time,  pumped  and  washed  out  the  stomach  of  his  patient. 

"  The  introduction  of  the  stomach-tube,  the  pumping  out,  and  the  wash- 
ing with  Vichy  water  were  unexpectedly  easy.  We  withdrew  three  liters  of 
acid,  dirty-grey,  sarcina-containing  fluid,  with  particles  of  food  of  all  kinds 
undergoing  softening  and  decomposition. 

■  "  Even  the  immediate  result  of  the  first  emptying  and  washing  of  the 
stomach  with  Vichy  water  was  a  surprisingly  beneficial  one.  The  patient, 
who  was  previously  always  exceedingly  disagreeable,  and  of  such  a  whining 
disposition  that  she  well  bore  out  her  name,  MVeiner'  (crier),  appeared  a 
few  hours  later  as  if  completely  transformed.  For  the  first  time  she  was 
agre(>able  and  appeared  comfortable  in  her  bed,  and  she  declared  that  for 
years  she  had  not  been  in  such  good  spirits.  She  at  once  digested  and 
slept  much  better,  and  for  two  days  was  entirely  free  from  depressing  sen- 
safions  in  the  stomach.  After  repeated  employment  of  the  pump,  at  the 
eud  of  fourteen  days  the  patient  had  a  more  healthy  appearance,  and  had 
become  another  being.  She  who  had  always  been  disagreeable,  had  lain 
in  bed  or  reclined  in  an  arm-chair,  was  up  the  whole  day,  was  very  friendly, 
and  attemi)ted  to  make  herself  useful  about  the  room,  and  soon  in  other 
]iarts  of  the  house.  In  the  first  three  months  of  her  stay  in  the  hospital, 
and  l)(^fore  the  employment  of  the  pump,  she  had  gained  at  most  about  5^ 


THE  HISTORY  OF  GASTRIC  LAVAGE  35 

pounds  in  weight;  two  months  afterward  she  had  gained  at  least  16^  pounds, 
and  in  not  quite  six  months,  24  to  25  pounds.  For  two  years  recovery  has 
been  complete,  although  the  patient  is  by  no  means  in  easy  circumstances." 

The  first  communication  regarding  this  new  method  of  treatment  of 
gastric  dilatation  was  reported  by  Kussmaul  at  the  first  meeting  of  the 
Section  of  Internal  Medicine  of  the  Forty-first  Congress  of  German  Natu- 
ralists and  Physicians  in  Frankfort-on-the-Main  in  September,  1867.  Fur- 
ther observations  and  experience  regarding  this  treatment,  which,  in  the 
meantime,  had  become  a  method  of  gastric  dilatation,  were  communicated 
by  Kussmaul  in  his  Freiburg  pro-rector  oration  on  the  9th  of  September, 
1869,  and  in  his  classic  treatise  in  the  Deutsches  Archiv  fiir  Klinische' 
.  Medicin,  vol.  vi,  1869,  which  has  become  widely  celebrated :  "  On  a  New 
Method  of  Treatment  of  Gastric  Dilatation  by  means  of  the  Stomach 
Pump." 

Besides  the  new  method  of  treatment,  this  epoch-making  work  of  Kuss- 
maul's  furnished  such  an  enormous  amount  of  clinical  material  and  so 
many  new  points  of  view  for  pathology,  diagnosis  and  treatment  that  it 
became  the  foundation,  and  even  a  treasury,  for  most  of  the  later  investi- 
gations in  gastric  disease.  Besides  benign  constriction  of  the  pylorus  from 
ulcers,  cicatrices,  hypertrophy,  and  malignant  constrictions  from  cancer, 
here  was  found  the  complete  clinical  investigation  of  the  simple  dilatations 
of  the  stomach  not  dependent  upon  stenosis  of  the  pylorus  or  of  the  duo- 
denum, those  due  to  atony  of  the  musculafis  in  consequence  of  too  great 
weight  and  extension  of  the  stomach  beyond  its  elasticity  from  polyphagia, 
or  paralytic  weakness  in  convalescence  from  exhausting  diseases,  for  exam- 
ple, enteric  fever,  or  which  had  been  produced  in  nervous  anemic  condi- 
tions, as  well  as  paresis  of  the  gastric  musculature  in  consequence  of  fatty 
and  choloid  degeneration  of  the  muscular  fibers.  The  definite  mechanical 
factors  were  also  considered  which  occasionally  during  life  had  caused  symp- 
toms of  complete  closure  of  the  pylorus  while  in  the  cadaver  a  small  finger 
could  readily  be  passed  through  the  narrowed  pylorus  into  the  duodenum. 
The  descent  in  gastric  dilatation  of  the  pyloric  portion  of  the  stomach  which  ■ 
is  most  bulged  out  and  implicated,  and  the  formation  of  the  fetal  (vertical) 
position  of  the  stomach  were  also  discussed,  as  well  as  the  possibility  of  a 
reflex  tonic  spasm  of  the  hypertrophied  pylorus,  which  is  manifest  to  a 
decided  degree  in  consequence  of  the  irritation  of  the  sensory  nerves  of 
the  pjdoric  region  produced  by  the  acid  contents  which  cause  increased 
peristalsis  in  this  neighborhood. 

That  this  increased  irritation  of  the  gastric  mucous  membrane  from 
stagnating  gastric  contents  produces  reflexly  an  increased,  even  continuous 
secretion  of  fluid,  and  not  only  of  HCl-containing  gastric  juice,  was  at 
that  time  unknown  to  Kussmaul.  It  did  not.  however,  escape  the  sharp 
eye  of  the  investigator  that  in  his  patient  suffering  from  tonic  muscular 
spasm  the  amounts  of  fluid  ejected  by  vomiting  and  brought  up  with  the 


36        HISTORY  AND  CLINICAL  INDICATIONS  OF  GASTRIC  LAVAGE 

stomach-pump  were  much  greater  than  those  introduced;  he  also  noted 
the  decidedly  diminished  amounts  of  urine  in  such  patients.  Kussmaul 
believed  for  a  long  time,  as  I  know  from  his  personal  communications,  in 
a  kind  of  transudation  into  the  stomach,  but  he  was  unable  to  furnish 
exact  clinical  proof  of  such  an  influx  of  fluids;  as  is  well  known,  this  ex- 
perimental success  was  achieved  only  a  few  years  ago  (1893)  by  v.  Mering. 
On  the  other  hand,  the  significance  of  the  marked,  and  often  rapidly 
occurring,  losses  of  water  in  some  cases  of  gastric  dilatation  was  quite  clear 
to  Kussmaul;  he  considered  the  tonic  muscular  spasms  which  were  first 
described  by  him  (so-called  gastric  tetany)  to  be  the  consequences  of  rapid 
inspuisation  of  the  blood  and  a  drying  of  the  nerve  and  muscle,  and  con- 
sequently, at  that  time,  he  laid  great  stress  upon  the  introduction  of  fluid 
in  the  form  of  meat,  broth,  and  wine  enemata,  which  were  absorbed  in  the 
intestine  with  beneficial  effect.  As  an  additional  therapeutic  resource  which 
we  obtained  simultaneously  with  the  stomach-pump,  we  must  mention  Kuss- 
maul's  experience  that  the  dilated  stomach  which  is  no  longer  capable  of 
retaining  large  amounts  of  fluid  or  food  is  still  able  to  force  into  the 
intestine  small  portions  given  at  stated  intervals,  and,  finally,  the  employ- 
ment of  the  hypogastric  bandage  to  prop  up  the  descended  and  dilated 
stomach. 

Kussmaul,  in  his  classic  work,  refers  at  different  points  to  the  variation 
of  the  stagnant  contents  of  dilated  stomachs  in  regard  to  amount,  and  to 
the  appearance,  the  composition,  and  the  degeneration  of  the  gastric  juice, 
in  such  a  manner  as  to  sound  like  a  challenge  to  investigators  to  attack 
these  questions.  In  truth,  all  of  the  clinical  laboratories,  particularly  in 
Kussmaul's  Clinic,  were  actively  at  work  on  this  line,  but  were  interrupted 
by  the  Franco-Prussian  war  and,  later,  by  the  great  clinician's  removal 
from  Freiburg  to  Strassburg.  The  contents  of  diseased  stomachs  and, 
later,  those  also  of  healthy  stomachs,  were  subjected  to  chemical,  physiologic, 
and  subsequently  also  to  bacteriologic,  investigations.  Normal  and  patho- 
logic processes  of  digestion  attained  more  and  more  prominence,  both  from 
a  clinical  and  a  professional  standpoint.  "With  an  eagerness  without  parallel, 
the  tube  was  introduced  into  the  stomach  and  gastric  contents  were  brought 
up  as  if  buried  treasures  were  being  restored  to  daylight. 

Thanks  to  these  eager  investigators,  we  gradually  became  aware  of  the 
importance  in  diagnosis  and  prognosis  of  the  presence  or  absence  of  hydro- 
chloric acid,  not  only  in  gastric  dilatation  but  also  in  gastric  affections  in 
general.  Simple  color  reactions  were  found  which,  even  at  the  bedside, 
sliowod  the  qualitative  presence  of  hydrochloric  acid  and  of  organic  acids, 
wliilo  analytical  methods  by  measure  and  weight  were  formulated  in  great 
uutiihiTs  to  determine  quantitatively  the  gastric  acids.  In  connection  with 
physiologic  experiments  in  digestion  to  show  the  activity  of  the  enzymes  of 
the  gastric  juice,  and  their  presence  or  absence,  these  quantitative  analyses 
also  made  it  possible  to  test  the  function  of  secretion  of  the  gastric  mucous 


THE  HISTORY  OF  GASTRIC  LAVAGE  37 

membrane  and  the  digestive  power  of  the  gastric  juice.  We  learned  to 
recognize  an  amylolytic  and  a  proteolytic  stage  of  gastric  digestion,  also 
the  difference  between  combined  and  free  hydrochloric  acid.  Gradually  a 
period  dawned  in  which  we  believed  that  the  activity  of  the  stomach  and 
the  degree  of  its  digestive  disturbance  could  be  definitely  measured  accord- 
ing to  the  amount  of  hydrochloric  acid  present,  and  the  other  functions 
of  the  stomach,  especially  its  motor  activity,  were  not  sufficiently  appre- 
ciated. A  reaction  took  place.  In  the  meantime,  however,  the  number 
of  methods  for  estimating  free  and  combined  hydrochloric  acid  became 
enormous,  and  the  literature  of  this  subject  has  become  so  extensive  that 
it  can  scarcely  be  reviewed ;  the  future  will  determine  what  portion  of  this 
is  necessary,  useful,  and  of  permanent  value. 

But,  to  return  to  our  theme  of  gastric  lavage,  we  must  first  mention 
the  instrument  vfhich  Kussmaul  used  to  empty  and  wash  out  the  stomach. 

Kussmaul  first  employed  the  stomach-pump  of  the  American  physician, 
Wyman,  which,  according  to  Bowditch's  reports  (1852),  was  also  utilized 
in  draining  empyemata.  Then,  however,  he  had  pumps  manufactured  by 
the  instrument  maker,  Fischer,  in  Freiburg,  after  Wyman's  drawings,  and 
these  were  also  made  use  of  by  Keich  in  Stuttgart  who  designated  them 
as  Fischer's  stomach-pump,  without  any  mention  of  Kussmaul's  authorship. 

V.  Ziemssen  later  ascertained  that  the  honor  of  inventing  this  very  use- 
ful instrument  belongs  neither  to  Wyman  nor  to  Bowditch,  but  to  a  Grerman 
instrument  maker  by  the  name  of  Weiss,  who  lived  in  London  in  the  second 
decade  of  the  last  century.  Ziemssen  therefore  proposed  in  1870  that  "  the 
instrument  which,  by  Kussmaul's  brilliant  discovery,  rapidly  attained  such 
great  distinction  in  the  treatment  of  gastric  diseases,  should  hereafter  be 
designated  as  the  Weiss  stomach-pump."  At  first  Kussmaul,  after  once 
emptying  and  cleansing  a  dilated  stomach,  only  employed  the  gastric  pump 
when  new  difficulties  arose,  such  as  burning  in  the  stomach,  acid  eructation, 
pain,  a  tendency  to  vomit  and  similar  symptoms. 

In  consequence,  the  daily  employment  of  the  stomach-pump,  particu- 
larly in  severe  cases,  became  more  and  more  obvious,  and  it  was  also  ascer- 
tained that  for  emptijing  and  washing  the  dilated  stomach,  the  time  when 
the  stomach  was  still  empty,  therefore,  the  early  morning,  was  the  best  time. 

As  long  as  the  patients  remained  in  the  hospital,  this  operation  could 
be  easily  and  regularly  carried  out  early  in  the  morning  upon  an  empty 
stomach.  After  discharge  from  the  hospital,  however,  the  patients  are 
unfortunate,  "  for  a  busy  physician  cannot  find  time  to  use  the  pumps 
for  such  patients  for  weeks  or  even  for  many  months  with  the  desirable 
regularity."  These  reasons  induced  Kussmaul  to  teach  the  patients  them- 
selves to  introduce  the  stomach-tube,  and  to  wash  out  their  stomachs.  His 
patients  who  had  learned  to  introduce  the  stomach-tube  and  the  stomach- 
pump  for  themselves — as  the  clinical  histories  of  the  year  1869  show — left 
the  Freiburg  Clinic  with  these  instruments  in  their  possession.     It  is  very 


38       HISTORY  AND  CLINICAL  INDICATIONS  OF  GiVSTRIC  LAVAGE 

interesting  to  note  the  use  which  a  patient  of  Kussmaul's,  a  wool-spinner 
by  occupation,  made  of  the  stomach-pump  as  soon  as  indigestion  appeared. 
This  patient  by  no  means  adhered  to  the  directions  which  he  had  received 
in  the  Clinic,  but,  nevertheless,  he  improved  steadily.  If  the  foods  which 
were  forbidden,  pastry,  bacon,  poor  beer,  or  others,  caused  any  great  diffi- 
culty, he  used  the  pump  and  washed  them  out — often  twice  daily. 

"In  comparison  to  this  refined  behavior  of  the  Black  Forest  wool-spinner, 
how  insignificant,"  says  Kussmaul  (1.  c,  page  498)  "is  the  classic  con- 
suetudo  vomitandi  of  Vitellius  and  other  celebrated  gourmands  of  ancient 
Rome,  who  had  at  command  only  the  maneuver  of  the  palate-tickling  finger 
or  the  feather." 

But,  from  the  onset,  Kussmaul  was  not  content  with  the  simple  evacua- 
tion of  the  stagnating  gastric  contents.  On  the  contrary  he  sometimes  also 
employed  the  stomach-pump  for  irrigating  the  diseased  gastric  mucous 
membrane  with  suitable  fluids,  designed  to  have  a  curative  effect,  or  to 
limit  processes  of  decomposition  and  the  proliferation  of  fungi  (sarcina). 

First,  natural  alkaline  waters  were  employed,  Vichy  and  Vals,  which, 
however,  were  gradually  replaced  by  corresponding  artificial  soda  solutions. 
For  the  latter  purpose,  borax  solutions  (4-400),  phenyl  acid  solutions  (25.0 
creosote  water  to  400  of  water),  solution  of  sodium  hyposulphite  (4  to  8 
grams  to  400  of  water),  which,  i\  was  expected,  would  cause  the  formation 
of  disinfecting  sulphurous  acid  in  the  stomach,  also  lign,  quassiae  amar. 
raspat.,  of  which  30  grams  were  covered  with  400  grams  of  cold  water, 
and,  after  macerating  for  twelve  hours,  the  colature  was  employed.  The 
action  of  stomach  washing  was  assisted  by  dietetic  treatment,  which  com- 
prised the  ingestion  of  small  but  frequent  meals  consisting  of  food  which 
could  be  easily  digested  and  contained  nothing  that  might  produce  abnormal 
acids;  also  the  employment  of  soda-containing  mineral  waters  (Vichy,  Vals) 
given  in  amounts  of  a  ^  schoppen,  one-half  to  one  hour  before  breakfast  or 
before  the  first  meal,  for  the  purpose  of  dissolving  the  tough  mucus  which 
had  formed  in  surplus,  to  neutralize  the  abnormal  acid,  and  to  stimulate 
the  secretion  of  normal  gastric  juice;  finally,  keeping  the  bowels  open  by 
means  of  sour  milk,  buttermilk,  simple  warm  water  enemata,  and  rhubarb. 

The  great  enthusiasm  aroused  by  the  first  communication  of  Kussmaul 
before  the  Frankfort  Naturalist  Congress,  and,  even  more,  the  general 
recognition  in  all  professional  circles  of  the  world  of  the  wonderful  suc- 
cess of  his  method  of  treatment,  when  compared  with  other  modes,  as 
detailed  explicitly  in  the  Deutsches  Archiv  fiir  Klinische  Medicin,  led  to 
tlie  rapid  introduction  of  the  stomach-pump  into  hospital  and  private  prac- 
tice. \\  ith  the  publication  of  Kussmaul's  method  of  treatment,  voluminous 
literature  of  the  subject  rapidly  appeared  which  at  first  brought  only  novelty 
in  rpi,rard  to  technic,  various  processes  being  described  which  permitted  the 
nmi-cmployment  of  the  stomach-pump,  as  this  could  not  always  be  readily 
obtained. 


THE  HISTORY  OF  GASTRIC  LAVAGE  39 

In  Kiel,  Dr.  Schorer,  the  assistant  of  Bartels,  in  the  absence  of  a  Wyman 
pump  used  the  ordinary  laboratory  air-pump.  Jiirgensen,  at  that  time 
professor  in  Kiel,  inserted  between  pump  and  stomach  a  two-necked  Woulff's 
bottle,  in  order  to  meet. the  objection  that  all  fluids  discharged  from  the 
stomach  passed  through  the  metal  boot,  and  thus  corroded  and  damaged 
the  pump  which  was  very  difficult  to  clean. 

Jiirgensen,  however,  soon  noticed  that  the  stomach-pump  was  only  neces- 
sary until  the  tube  was  filled  which  led  from  the  stomach  to  the  low-lying 
Woulff's  bottle :  From  that  time  on  the  indications  for  emptying  the  stomach 
by  the  action  of  a  lever  were  given.  Jiirgensen  obtained  the  latter  just  as 
well  by  abdominal  pressure  as  by  the  suction  pump.  For  this  reason  the 
use  of  the  stomach-pump  was  discontinued^  the  stomach  was  no  longer 
pumped  out  but  evacuated. 

In  his  article :  "  An  Addition  to  the  Local  Treatment  of  Gastric  Dis- 
eases "  (in  the  Deutsclies  Archiv  fiir  KUnische  Medicin,  vii,  1870),  Jiirgen- 
sen describes  the  simplest  method  embodying  the  lever  principle,  which  he 
advises  for  the  busy  practitioner  as  the  most  serviceable,  in  the  following: 

"  By  the  aid  of  the  tube  which  is  introduced  into  the  stomach  the  lat- 
ter, if  empty,  is  filled  with  a  fluid  to  be  utilized  in  washing;  naturally,  if 
the  stomach  contains  sufficient  fluid  this  is  unnecessary;  then  by  means 
of  a  glass  tube  or  a  hard  rubber  and  glass  tube  (1.5-2  meters  long,  and  one 
centimeter  in  diameter)  an  ordinary  rubber  tube  is  attached  to  a  sound. 

"  The  patient  now  stands  upon  a  chair,  and  either  coughs  or  retches. 
The  flow  from  the  stomach  immediately  begins.  The  emptiness  of  the 
stomach  is  indicated  by  a  sudden  jerking  of  the  rubber  tube;  and  the  stream 
of  outflowing  water  at  once  becomes  thinner. 

"  Thus,  in  a  brief  time,  a  large  amount  of  fluid  may  be  forced  through 
the  stomach.  To  be  certain  that  my  lever  may  actually  be  filled  without 
difficulty  by  the  prelum  abdominale,  I  fill  the  stomach  with  water,  and 
pay  no  attention  to  the  slight  inconvenience  which  the  patient  appears  to 
experience."     ( Jiirgensen. ) 

Compared  with  gastric  lavage  as  practised  to-day,  this  method  described 
by  Jiirgensen  as  the  simplest  appears  to  require  considerable  assistance  from 
the  patient  who  must  get  upon  a  chair  with  a  sound  in  his  stomach.  Never- 
theless, we  owe  it  to  Jiirgensen  that  the  pump  was  proven  to  be  unnecessary. 

Jiirgensen  did  us  the  further  service  of  attempting  to  substitute  soft 
rubber  sounds  for  the  stiff  French  and  English  stomach  sounds  which  were 
then  in  use. 

These  stomach  sounds  were  of  very  small  caliber,  and  had  upon  their 
anterior  end  two  or  four  small  fenestra,  in  consequence  of  which  they  very 
readily  became  clogged  with  the  remains  of  food  and  even  with  mucus.  A 
very  disagreeable  feature  for  the  patient  was  that,  as  soon  as  clogging 
occurred,  the  sound  was  taken  from  the  stomach,  cleansed,  and  reintro- 
duced.    This  process  was  improved  by  Jiirgensen  who  obtained  from  the 


40        HISTORY  AND  CLINICAL  INDICATIONS  OF  GASTRIC  LAVAGE 

factory  of  Galante  in  Paris  an  excellent  tube  having  a  length  of  70  cm., 
the  walls  being  2  mm.  in  thickness,  and  10  mm.  in  diameter.  This  he 
tied  with  a  silk  thread  over  an  acorn-shaped  ivory  button  2  cm.  long  in 
such  a  manner  that  the  tube  nowhere  extended  aboVe  the  level  of  the  acorn. 

In  the  base  of  the  lumen  of  the  tube  the  ivory  button  had  an  indenta- 
tion 3  mm.  deep,  which  was  intended  to  receive  the  anterior  end  of  a 
whalebone  sound  acting  as  a  director  to  prevent  its  lateral  deviation. 

Laterally,  2-2^  cm.  above  the  ivory  button,  a  hole  was  cut  in  the  tube 
corresponding  to  its  lumen.  Jiirgensen  preferred  one  opening  to  several, 
chiefly  because  of  the  durability  of  the  tube.  If  he  poured  water  into 
one  opening  of  the  sound  this  flowed  from  it  in  a  full  stream,  while  the 
sound  itself,  owing  to  the  well-known  phenomenon  of  "  rebound,"  would 
move  with  great  rapidity  in  the  direction  opposite  to  the  outflow.  By  this 
lateral  deviation  of  the  tube,  Jiirgensen  believed,  especially  by  turning  the 
sound  on  its  longitudinal  axis,  that  he  was  able  to  douche  the  stomach  by 
the  instreaming  water. 

When  it  was  desirable  to  prevent  the  lateral  motion  of  the  sound  in 
tlie  stomach,  a  second  small  opening,  opposite  the  outlet,  was  sufficient  for 
this  purpose. 

The  tube-sound  was  so  prepared  that  the  stylet  was  at  first  introduced 
into  the  hollow  orifice  of  the  acorn-like  attachment,  then  the  tube  was 
drawn  over  it  and  stretched,  and,  finally,  a  clamp  was  attached  at  the  end 
of  the  tube  opposite  the  acorn,  over  the  tube  and  the  directing  staff. 

"  When  the  sound  equipped  in  this  manner  has  been  inserted  about 
5  cm.  into  the  esophagus,  the  clamp  is  removed,  the  whalebone  staff  (man- 
drin)  may  be  withdrawn,  and  the  soft  tube  is  passed  down  into  the  stomach 
and  held  so  that  it  cannot  be  forced  up  by  the  retching"  (Jiirgensen). 

A  further  simplification  of  the  technic  of  gastric  lavage  was  the  inser- 
tion, by  Eosenthal,  of  a  T-shaped  tube  with  a  cock  into  the  apparatus, 
which,  being  placed  in  different  positions,  might  be  connected  with  the 
vessel  containing  the  water,  with  the  descending  outflow  tube,  or  the 
stomach-tube  with  the  outflow  tube,  or  the  vessel  containing  water  with 
the  stomach-tube.     A  similar  technic  was  recommended  by  Schiffer. 

Then  experiments  were  made  with  double  stomach  sounds,  first  by  Dr.- 
Auerl)aeh  in  the  Clinic  at  Kiel,  then  by  Ploss,  Hodgen,  Apolant  and  others. 
Hodgen  (St.  Louis)  invented  a  simple  hard  rubber  pump  in  which  the 
hall  valves  were  so  arranged  that  the  mere  turning  of  the  hand  in  a  con- 
trmv  direction  was  sufficient  to  reverse  the  stream.  Hodgen  even  simplified 
the  method  of  emptying  the  stomach  by  connecting  a  rubber  tube  with  the 
gastric  sound,  and  filling  it  with  water  before  introducing  the  sound  into 
the  stomach. 

According  to  whether  the  vessel  containing  the  end  of  the  rubber  tube 
is  higher  or  lower  than  the  stomach,  fluid  may  be  allowed  to  flow  into  the 
stomach  or  may  be  withdrawn  from  it. 


THE  HISTORY  OF  GASTRIC  LAVAGE  41 

Extreme  simplicity  seemed  to  be  attained  in  the  apparatus  employed 
by  Th.  Biedert ;  it  consisted  of  a  stomach-tube,  a  glass  tube  6  to  8  cm.  long, 
which  was  inserted  into  the  former,  and  which  at  its  other  extremity  was 
connected  with  a  long  rubber  tube,  and,  finally,  with  a  funnel  into  which 
the  water  could  be  poured  (1873).  To  permit  the  water  to  flow  from  the 
stomach,  Jiirgensen,  as  mentioned,  still  believed  it  necessary  that  the  patient 
with  the  full,  or  even  distended,  stomach  get  up  on  a  chair.  In  1875, 
Holland  Cotton  thought  it  sufficient  for  the  patient  to  stand  during  the 
lavage;  Biedert  filled  and  emptied  the  stomach  by  raising  and  lowering 
the  funnel. 

A  fortunate  advance  in  the  technic  of  gastric  lavage  was  the  introduc- 
tion of  soft  stomach-tubes  by  Jiirgensen.  These  instruments  had  the  dis- 
advantage that  their  flexibility  was  soon  lost,  from  the  fact  that  a  mandrin 
of  whalebone  or  rattan  was  introduced  into  them,  to  stiffen  them  until  the 
larynx  was  passed.  It  is  greatly  to  Ewald's  credit  to  have  shown  (1874) 
in  a  case  of  nitrobenzol  poisoning  that  even  a  very  soft  rubber  tube,  or  an 
ordinary  smooth  gas  tube,  may  be  introduced  into  the  stomach  and  utilized 
for  gastric  lavage.  In  a  discussion  of  Oser's  communication  ("  Die  Magen- 
spiilung  mittels  des  elastischen  Schlauches,"  Wiener  med.  Presse,  1877,  1), 
Nothnagel,  however,  emphasizes  (in  Virchow-Hirsch's  Jahresberichten)  that 
he  also,  without  any  knowledge  of  Ewald's  publication,  employed  in  his 
Clinic  for  some  years  a  smooth  rubber  tube  with  a  funnel  for  simple  gastric 
lavage. 

Ewald's  gas  tubing  was  the  prototype  of  the  improved  tube  which  later 
came  into  use, — stomach-tubes  which  were  open  below,  i.  e.,  with  one  cen- 
tral opening  only.  Jiirgensen's  ivory  knob  at  the  end  of  a  soft  tube  fell 
into  disuse  when,  with  the  technical  improvement  in  the  rubber  industry, 
closed,  rounded  tubes,  with  one  or  two  lateral  openings,  stomach-tubes  pat- 
terned after  the  Nelaton  catheter,  were  then  manufactured.  Such  tubes 
were  first  employed  by  Leube;  by  and  by,  however,  they  came  into  general 
use,  and  have  been  exclusively  employed  in  gastric  lavage. 

The  technic  of  the  introduction  of  the  sound  in  gastric  lavage  which 
was  carefully  constructed  and  practised  in  Kussmaul's  Clinic,  had  then  to 
be  learned  and  practised  by  others  who  desired  to  utilize  this  new  method 
of  treatment.  It  goes  without  saying  that  in  such  mostly  autodidactic 
handling  of  the  sound  the  patients  must  have  been  obliged  to  bear  a  great 
deal.  I  do  not  believe  I  am  far  wrong  in  assuming  that  the  widely  prevalent 
fear  of  the  stomach-pump  which  still  exists  in  the  minds  of  many  patients 
originated  in  that  period  when  physicians  were  learning  to  use  the  stomach 
sound  and  the  stomach-tube. 

Eecognizing  these  evils,  v.  Ziemssen  was  the  first  to  advise  care  in  the 
employment  of  the  stomach-pump  (1872).  Then  Biermer  (1874)  pub- 
lished a  communication  concerning  inflammation  of  the  esophagus  and 


42        HISTORY  AND  CLINICAL  INDICATIONS  OF  GASTRIC   LAVAGE 

of  the  pcri-esophageal  connective  tissue  following  injuries  from  the  sound. 
This  author  was  later  followed  by  Leube  and  others.  In  the  introduction 
of  the  stomach  sound,  as  well  as  also  in  the  use  of  the  stomach-pump,  and 
in  withdrawal  of  the  sound  from  the  stomach,  now  and  then  injuries 
occurred  which,  under  some  circumstances,  made  these  procedures  danger- 
ous. It  repeatedly  happened  that  portions  of  the  mucous  membrane  were 
torn  off  by  the  sound,  sometimes  fragments  from  1  to  3  cm.  long  and  3  to  5 
nun.  in  breadth,  therefore  presenting  quite  a  surface.  In  none  of  these 
cases  of  injury  to  the  gastric  mucous  membrane  were  serious  consequences 
noted ;  now  and  then  more  or  less  decided  hemorrhage  and  syncope  followed, 
1)11 1  recovery  was  rapid  and  so  complete  that  even  in  those  cases  in  which 
there  was  an  opportunity  later  to  hold  a  necropsy  no  visible  cicatrices  were 
found  in  the  stomach.  Besides  these  lacerations  in  the  mucous  membrane 
of  llie  stomach,  there  are  reports  in  literature  of  injuries  to  the  pharyngeal 
and  esophoageal  mucous  membranes,  perforations  of  aortic  aneurysms,  hem- 
orrhages from  esophageal  varices,  of  erosions  and  superficial  excoriations  of 
the  gastric  mucous  membrane.  Moreover,  the  mucous  membrane  has  been 
perforated  by  iising  hard  sounds,  and  the  overfilling  of  the  stomach  with 
fluid  has  caused  decided  ruptures  of  continuity  in  the  gastric  mucous 
meml)rane. 

The  number  of  accidents  of  this  kind  noted  in  literature  is  exceedingly 
small  when  we  consider  the  extensive  and  world-wide  use  of  the  stomach- 
tube.  However,  in  the  opinion  of  a  celebrated  author  (Ebstein)  they  do 
not  exactly  represent  actual  conditions.  For  instance,  the  tearing  away 
of  particles  of  the  gastric  mucous  membrane  with  a  stomach  sound  is  even 
now  said  to  be  much  more  frequent  than  might  be  assumed  from  the 
publications. 

In  the  year  1872  Ziemssen  also  advised  us  to  be  careful  in  the  use  of 
certain  sounds,  particularly  the  black  ones  (French),  and  of  such  as  had 
friable  borders  at  their  openings,  Emminghaus  did  the  same.  Luube  com- 
pared the  action  of  a  sharp  opening  in  the  sound  with  that  of  a  hollow 
chisel,  and  he  believed  the  central  opening  in  the  sound  to  be  dangerous, 
as  had  previously  been  stated  by  Emminghaus.  Ziemssen  (1872)  gave 
minute  directions  for  preventing  injuries  with  the  sound  as  follows:  1. 
]\Ieasure  the  distance  between  the  epigastrium  and  the  teeth  with  a  sound 
before  its  introduction,  and  mark  upon  the  latter  a  line  so  that  the  instru- 
ment will  not  be  forced  so  deeply  into  the  stomach  as  to  damage  the  greater 
curvature  ;  2.  Xever  begin  to  pump  out  the  stomach  before  previously  inject- 
ing warm  water  (at  least  half  a  liter),  unless  a  short  time  previously  large 
amounts  of  fluid  have  been  ingested;  otherwise,  the  gastric  mucous  mem- 
brane may  be  drawn  by  suction  into  the  opening  of  the  tube,  and  thus  be 
torn  away. 

With  the  general  introduction  into  practice  of  the  soft  stomach-tube 
these  dangers  have  been  almost  obviated.      Gastric  lavage  may  now  be 


THE  HISTORY  OF  GASTRIC  LAVAGE  43 

regarded  as  a  harmless  procedure  provided  the  cases  are  suitable  for  lavage 
and  the  instruments  correctly  chosen,  and  that  we  adhere  to  the  technical 
rules  primarily  given  by  Kussmaul,  which  are  still  to  be  explicitly  discussed. 
The  greater  certainty  which  has  resulted  from  this  manner  of  handling 
the  stomach-tube  no  longer  limits  the  employment  of  lavage  to  the  dilated 
stomach.  Kussmaul  advised  the  employment  of  lavage  as  early  as  possible 
in  reflex  spasm,  in  stenosis  of  the  pylorus,  and  in  pathologic  conditions  lead- 
ing to  degeneration  of  the  gastric  walls.  In  consequence  of  this  Eeich 
in  Stuttgart  (1869  and  1870)  and  Schliep  in  London  treated  chronic  dis- 
eases of  the  stomach,  catarrh,  ulcers,  and  digestive  disturbances  from  other 
causes  with  the  stomach-pump,  and  also  employed  the  remedies  advised  by 
Kussmaul  in  irrigating  the  affected  gastric  mucous  membrane, — solutions 
of  sodium  bicarbonate,  potassium  permanganate  (1  to  100,  of  this  2  to  4 
ounces  in  a  vessel  filled  with  water),  carbolic  acid,  chloralum  (an  English 
preparation),  boric  acid  and  tincture  of  myrrh.  In  an  article  from  Kuss- 
maul's  Clinic,  "  On  the  Treatment  of  Gastralgia  with  the  Internal  Stomach 
Douche,  and  Remarks  Regarding  the  Technic  of  Sounding  the  Stomach," 
Malbranc  (1878)  described  the  anodyne  effect  of  sprinkling  the  gastric  wall 
with  warm  water,  and  particularly  with  warm  carbonated  water  (100.4°  F.). 
Rosenheim,  in  1892,  advised  a  particular  sound  with  many  small  lateral 
openings  for  douching  the  stomach.  In  the  same  year  Lowenthal  suggested 
in  the  treatment  of  hyperchlorhydria  and  gastralgia  spraying  the  gastric 
mucous  membrane  with  solutions  of  silver  nitrate  (1  to  1000)  and  Einhorn 
employed  the  spray  in  various  gastric  affections. 

The  communications  of  Cahn,  from  Kussmaul's  Clinic,  upon  the  treat- 
ment of  intestinal  obstruction  .by  gastric  lavage  (1884),  received  merited 
attention.  In  many  cases  of  ileus,  the  results  of  repeated,  even  of  a  single, 
irrigation  of  the  stomach,  as  I  later  had  abundant  opportunity  of  convinc- 
ing myself,  were  remarkable.  The  benefit  was  brought  about  by  the  removal 
of  gas  and  fecal  masses  lodged  above  the  stenosed  area.  This  removes  ten- 
sion and  the  limitation  of  space.  Decided  peristalsis  and  vomiting  cease, 
and  food  may  then  be  introduced. 

I  must  also  attribute  to  Kussmaul's  initiative  the  method,  which  I  have 
systematically  described  and  practised,  of  covering  with  bismuth  the  ulcer- 
ated and  bleeding  surfaces  in  the  stomach,  these  having  first  been  cleansed 
(1893). 

The  beneficial  effect  of  gastric  lavage  upon  the  bowels  in  dilatation  of 
the  stomach,  Kussmaul  mentioned  in  his  article  to  which  we  have  so  often 
referred.  Tin's  was  noted  in  all  cases  in  which  gastric  lavage  was  at  all 
serviceable,  and  he  looked  upon  it  as  a  suspicious  sign  if,  after  prolonged 
gastric  lavage,  amelioration  took  place,  and  the  gastric  symptoms  improved, 
but  constipation  stubbornly  persisted. 

In  conjoined  labor  with  the  venerable  master  for  almost  ten  years, 
I  have  availed  myself  of  the  benefits  of  gastric  lavage  in  intestinal  disturb- 


44       HISTORY   AND  CLINICAL  INDICATIONS  OF  GASTRIC  LAVAGE 

ante  to  an  enormous  extent,  not  only  when  constipation  existed,  but  even 
more  frequently  when  prolonged  diarrheas  were  present  which  so  often  have 
their  origin  in  disturbances  of  gastric  function  and  organic  disease  of  the 
stomach.  Here  I  cannot  refrain  from  mentioning  the  favorable  effect  of 
gastric  lavage  in  many  diseases  of  the  liver,  in  diseases  of  the  gall-bladder 
combined  with  jaundice,  in  chlorosis  and  anemia,  in  many  disturbances 
of  metabolism,  and  in  intoxications.  Gastric  lavage  has  not  only  a  local 
effect,  but,  in  those  cases  where  the  pylorus  opens  during  lavage,  also  a 
general  effect  in  that  the  water  which  streams  into  the  small  intestine,  if 
not  regurgitated  into  the  stomach,  and  not  expelled  externally,  reaches  the 
blood  and  the  liver,  washes  out  the  blood  and  the  vessels,  and,  in  particular, 
cleanses  and  washes  out  the  kidneys  just  as  effectually  as  the  best  mineral 
spring  cures. 

Furthermore,  I  must  call  attention  to  the  value  of  gastric  lavage  in 
diagnosis;  this  was  evident  from  the  beginning  and  has  become  still  more 
apparent  in  the  course  of  time.  "  We  first  empty  the  stomach,  and  then 
the  palpating  finger  may  detect  tumors  which  cannot  be  made  out  when 
the  stomach  is  filled.  Secondly,  lavage  is  a  very  valuable  means  by  which 
to  differentiate  dilatation  of  the  stomach  from  dilatation  of  the  transverse 
colon;  this  was  formerly  very  difficult,  so  much  so  that,  as  I  know  from 
my  own  experience,  the  greatest  clinicians  occasionally  made  gross  mis- 
takes"  (Kussmaul,  1869). 

Finally,  gastric  lavage  enables  us  to  arrive  at  conclusions  regarding  the 
motor  condition  of  the  stomach,  and  Leube  did  us  a  lasting  service  in 
utilizing  gastric  lavage  to  estimate  the  time  necessary  for  gastric  digestion 
and  for  the  diagnostic  determination  of  the  motility  of  the  stomach.  By 
systematic  washing  out  of  the  stomach  a  certain  time  after  the  ingestion 
of  various  foods  and  drinks  Leube,  and,  following  him,  Penzoldt,  gained 
absolute  knowledge  concerning  the  activity  of  the  stomach,  and  the  gastric 
digestibility  of  food.  The  results  obtained  became  the  basis  of  scientific 
dietetics.  This  was  the  origin  of  the  well-known  diet  schemes  of  Leube, 
as  well  as  the  tables  of  Penzoldt,  which  are  so  useful  in  practice,  showing 
the  gastric  digestibility  of  ordinary  food  and  drink. 

The  motor  function  and  the  activity  of  the  stomach  were  considered 
by  Leube  as  sufficiently  good  if,  in  the  course  of  from  five  to  seven  hours, 
after  a  test-meal  at  midday  consisting  of  soup,  meat  and  a  roll,  an  evening 
washing  of  tlie  stomach  showed  it  to  be  almost  or  entirely  empty.  If,  at 
this  time,  considerable  quantities  of  the  midday  meal  are  still  found  in 
the  stomach,  digestion  is  slow  or  imperfect.  Such  a  stomach,  however,  as 
is  taught  by  clinical  experience,  will  during  the  night  rid  itself  of  its  con- 
tents and  become  empty  by  the  morning  even  if  another  meal  has  been 
eaten  in  the  evening  before  complete  emptying.  I,  therefore,  regard  a 
stomach  which  does  not  become  empty  during  the  night,  and  in  which  early 
in  the  morning  remains  of  food  from  the  previous  day  are  still  present, 


THE  HISTORY  OF  GASTRIC  LAVAGE  45 

as  deficient  in  a  motor  respect  only.  A  flaccid  or  atonic  stomach  is  occa- 
sionally not  empty  early  in  the  morning  on  account  of  an  error  in  diet, 
either  by  overloading  and  over-distending  it,  or  because  of  improper  food 
and  an  improper  mode  of  life,  while  it  may  be  quite  capable. of  digesting 
and  assimilating  suitable  food.  On  the  other  hand  a  dilated  stomach  in 
consequence  of  moderate  stenosis  of  the  pylorus  may,  for  a  long  time — 
until  improved  by  washing — show  motor  insufficiency,  but  in  severe  cases 
it  is  permanently  in  this  condition,  in  which  case  it  is  never  empty  early  in 
the  morning,  and  is  therefore  incurable  by  gastric  lavage. 

At  this  point  I  shall  mention  what  Kussmaul  found  to  be  the  limita- 
tions of  his  method  in  the  treatment  of  gastric  dilatation.  He  was  able 
to  cure  dilatation  of  the  stomach  by  gastric  lavage  when  no,  or  only  mod- 
erate, constriction  of  the  pylorus  or  duodenum  was  present.  No  cure,  hut 
amelioration  only,  could  be  brought  about  by  gastric  lavage  in  the  follow- 
ing conditions: 

1.  In  malignant  stenosis  of  the  pylorus, 

2.  In  very  decided  cicatricial  narrowing  of  the  pylorus,  and 

3.  In  moderate  narrowing,  when  the  gastric  wall,  in  consequence  of 
chronic  gastritis,  had  suffered  such  extreme  degeneration  as  no  longer  to  he 
capable  of  retrogression. 

For  the  cases  which  at  that  time  (1869)  were  looked  upon'as  incurable, 
gastric  lavage  was  evidently  a  remedy  that,  if  employed  early,  would  decid- 
edly prolong  life  and  markedly  improve  the  nutrition. 

"  N^aturally,  a  cicatricial  narrowing  which  cannot  be  dilated  even  to 
the  extent  that  a  goose  quill  may  pass  through  the  pylorus,  can  never  be 
cured  by  gastric  lavage."  With  keen  discernment,  the  great  master  con- 
tinues: ""  Whether  in  the  most  daring  ages  of  a  distant  future,  an  attempt 
may  he  made  to  produce  radical  results  hy  gastrostomy,  and  to  form  a 
gastric  fistula  and  dilatation  of  the  stricture  hy  the  Jcnife  or  sound,  no  one 
can  to-day  positively  assert.  We  fear  that  even  the  proposal  of  such  a 
method  of  relief  may  expose  us  to  silent  or  expressed  ridicule."  Kussmaul, 
DeutscJi.  Archiv  fiir  Klin.  Medicin,  vi,  p.  485. 

Perhaps  it  was  the  inspiration  of  this  ingenious  thought  of  Kussmaul's 
which  stimulated  his  friend  Billroth  (who  was,  unfortunately,  too  early 
removed  from  his  sphere  of  activity)  to  attempt  the  cure  of  heretofore 
incurable  gastric  diseases,  in  which  internal  treatment  had  been  of  no  avail, 
by  operative  procedures. 

But  this  was  by  no  means  left  to  a  later  race  of  surgeons;  by  means 
of  antisepsis  and  asepsis  the  contemporaries  of  Kussmaul  have  been  enabled 
to  operate  on  diseased  organs  within  the  cavities  of  the  body.  Since  that 
time  surgery  of  the  abdominal  organs — and,  by  no  means  least,  gastric  sur- 
gery— has  had  a  brilliant  and  wonderful  success.  At  the  turn  of  the  cen- 
tury the  realms  of  internal  medicine  and  surgery  are  no  longer,  as  a  few 
decades  ago,  sharply,  almost  diametrically,  opposed  to  each  other,  but,  in 


46        HISTORY   AND  CLINICAL  INDICATIONS  OF  GASTRIC  LAVAGE 

united  labor,  such  as  Kussmaul  saw  with  his  mind's  eye  or  hoped  for,  the 
physician  and  the  surgeon  are  working  hand  in  hand  to  reach  the  same 
high  goal:  To  cure! 

THE   CLINICAL  EMPLOYMENT   OF   GASTRIC   LAVAGE 

Owing  to  the  results  achieved  by  gastric  lavage  and  diet,  the  treatment 
of  diseases  of  the  stomach  has  become  one  of  the  most  grateful  tasks  of 
the  internal  clinician.  In  the  interest  of  the  practising  physician  it  is 
to  be  greatly  deplored  that  this  realm,  which  is  constantly  extending, 
threatens  to  become  the  domain  of  specialists.  For  the  peculiar  sense  of 
satisfaction  which  springs  from  the  consciousness  of  having  relieved  the 
sick  from  distress,  and  which  richly  compensates  the  physician  for  many 
wearv  hours  of  his  professional  life,  can  scarcely  be  greater  after  a  fortunate 
version  or  forceps  extraction,  after  the  curative  removal  of  pus  from  a  con- 
cealed abscess,  after  the  removal  of  an  obstruction  to  respiration  by  the 
aspiration  of  a  pleural  exudate  or  of  ascites,  or  after  the  instrumental 
relief  of  an  over-distended  bladder  difficult  to  reach — than  after  a  gastric 
lavage,  whicli  frees  from  his  painful  condition  an  unfortunate  whose 
stomach  has  no  longer  the  power  to  empty  itself. 

The  dread  of  disagreeable  consequences  which  the  first  trial  of  gastric 
lavage  brings  to  the  physician  as  well  as  to  the  patient,  and  also  the 
possible  danger  of  certain  unfortunate  errors  in  technic  for  which  we  are 
responsible,  may  restrain  some  physician,  whose  position  in  regard  to  his 
patient  is  often  very  difficult,  from  employing  this  otherwise  most  useful 
method.  Nevertheless,  particularly  in  severe  disease,  the  value  of  gastric 
lavage  carried  out  at  the  right  time  is  so  great,  and  the  injury  which 
ensues  from  neglecting  the  necessary  emptying  of  the  stomach  may  be 
so  considerable,  that  personal  considerations  must  be  set  aside.  Besides, 
with  the  methods  in  vogue  to-day  it  is  quite  possible  to  use  the  stomach- 
tube  for  diagnostic  and  therapeutic  purposes  in  such  a  way  that  harm 
to  the  patient  may  be  absolutely  avoided. 

The  technic  of  gastric  lavage  has  become  of  such  vast  practical  impor- 
tance, for  the  physician  as  well  as  for  the  patient,  that  I  am  led  minutely  to 
detail  some  old,  well-tried  Titles  which  I  learned  and  constantly  used  in 
association  with  my  highly  honored  teacher,  Kussmaul. 

Tlie  stomach-tube,  as  is  well  known,  serves  for  diagnostic  and  therapeutic 
purposes.  We  test  the  function  of  the  stomach  to  aid  us  in  the  diagnosis 
of  a  gastric  alTection  or  in  the  correct  decision  as  to  the  part  which  the 
stomacli  ])erforins  in  a  complex  of  pathologic  phenomena.  This  test  com- 
])rises  two  parts:  A  test  of  the  gastric  contents  at  the  height  of  digestion, 
and  a  test  lavage. 

A  test  of  the  gastric  contents  is  made  a  certain  time  after  the  admin- 
istration of  a  test-meal,  usually  from  three  to  three  and  a  half  hours  after 


THE  CLINICAL  EMPLOYMENT  OF  GASTRIC  LAVAGE  47 

a  meal  consisting  of  gelatinous  soups  (250),  roast  beef  (200),  and  mashed 
potatoes  (200),  or  one  hour  after  a  trial  breakfast  consisting  of  tea  and 
a  roll.  By  means  of  the  stomach-tube  a  sufficient  quantity  of  the  gastric 
contents  is  obtained  for  chemical,  physiologic  and  microscopic  investiga- 
tion, so  that  we  may  examine  the  secretory  and  fermentative  processes  in 
the  stomach. 

The  trial  lavage  of  the  stomach  takes  place  early  in  the  morning,  the 
stomach  of  the  patient  being  empty,  and  enables  us  to  form  conclusions 
regarding  its  motor  activity,  as  well  as  also  in  regard  to  many  pathologic 
conditions,  such  as  catarrh,  secretory  irritative  phenomena,  continuous 
secretion  of  gastric  juice,  and  stagnation  and  decomposition  of  food. 

In  the  trial  lavage  of  the  stomach,  which  naturally  should  be  empty,  we 
must  not  neglect  to  secure  separately  the  stagnating  contents  or  the  first 
fluid  which  comes  from  the  stomach,  and  these  should  be  examined  chemi- 
cally and  microscopically — at  least,  with  litmus  paper  and  with  Congo 
paper.  If  circumstances  permit,  a  test  of  the  gastric  contents  should  first 
be  made,  and  then  the  trial  lavage  should  be  attempted;  there  should  be 
'a  day  of  rest  between  these  procedures. 

How  these  results  assist  in  the  diagnosis  and  indications  for  treatment 
will  be  described  later. 

The  therapeutic  indications  obtained  by  the  aid  of  the  gastric  tube  are 
manifold.  * 

Frequently  the  stomach-tube  is  used  for  the  purpose  of  emptying  and 
washing  the  stomach.  Such  stomach  washings  are  indicated  in  all  cases 
in  which  the  stomach,  early  in  the  morning,  is  not  empty,  but  in  which 
are  found  remains  of  food  from  the  preceding  day  (or  even  earlier),  mucus 
or  gastric  juice  containing  hydrochloric  acid  such  as  occurs  in  chronic  gas- 
tric catarrh,  and  a  continuous  flow  of  gastric  juice  in  consequence  of  perma- 
nent irritative  conditions  of  the  gastric  mucous  membrane. 

Even  if  the  stomach  early  in  the  morning  is  quite  empty,  gastric  lavage 
is  often  performed.  Washing  or  spraying  the  gastric  wall  with  the  stomach- 
douche  may  be  designated  as  the  best  remedy  to  stimulate  the  appetite,  the 
flaccid  gastric  musculature  and  the  secretory  glandular  apparatus,  and  also 
to  relieve  irritative  conditions  and  pain  or  vomiting.  All  of  the  symptoms 
just  mentioned  are  indications  for  the  employment  of  the  stomach-douche. 
Instead  of  water  of  varying  temperature  (usually  from  86°  to  95°  F.) 
saline  solution,  mineral  water  and  diluted  drugs  of  various  kinds  are  em- 
ployed, according  to  circumstances. 

Gastric  lavage  is  also  frequently  and  successfully  employed  in  disturb- 
ances of  function  and  in  diseases  of  the  intestine  and  of  the  liver,  in  con- 
ditions of  abnormal  blood-mixture,  in  renal  diseases,  and  in  acute  poison- 
ing, as  well  as  in  chronic  states  of  intoxication,  for  example,  uremia. 

The  indication  for  gastric  lavage  in  ileus  (intestinal  obstruction)  deserves 

special  mention. 
5 


48       HISTORY  AND  CLINICAL  INDICATIONS  OF  GASTRIC  LAVAGE 

Before  each  introduction  of  the  stomach-tube  or  of  the  sound  the  patient 
must  be  carefully  examined,  since  this  alone  makes  it  possible  to  discrim- 
inate in  the  choice  of  patients,  and  to  exclude  those  in  whom  gastric  lavage 
might  be  dangerous. 

In  deciding  what  cases  are  suitable  for  gastric  lavage  it  must  be  remem- 
bered that  the  first  introduction  of  the  stomach-tube  almost  invariably 
produces  excitement,  retching,  and  nausea,  sometimes  also  difficulty  in 
respiration  and  cardiac  palpitation.  Some  patients,  in  consequence  of 
psychic  stimulation,  hold  the  breath,  become  cyanotic,  and,  by  a  mighty 
exertion  of  the  prelum  abdominale,  bring  about  a  decided  rise  in  blood- 
pressure.  In  irritable  and  anxious  patients,  all  these  symptoms  appear 
more  rapidly  and  reach  a  higher  degree  than  in  persons  of  more  quiet 
temperament  who  are  able  to  control  themselves.  The  same  is  true 
of  those  who  suffer  from  diseases  of  the  respiratory  and  circulatory 
organs. 

For  this  reason  persons  who,  on  account  of  diseases  of  the  respiratory 
passages,  the  lungs  or  the  pleura,  can  only  complete  their  respiratory  inter- 
change of  gases  with  difficulty,  are  markedly  disturbed  by  gastric  lavage, 
and,  under  some  circumstances,  to  them  it  even  becomes  dangerous.  The 
effect  is  similar  in  those  who  have  a  disease  of  the  heart,  whose  myocardium 
is  weakened  or  degenerated,  or  whose  valvular  disease  is  so  defectively 
compensated  for  as  to  be  unable  to  withstand  great  variations  in  blood- 
pressure.  Therefore,  we  refrain  from  stomach  washing  and  also  stomach 
evacuation  to  promote  the  diagnostic  investigation  of  the  stomach  contents 
ivhen  severe  pulmonary  and  cardiac  affections  are  present.  If,  however, 
the  conditions  are  such  as  to  necessitate  the  introduction  of  a  gastric  tube, 
and  if  it  is  believed  that  the  value  of  this  procedure  will  outweigh  the 
possible  danger  from  its  use,  the  expert,  relying  upon  the  accurate  handling 
of  the  stomach-tube  while  carefully  regarding  the  rules  of  the  technic,  will, 
nevertheless,  attempt  to  introduce  the  instrument.  If  the  first  trial  is 
successful,  with  like  caution  others  may  follow,  for  a  sensible  patient  soon 
becomes  accustomed  to  its  use.  Many  a  phthisical  patient  by  the  washing 
out  of  the  stomach  has  gained  an  appetite,  acquired  new  strength,  and 
prolongation  of  life.  I  even  believe  that  incipient  phthisis  in  many  per- 
sons may  be  arrested  with  the  removal  of  the  anorexia  by  gastric  lavage 
and  subsequent  plentiful  feeding,  and  that  in  this  way  a  cure  may  be 
brouglit  about. 

As  a  rule,  we  avoid  the  use  of  the  stomach-tube  if  we  have  reason  to 
suspect  that  the  walls  of  the  vessels  in  any  part  of  the  body  are  not  able 
to  witlistand  a  rise  in  blood-pressure  brought  about  by  the  introduction  of 
tlio  sound,  wliieh  is  apt  to  produce  retching,  vomiting,  or  decided  action 
of  tlie  alxlominal  press.  Preceding  hemorrhages  (hemoptysis,  hematemesis, 
inolena,  apoplexy)  or  a  tendency  to  hemorrhage  still  present,  also  atheroma- 
Idiis  (irfi-rirs.  valvular  disease  of  the  heart  demonstrable  by  perciission  and 


THE  CLINICAL  EMPLOYMENT  OF  GASTRIC  LAVAGE  49 

auscultation,  and  even  suspected  aneurysmal  dilatation  of  the  aorta,  are 
valuable  guides. 

Recent  and  profuse  hemorrhages  from  the  stomach  or  from  the  lungs, 
high-graded  atheroma,  severe  cardiac  disease,  and  aortic  aneurysm  are 
always  contraindications  to  the  employment  of  the  stomach-tube. 

Capillary  hemorrhages  from  the  inflamed,  perhaps  also  eroded,  gastric 
mucous  membrane,  and  parenchymatous  bleeding  from  ulcerated,  decom- 


FiG.  2. — Terminal  piece  of  a  soft  tube  as  found  in  the  instruments  usually  on  the  market. 

posing  growths  in  the  gastric  wall,  may,  under  sOme  circumstances,  also 
be  contraindications ;  usually,  however,  they  are  not ;  but  such  hemorrhages 
generally  cease  if,  after  the  discharge  of  accumulated  and  decomposed 
masses,  the  stomach  is  again  able  to  contract.  In  hemorrhages  of  any  kind, 
even  during  the  menstrual  period,  I  only  very  exceptionally  make  a  gastric 
examination  with  the  stomach-tube  and  perform  gastric  lavage.  During 
menstruation  the  gastric  mucous  membrane  of  many  women  is  somewhat 
inclined  to  hemorrhage.  For  this  reason  I  interrupt  the  treatment  by  gas- 
tric lavage,  and  resume  it  only  two  or  three  days  after  the  menstrual  period. 
According  to  experience,  women  during  menstruation  digest  food  less  well, 
and  they  secrete  a  weaker  gastric  juice  than  at  other  times,  therefore  it 
is  well  to  defer  the  investigation  of  the  gastric  contents. 

To  obtain  the  gastric  contents  and  for  gastric  lavage  we  employ  exclu- 
sively soft  stomach-tuhes,  and  preferably  those  of  English  manufacture 
(Jaques's  esophagus  tube)  on  account  of  their  smooth  surface  and  great 
flexibility.     However,  these  English  tubes  have  glaring  defects  which  for 


Fig.  3. — ^Terminal  piece  of  a  soft  tube  with  a  lateral  opening,  and  a  central  opening  in  the 
longitudinal  axis  of  the  tube.  This  tube  appears  to  me  to  be  most  dangerous  to  the 
mucous  membrane  of  the  pharynx,  of  the  esophagus,  and  of  the  stomach. 

some  unaccountable  reason  the  manufacturers  do  not  remedy.  Their  open- 
ings are  frequently  not  large  enough,  and  the  margins  of  the  openings,  with- 
out exception,  are  so  sharp  that  they  readily  injure  the  mucous  membrane, 
particularly  the  mucous  memhrane  of  the  stomach,  as  may  be  seen  from 
Figures  2,  3,  and  4,  which  show  the  configuration  of  the  tubes  in  natural 
size.  This  defect  may  be  remedied  by  burning  out  the  openings,  and  round- 
ing off  the  edges  with  a  hot  darning  needle  or  a  hot  glass  rod,  as  may 
be  seen  in  Figures  5  and  6.     But,  after  this  treatment  of  the  margins  of 


50       HISTORY  AND  CLINICAL  INDICATIONS  OP  GASTRIC  LAVAGE 

the  openings,  the  rubber  is  rough  for  a  time,  and  must  be  rubbed  down 
with  pumice  stone.  Besides,  the  tube  has  for  days  an  odor  of  burnt  rub- 
ber, and,  sooner  or  later,  small  rents  appear  in  the  edges  which  have  been 
burnt  and  soon  render  the  tube  unfit  for  use.     It  is  to  be  hoped  that  the 


Fig.  4. — Terminal  piece  of  a  soft  tube  with  a  central  and  numerous  lateral  openings,  and 
said  to  be  more  suitable  for  irrigation  of  the  stomach  than  tubes  with  only  two  large 
lateral  openings. 

manufacturers  will  speedily  place  on  the  market  more  serviceable  tubes 
with  rounded,  polished  edges  that  will  meet  practical  requirements. 

The  introduction  of  a  staff  or  mandrin  into  a  soft  stomach-tube  is 
decidedly  objectionable,  for,  with  a  mandrin  inside,  the  soft  tube  again 
becomes  a  hard  sound  with  all  of  its  defects  and  dangers.  They  are  only 
required  in  gastric  lavage  and  artificial  nutrition  when  it  is  necessary  to 
overcome  an  obstruction  in  the  front  of  the  stomach,  in  narrowing  of  the 
esophagus,  or  in  deep-seated  dilatations  of  the  esophagus,  for  example,  in 
some  ante-stomachs. 

Preparation  of  the  Patient. — Before  the  first  introduction  of  the 
stomach-tube  I  have  never  failed  minutely  to  inform  patients  who  are  at 
all  intelligent  regarding  the  purpose  and  utility  of  the  proceeding,  to  call 
their  attention  to  its  harmlessness,  and  to  teach  them  how  to  conduct  them- 
selves during  the  operation.      Whenever  possible,  I  have  always  allowed 


Figs.  5  and  6. — Terminal  piece  of  soft  tubes  whose  openings  have  been  rounded  off  by  a 
hot  glass  rod  and  thereby  rendered  harmless. 

nervous  patients  an  opportunity  to  see  how  willingly  other  patients  with 
practice  swallow  the  tube  themselves  and  permit  lavage. 

The  patient  now  sits  erect  in  a  chair,  or,  if  in  bed,  sits  upon  the  edge 
of  the  l)ed.  A  basin  is  given  him  in  which  to  catch  the  saliva  which  flows 
from  tlie  mouth,  or  the  vomited  material,  and  which  he  holds  with  both 
hands,  so  as  not  to  disturb  the  physician  by  making  motions  to  oppose  him. 
if  dealing  with  patients  who  have  very  sensitive  pharyngeal  mucous  mem- 
branes, such  as  smokers  who  retch  easily  and  show  a  tendency  to  vomit. 


THE  CLINICAL  EMPLOYMENT  OF  GASTRIC  LAVAGE  51 

the  introduction  should  be  preceded  by  gargling  with  a  watery  solution  of 
potassium  bromid,  or  by  painting  the  pharynx  with  cocain,  when  the  sensi- 
tiveness and  reflex  irritability  of  the  structures  of  the  pharynx  may  be  so 
controlled  that  we  may  proceed  with  the  introduction  of  the  tube.  Arti- 
ficial teeth  must,  naturally,  be  removed.  The  patient  should  be  allowed 
to  drink  some  water  before  the  lavage,  so  that  the  mucous  membrane  of 
the  mouth,  tongue,  palate,  pharynx  and  esophagus  may  be  moistened  and 
more  readily  permit  the  passage  of  the  tube.  Where  there  is  a  very  irrita- 
ble stomach  and  a  great  tendency  to  vomit,  the  patient  should  even  be 
made  to  swallow  a  considerable  quantity  of  water  before  the  introduction 
of  the  tube,  so  that  this  will  not  reach  an  entirely  empty  stomach  and, 
by  direct  contact  with  its  walls,  produce  great  irritation. 

Naturally,  if  we  desire  to  obtain  the  gastric  contents  for  the  purpose 
of  analytical  examination,  water  is  not  permitted  before  the  introduction 
of  the  tube.  In  this  case  the  prevention  of  retching  and  a  tendency  to 
vomit  are  not  at  all  necessary  for,  under  these  circumstances,  the  evacua- 
tion of  the  gastric  contents  is  only  facilitated.  In  this  latter  operation 
— in  case  it  is  done  without  a  pump  or  aspiration  apparatus — injury  to  the 
gastric  wall  is  unlikely,  since  the  stomach  is  not  empty,  and  the  tube  can 
hardly  come  in  contact  with  the  walls  of  the  stomach. 

Preparation  of  the  Stomach-Tube. — According  to  Luschka's  plates,  the 
ninth  spinous  process  of  the  thoracic  vertebrae  corresponds  exactly  to  the 
position  of  the  cardia,  provided  the  location  of  the  abdominal  organs  is 
normal.  Before  the  first  introduction  of  the  tube  we  count  on  the  patient's 
back  the  spinous  processes  of  the  vertebral  column  up  to  this  point,  to  which 
we  apply  the  upper  opening  of  the  tube,  and  measure  along  the  vertebral 
column,  passing  alongside  the  ear  to  the  incisor  teeth,  and  mark  this  point 
upon  the  tube  with  a  waxed  silk  thread  which  we  tie  around  the  tube, 
or  with  a  colored  pencil.  If  the  tube  is  now  introduced  up  to  this  point 
it  is  certainly  in  the  stomach,  provided  this  organ  is  in  its  normal  situa- 
tion, and  it  is  unnecessary  to  shove  the  tube  up  and  down  to  ascertain 
whether  it  is  in  its  proper  position,  as  this  will  cause  retching  and  a  ten- 
dency to  vomit.  Before  the  introduction  is  begun  the  end  of  the  stomach- 
tube  is  moistened  in  luke-warm  water. 

While  the  patient  sits  erect  in  a  comfortable  position,  with  the  head 
raised,  the  mouth  open  wide,  and  the  point  of  the  tongue  placed  against 
the  lower  incisor  teeth,  the  rounded  end  of  the  stomach-tube  is  pushed 
over  the  dorsum  of  the  tongue  up  to  the  posterior  pharyngeal  wall.  The 
moment  the  tube  reaches  this  point,  the  patient  slowly  bends  his  head  for- 
ward and  simultaneously  attempts  to  swallow.  The  sound  glides  along  the 
posterior  wall  of  the  pharynx,  along  the  vertebral  column  to  the  cricoid 
cartilage,  often  even  beyond  this.  Now  we  pause  for  a  moment,  ask  the 
patient  to  breathe  deeply  and  recrnlarly,  and  then  to  swallow  again,  when 
the  tube  will  slide  downward  behind  the  larynx,  and  with  a  slight  push 

I  t_;  u  a  .^  A  »     wi 

CO  LLl£v£l£   CI--   Obn'lZUl 


52       HISTORY  AND  CLINICAL  INDICATIONS  OF  GASTRIC  LAVAGE 

on  the  part  of  the  physician  the  instrument  is  rapidly  introduced  up  to 
the  required  mark.  When  this  is  accomplished  the  tube  is  held  firmly  until 
the  patient  breathes  quietly  and  regularly,  and,  in  the  meantime,  a  ring 
of  hard  rul)ber  which  encircles  the  tube,  is  put  between  his  teeth,  and  upon 
this  ring  he  may  bite. 

Tiie  further  procedure  depends  upon  the  purpose  for  which  the  tube 
has  been  introduced. 

To  Test  the  Gastric  Contents. — If  it  is  desirable  to  obtain  some  of  the 
gastric  contents  for  a  test  of  the  chemism  of  the  stomach,  we  direct  the 
patient,  after  the  tube  has  been  introduced  and  is  in  the  right  position,  to 
contract  his  abdominal  muscles  as  if  he  were  having  an  evacuation.  By 
this  exertion  of  the  abdominal  press,  the  gastric  contents  are  brought  up 
through  the  tube  and  mpy  be  caught  in  a  vessel  held  for  the  purpose. 

It  may  happen  that,  on  pressing,  only  air  comes  up  through  the  tube 
and  none  of  the  ingesta.  The  tube  is  then  gently  pushed  further  down, 
and  after  a  few  deep  respirations  renewed  attempts  at  expression  are  made. 
"\\'ilh  very  flabby  abdominal  walls,  the  result  may  sometimes  be  brought 
about  by  jiressing  a  hand  upon  the  back  and  one  upon  the  abdomen  to 
assist  the  abdominal  press,  or  by  raising  the  protruding  abdomen  so  as 
to  bring  the  descending  stomach  and  its  contents  nearer  the  vicinity  of 
the  tube. 

//  these  manipulations  are  futile,  either  the  stomach  is  empty  or  the 
tube  is  clogged  by  insuMciently  masticated  particles  of  meat  of  the  test- 
meal  which  have  not  yet  been  dissolved  in  the  stomach  and  are  too  large 
to  pass.  It  is  not  always  easy  to  determine  which  of  these  two  possibilities 
is  the  case.  If,  on  repeated  attempts  at  pressing,  only  air  comes  up 
tlirough  the  tube — and  this  may  be  recognized  by  the  sound  which  accom- 
panies it — this  is  in  favor  of  the  stomach  being  empty.  If,  on  the  other 
hand,  upon  attempts  at  pressure  nothing  or  only  the  sound  of  air  is  heard, 
which  suddenly  ceases,  or  if  the  stream  of  stomach  contents  suddenly  stops 
flowing  from  the  tube  and  does  not  again  flow  when  pressure  is  made,  the 
tube  is  clogged.  It  may  be  that  the  tube  is  not  clogged  by  particles  of 
food,  but  that  a  fold  of  the  gastric  mucous  memirane  is  sucked  into  the 
opening  of  the  tube  and  thus  closes  the  opening.  The  latter  possibility 
must  be  l)orne  in  mind  if,  upon  pressure,  neither  air  nor  stomach  contents 
eonie  forth. 

In  such  cases  there  is  danger,  by  rapid  displacement  of  the  tube,  of 
injuring  the  gastric  mucous  membrane,  or  of  tearing  off  a  fold  of  the 
mucous  membrane  which  has  been  sucked  into  the  opening  of  the  tube. 
(Jreat  care  is  necessary  in  moving  or  in  withdrawing  the  tube.  To  be 
assured  of  the  results  when  gastric  contents  are  not  brought  up  through 
tlie  tube,  hold  it  firmly,  connect  it  with  the  other  parts  of  the  lavage 
a]iparatus.  and  permit  a  measured  quantity  of  lukewarm  water  to  fiow  into 
iho  stomach.     If  this  water,  upon  lowering  the  funnel,  regurgitates  quite 


THE  CLINICAL  EMPLOYMENT  OF  GASTRIC  LAVAGE 


53 


pure,  the  stomach  has  passed  the  test-meal  into  the  intestine,  and  the  tube 
may  now  be  removed  with  the  observance  of  the  necessary  precautions.  The 
attempt  to  obtain  the  gastric  contents  has,  under  such  circumstances,  failed, 
and  if  we  desire  to  obtain  further  insight  into  the  chemism  of  the  stomach 
the  test-meal  must  be  repeated 
at  some  other  time,  and  at  an 
earlier  hour.  At  all  events,  the 
operation  gives  proof  of  a  nor- 
mal, even  increased,  motor  activ- 
ity (hypermotility)  which  com- 
pensates for  secretory  disturb- 
ances. 

A  proof  that  the  tube  has 
been  clogged,  and  that  the  stom- 
ach is  not  empty,  is  the  fact  that 
water  poured  into  the  stomach 
reappears  mingled  with  gastric 
contents  when  the  funnel  is  low- 
ered. Qualitative  investigation 
for  hydrochloric  acid,  at  least 
with  Congo  paper,  may  be  made 
in  the  fluid  thus  obtained,  but 
no  quantitative  results  are  fur- 
nished. Under  these  circum- 
stances, therefore,  another  test- 
meal  must  be  given,  the  attempt 
be  repeated  another  day,  with  due 
care  that  the  meat  has  been  fine- 
ly chopped  so  as  to  avoid  clog- 
ging of  the  stomach-tube.  In  the 
first  attempt,  I  do  not  have  the 
meat  for  the  test-meal  chopped,  for  it  often  aids  us  in  the  etiology  and 
treatment  of  many  digestive  disturbances  to  know  how  the  patient  chews. 

Gastric  Lavage. — For  stomach  washing  we  require  an  apparatus  (Fig.  7) 
which  is  composed  of  (he  already  mentioned  stomach-tube  and  the  ring 
which  is  placed  over  it  and  held  between  the  incisor  teeth  (Fig.  8)  for 
biting,  a  glass  funnel  holding  from  one-half  to  three-quarters  of  a  liter, 
and  a  rubber  tube  one  and  one-half  meters  long  interrupted  in  its  lower 
third  by  a  short  glass  tube  which  is  connected  with  the  funnel,  also  an 
inserted  piece  by  which  the  rubber  tube  is  readily  attached  to  the  stomach- 
tube.  This  enclosed  piece  (Fig.  9)  is  made  of  hard  rubber,  and  is  of  the 
form  and  size  depicted  in  the  illustration.  The  round  end,  a,  is  placed 
toward  the  funnel  and  attached  to  the  rubber  tube.  At  h  there  is  a  faucet 
which  is  usually  firm  and  air-tight,  but,  under  certain  conditions  which  we 


Fig.  7. — Complete  apparatus  for  washing  the 
stomach.  (After  Kussmaul.)  a,  funnel;  b, 
rubber  tube,  one  and  one-half  meters  long; 
c,  glass  connecting  piece;  d,  enclosed  piece 
of  hard  rubber  with  cock;  e,  stomach-tube; 
/,  ring  of  hard  rubber  on  which  to  bite. 


54       HISTORY  AND  CLINICAL  INDICATIONS  OF  GASTRIC  LAVAGE 


will  learn  to  recognize,  may  be  removed  for  a  short  time.  The  conically 
narrowing  end,  c,  of  the  inserted  piece  answers  the  purpose  of  connecting 
the  tube  with  the  stomach-tube  and,  on  account  of  its  shape,  fits  a  tube  of 
any  caliber. 

If  the  stomach-tube  has  been  introduced  according  to  the  directions 
given,  the  biting  ring  is  between  the  incisor  teeth,  and  everything  else  in 
position,  we  fill  the  lowered  funnel  with  lukewarm  water,  and  then  raise 
it  so  that  the  water  fiows  into  the  stomach.  When  proper  assistance  is 
given  I  permit  the  funnel  to  be  filled  as  soon  as 
the  tube  has  passed  the  larynx  and  before  it  is 
introduced  and  elevated. 

The  rapidity  with  which  the  water  flows  into  the 
stomach  depends  upon  the  pressure  of  the  column 
of  water,  i.  e.,  upon  the  elevation  of  the  funnel,  upon 
the  degree  of  contraction  of  the  gastric  muscula- 
ture, and  upon  the  pressure  of  the  prelum  abdomi- 
nale.  Under  some  circumstances,  as  in  retching  or 
coughing,  nothing  flows  into  the  stomach,  and  even 
when  the  funnel  is  raised  very  high  either  the  water 
for  washing  or  some  of  the  gastric  contents  returns 
through  the  tube.  On  the  other  hand,  if  the  stom- 
ach walls  are  flaccid,  on  deep  inspiration  and  in 
consequence  of  the  diminished  intra-abdominal  pres- 
sure the  water  is  aspirated  into  the  stomach  and 
actually  streams  into  this  organ.  It  may  then  occur, 
if  the  funnel  is  raised  high,  that  a  bubble  arises  and 
by  means  of  this,  simultaneously  with  the  water,  air 
is  aspirated  into  the  stomach  and  causes  an  over- 
distention  of  the  organ.  A  simple  artifice,  namely, 
slanting  the  funnel,  may  prevent  this  difficulty. 

Before  the  funnel  becomes  quite  empty,  it  must  be 
rapidly  lowered  so  that  no  air  can  pass  into  the  tube, 
and  the  continuous  fiow  of  water  through  the  tube  is 
not  interrupted.  On  lowering  the  funnel,  a  siphon 
action  takes  place,  and  the  water  regurgitates  into  the  funnel.  It  may  now 
be  collected,  examined,  its  reaction  tested  with  litmus  or  Congo  paper,  and 
we  should  carefully  observe  whether  as  much  water  flows  out  of  the  stomach 
as  has  been  poured  in.  By  this  precaution,  it  is  quite  impossible  to  damage 
the  stomach  by  over-filling  it  with  fluid.  In  the  stomach-tube  and  in  the 
wash-tube,  even  after  emptying  the  funnel,  a  column  of  fluid  remains.  A 
glance  at  the  glass  tube  within  the  stomach-tube  will  show  of  what  this  fluid 
column  consists.  If  it  is  clear,  or  but  slightly  turbid,  we  should  continue 
the  lavage.  The  lowered  funnel  is  refilled  with  water,  is  raised  and  low- 
ered again,  the  water  used  for  washing  is  collected  and  emptied,  as  before. 


Fig.  8. — Ring  on  which 
to  bite  (of  hard  rub- 
ber) drawn  over  the 
sound,  and  readily 
moved  about  upon  it. 


THE  CLINICAL  EMPLOYMENT  OF  GASTRIC  LAVAGE  55 

If,  however,  the  fluid  in  the  tube  is  quite  turbid,  or  decidedly  mixed  with 
mucus,  remains  of  food  or  the  like,  the  faucet  at  the  inserted  piece  is 
removed  for  a  moment  so  that  air  enters  the  tube  and  the  contents  flow 
toward  the  funnel.  When  this  is  done,  the  faucet  is  reintroduced,  the 
washing  is  continued,  the  faucet  is  again  removed,  and  if  the  water  returned 
a  second  or  third  time  through  the  funnel  is  not  yet  clear,  this  process  is 
continued  until  the  water  flows  clear.  Without  the  enclosed  piece  with  the 
faucet — which,  by  the  way,  is  the  invention  of  an  artillery  oSicer  who  was 
treated  in  Kussmaul's  Clinic  for  dilatation  of  the  stomach — the  soiled  water 
is  again  forced  through  the  tube  and  returns  to  the  stomach.  The  process 
is  then  unnecessarily  prolonged,  and  this  is  an  evil  of  some  consequence  in 
debilitated  patients,  one  which  is  obviated  by  the  introduction  of  the  en- 
closed piece,  which  is  as  simple  as  it  is  ingenious. 

The  stomach,  as  a  rule,  is  washed  until  it  is  clean,  provided  the^  patient 
is  able  to  hear  it.  In  very  irritable  patients  we  must  reckon  upon  their 
resistance,  and,  particularly  in  the  first  lavage,  we  may  be  obliged  to  desist 


Fig.  9. — Inserted  piece  of  hard  rubber  with  cock. 

before  this  end  is  attained.  Even  with  patients  whose  activity  and  self- 
control  is  only  slightly  diminished,  days  frequently  pass  before  the 
remains  of  food  from  former  meals  can  be  removed  from  a  dilated 
stomach. 

Besides,  a  return  flow  of  clear  water  does  not  always  indicate  that  the 
stomach  is  actually  clean.  For  example,  mucus,  which  often  thickly  coats 
the  gastric  walls,  dissolves  hut  slightly  or  not  at  all  in  pure  water;  the  water 
may,  therefore,  flow  off  clear  while  a  mucus  coat,  rich  in  microbes  and  fer- 
ments, may  still  adhere  to  the  gastric  mucous  membrane.  If,  in  such  cases, 
alkaline  waters  or  solutions  of  soda  and  table  salt  are  used  for  washing,  it 
is  frequently  astonishing  to  see  the  amounts  of  mucus  brought  up. 

The  conditions  are  somewhat  different  in  a  flaccid  and  dilated  or 
abnormally-formed  stomach.  When  the  patient  is  in  a  sitting  posture,  the 
fluid  reaches  only  the  lower  segment  of  the  flaccid  sac,  and  sprays  the  pos- 
terior gastric  wall  and  the  small  curvature,  also  the  region  of  the  cardia 
and  the  fundus,  slightly  or  not  at  all.  If  the  patients  with  gastric  dilata- 
tion who  have  become  accustomed  to  the  sound  are  made  to  lie  down  after 
an  apparently  satisfactory  washing  carried  out  in  a  sitting  posture,  and 


56       HISTORY  AND  CLINICAL  INDICATIONS  OF  GASTRIC  LAVAGE 

lavage  is  continued  while  in  the  recumbent  posture,  surprisingly  large  quan- 
tities of  mucus  and  remains  of  food  are  brought  up  with  the  water.  Those 
who  have  become  accustomed  to  lavage  in  the  recumbent  posture  bear  it 
very  well,  so  that,  after  the  stomach  is  filled  with  water,  this  fluid  may  be 
moved  to  and  fro  in  the  stomach  by  movement  of  the  trunk.  The  gastric 
wall  is  thus  thoroughly  washed  up  to  the  small  curvature,  which  is  par- 
ticularly important  since  this  area  is  the  preferable  seat  of  the  severest 
gastric  diseases. 

In  hour-glass  stomachs,  those  with  deep  diverticulum-like  sacs  formed 
by  cicatrices,  also  in  such  as  have  a  markedly  developed  antrum  pyloricum 
and  antrum  cardiacum,  we  sometimes  observe  that,  after  an  apparently  thor- 
ough gastric  lavage,  turbid  gastric  contents  which  have  been  enclosed  in  a 
sac  suddenly  pour  into  the  funnel.  The  symptom  may  frequently  be  utilized 
in  diagnosis. 

In  removing  the  stomach-tube  when  the  washing  is  finished,  we  will 
note  that,  with  a  lowered  funnel,  a  column  of  fluid  remains  in  the  tube 
because  the  gastric  wall  contracts  firmly  around  the  lower  end  of  the  tube 
and  closes  the  opening.  By  the  siphon  action,  folds  of  mucous  membrane 
may  even  be  drawn  into  the  opening  of  the  tube,  and,  should  this  occur, 
the  flow  of  water  will  cease  suddenly  with  a  jerk  which  may  often  be  felt 
throughout  the  entire  tube.  If,  at  this  moment,  the  stomach-tube  should 
be  rapidly  withdrawn,  there  is  great  danger  of  injuring  the  mucous  mem- 
brane, or  even  of  tearing  off  a  portion  of  it  that  has  been  sucked  into 
the  tube. 

This  danger  may  very  readily  be  averted  by  holding  the  tube  without 
moving  it,  pouring  a  little  water  into  the  funnel  which  is  raised,  and  then 
slowly  withdrawing  the  tube,  when  water  will  again  flow  into  the  stomach, 
and  the  mucous  membrane  be  forced  away  from  the  opening  of  the  tube. 
When  the  tube  is  so  far  withdrawn  that  the  opening  is  above  the  cardia 
we  compress  it  in  order  to  prevent  any  fluid  from  entering  the  air  passages 
while  the  tube  is  passing  over  the  epiglottis. 

Immediately  after  lavage  the  patients  should  have  some  breakfast  and 
then  rest  for  a  little  while;  they  should  make  no  exertion  whatever  for  at 
least  an  hour  afterward. 

Individualization  and  Interruption  of  Gastric  Lavage. — Individuality 
of  character  and  will  power  exert  quite  an  influence  upon  the  course  of 
operations,  which,  like  most  stomach  washings,  necessitate  some  assistance 
on  the  part  of  the  patient.  Where  this  influence  is  a  deleterious  one,  the 
physician,  by  his  personality  and  skill,  may  be  able  to  overcome  it  after 
a  time. 

Moreover,  there  are  definite  pathological  conditions  to  be  considered  in 
the  case,  the  influence  of  which  upon  the  course  of  the  operation  cannot 
l)e  foreseen  nor  always  prevented,  and,  under  some  circumstances,  they  may 
be  so  great  that  lavage  must  be  discontinued.     We  refer  particularly  to 


THE  CLINICAL  EMPLOYMENT  OF  GASTRIC  LAVAGE  57 

the  danger  of  extraordinary  irritability  of  the  gastric  mucous  membrane 
and  the  danger  of  hemorrhage. 

According  to  experience  lavage  is  best  borne  by  patients  with  gastric 
dilatation,  therefore  by  those  to  whom  this  operation  is  most  necessary. 
The  mucous  membranes  of  the  stomach  and  esophagus  are  so  benumbed 
by  the  intense  irritation  of  the  stagnating  gastric  contents  and  by  vomit- 
ing that  they  do  not  react  to  the  irritation  of  the  tube  and  the  cleansing 
fluid.  Hence  the  danger  of  injury  to  the  mucous  membrane  by  the  stomach- 
tube  in  gastric  dilatation  is  very  slight. 

The  condition  is  different  in  irritable  stomachs  which  are  not  dilated, 
which  are  sometimes  even  decreased  in  size  (contracted  or  concentrically 
hypertrophied),  which  react  by  a  decided,  sudden  contraction,  by  retching 
and  vomiting,  or  by  cough,  to  the  least  irritation ;  for  example,  to  the  slight- 
est movement  of  the  introduced  stomach-tube,  to  a  touch  of  the  latter  against 
the  stomach  wall,  to  the  inflow  of  the  fluid,  or  to  the  temperature  or  com- 
position of  the  same.  Vomiting  in  such  cases  often  has  a  peculiar  expulsive 
character.  The  water  suddenly  gushes  from  the  mouth  with  great  force 
so  that  care  is  necessary  in  handling  the  stomach-tube. 

In  such  irritable  stomachs  another  grave  danger  is  that,  after  a  sudden 
attack  of  retching  with  severe  vomiting,  or  after  an  attack  of  coughing, 
the  gastric  wall  is  forced  against  the  stomach-tube,  and  consequently  the 
mucous  membrane  is  rubbed  against  the  opening  of  the  tube  and  becomes 
excoriated,  or  a  fold  of  the  mucous  membrane  is  sucked  into  the  opening 
and  torn  off,  or,  if  the  stomach-tube  has  not  been  adjusted  carefully  enough, 
it  is  forced  out  of  the  stomach. 

These  stormy  reactions  of  extremely  irritable  stomachs  frequently  cease 
if  the  patient  obeys  the  command  to  breathe  deeply  and  regularly.  In 
other  cases,  the  stream  of  luke-warm  water  flowing  from  the  funnel  held 
as  high  as  possible  quiets  the  irritable  gastric  walls.  If  this  is  not  the 
case,  it  is  risky  to  continue  the  lavage.  It  is  wise  to  observe  all  pre- 
cautions; we,  therefore,  slowly  withdraw  the  stomach-tube,  and  defer  the 
operation  until  another  morning.  Before  attempting  it  again,  we  should 
never  neglect  to  call  the  attention  of  the  patient  to  the  mistakes  of  the 
last  washing,  to  caution  him  to  breathe  deeply  and  regularly,  and  to  avoid 
this  or  that  bad  habit.  If  catarrh  of  the  pharynx  is  present,  this  also 
should  receive  the  necessary  treatment. 

In  another  category  of  gastric  affections,  lavage  is  disagreeable,  and 
even  dangerous,  because  of  the  great  tendency  of  the  gastric  mucous  mem- 
brane to  hemorrhage.  In  the  accidents  during  lavage  which  have  heen 
described  above,  hemorrhages  may  also  occur,  but  only  in  consequence 
of  previous  gross  mechanical  injuries.  Here  we  are  dealing  with  hemor- 
rhages which  occur  without  such  injuries. 

There  are  certain  catarrhs  of  the  stomach  in  which  the  mucous  mem- 
brane, particularly  at  the  height  of  its  folds,  is  enormously  hyperemic. 


58       HISTORY  AND  CLINICAL  INDICATIONS  OF  GASTRIC  LAVAGE 

The  dilated  capillaries  of  the  mucous  membrane  mostly  show  such  an 
extreme  permeability  that  quite  insignificant  variations  in  pressure  are 
sufficient  to  cause  mucous  membrane  hemorrhages.  Among  many  thousand 
cases  of  lavage,  I  have  known  about  ten  such  hemorrhages  to  occur.  Al- 
though they  were  slight  they  necessitated  the  interruption  of  the  opera- 
tion and,  because  they  recurred  with  every  attempt,  I  was  compelled  to 
discontinue  lavage  entirely  in  these  cases. 

In  hysterical  patients  vomiting  of  bloody  masses  and  of  pure  blood 
occasionally  occurs  without  any  loss  of  substance  of  the  mucous  mem- 
brane. Therefore,  in  such  patients  also,  we  may  be  forced  to  withdraw 
the  stomach-tube  on  account  of  the  hemorrhagic  staining  of  the  water; 
the  same  is  true  of  gastric  crises  of  spinal  origin. 

Hemorrhages  from  esophageal  varices  must  also  be  referred  to.  They 
are  more  profuse  than  the  previously  mentioned  form,  and  closely  resem- 
ble the  hemorrhages  originating  from  gastric  ulcers.  In  a  noteworthy  case 
of  this  kind  Avhich  was  at  first  believed  to  be  ulcer  of  the  stomach,  in 
which,  however,  this  diagnosis  was  abandoned  on  account  of  the  absence 
of  all  other  symptoms  of  ulcer,  the  hemorrhages  ceased  entirely  under  the 
influence  of  lavage.  Here,  apparently,  the  introduction  of  the  tube  com- 
pressed the  ectatic  veins  of  the  esophagus.  Similar  conditions  are  seen 
in  hemorrhage  from  the  ureter,  where  catheterization  or  souiiding  acts  as 
a  potent  curative  factor. 

If,  during  lavage,  congealed  hlood  is  found  in  the  stomach  such  as  is 
observed  in  ulcerating  carcinoma,  in  old  ulcers  of  the  stomach,  and,  par- 
ticularly, where  there  is  a  stenosis  of  the  pylorus  with  a  spastic  closure 
of  the  pylorus  caused  reflexly,  producing  hypersecretion,  there  is  no  reason 
for  interrupting  the  operation.  On  the  contrary,  in  cases  of  this  kind,  the 
thorough  emptying  and  cleansing  of  the  stomach  is  an  exceedingly  bene- 
ficial measure,  and  well  calculated  to  check  an  old  hemorrhage  and  pre- 
vent a  new  one.  The  empty  and  clean  stomach  is  again  able  to  contract 
properly,  and  by  contraction  the  bleeding  surface  becomes  smaller,  the 
borders  of  the  ulcer  are  approximated,  and  the  gaping  lumina  of  the  ves- 
sels closed.  The  fresh,  and  often  not  inconsiderable,  losses  of  substance 
caused  l)y  the  tearing  off  of  particles  of  mucous  membrane  by  the  tube 
most  distinctly  show  the  mighty  styptic  influence  of  the  muscular  con- 
traction of  the  stomach.  In  the  cases  that  have  been  reported,  the  hemor- 
rliago  lias  ceased  rapidly  and  no  ulcer  formation  has  taken  place  apparently 
for  lite  reason  that  the  margins  of  the  wound,  in  consequence  of  muscular 
contraction,  have  approximated  at  once,  have  closed  and  healed,  like  opera- 
tive wouiuls  of  the  stomach,  by  first  intention. 

If,  therefore,  during  lavage,  a  fresh  hemorrhage  should  unexpectedly 
appear  and  be  indicated  by  the  red  discoloration  of  the  water,  the  physi- 
cian must  have  the  presence  of  mind  not  to  withdraw  the  sound  at  once; 
he  must  very  gently,  even  though  with  some  force,  allow  the  stomach 


THE  CLINICAL  EMPLOYMENT  OF  GASTRIC  LAVAGE  59 

to  empty  itself,  and  thus  make  it  possible  for  it  to  contract  completely. 
Naturally  the  patient  in  whom  this  has  happened  must  be  treated  for  a 
time  after  his  hemorrhage  as  in  the  case  of  ulcer. 

The  remedies  used  in  lavage  vary  with  the  requirements  of  the  indi- 
vidual case. 

For  simple  cleansing  of  the  stomach,  lukewarm  water  is  sufficient  (at 
about  the  temperature  of  86°  F.) ;  if,  however,  we  wish  to  act  upon  the 
diseased  gastric  wall,  additions  must  be  made  to  the  fluid,  above  all,  soda 
for  gastric  catarrh,  and  table  salt  for  deficient  hydrochloric  acid.  A  mix- 
ture of  these  salts  is  most  serviceable : 

^     Sodium  carbonate part  1 

Sodium  chlorid "     2 

M.  D.     S. :  To  be  dissolved  in  water  (2  to  5  per  1000). 

But  even  water  alone  may  act  in  different  ways  upon  the  gastric  wall ;  lower 
temperatures  (less  than  86°  F.)  stimulate  and  irritate;  higher  than  86°  F., 
lessen  irritation,  have  a  soothing  effect  and  relax.  Under  the  influence 
of  warm  washings  the  pylorus  opens,  even  when  spastically  closed,  more 
quickly  than  under  the  influence  of  cool  washings.  If  in  the  individual 
case,  lavage  of  the  stomach  requires  a  long  time,  it  is  better  for  the  patient 
not  to  have  the  water  too  cool,  as  thus  too  much  heat  may  be  withdrawn 
from  him.  Debilitated  persons  for  this  reason  bear  warm  washings  better 
than  cool  ones. 

The  pressure  exerted  during  lavage  has  no  inconsiderable  influence  upon 
the  diseased  gastric  wall.  In  all  the  diseases  in  which  lavage  must  be  car- 
ried out  cautiously,  therefore  in  gastric  ulcer  and  in  corrosion  of  the  stomach 
after  poisoning  with  a  tendency  to  hemorrhage  and  extreme  irritability, 
the  funnel  must  not  be  held  too  high, — not  above  the  height  of  the  patient's 
head.  When  we  wish  to  produce  a  stimulating  effect  by  the  gastric  washing 
(gastric  douche),  it  should  be  held  as  high  as  possible. 

After  cleansing  the  stomach,  bitter  tonics  are  sometimes  sprayed  upon 
the  mucous  membrane,  and  are  allowed  to  remain  in  the  stomach  in  con- 
tact with  the  gastric  mucous  membrane  for  a  few  minutes;  among  these 
quassia  amara  (30  grams  in  half  a  liter  of  cold  water,  macerated  overnight, 
and  filtered  early  in  the  morning) ,  hop  tea  and  infusion  of  dried  hops,  and 
condurango  are  most  recommended.  I  employ  one  to  two  teaspoonfuls  of 
the  fiuid  extract  of  condurango  to  half  a  liter  of  lukewarm  water. 

Abnormal  fermentative  decomposition  in  the  stomach  is  best  combated 
by  thorough  and  regular  lavage.  We  possess  no  reliable  remedy  for  the 
relief  of  abnormal  decomposition,  fermentation  and  other  processes  of  de- 
composition, which,  without  danger  to  the  organism,  can  aseptically  change 
the  digestive  processes  in  the  stomach  and  intestine.  In  an  abnormal  pro- 
duction of  organic  acids  in  the  stomach  I  have  most  often  employed  wash- 
ings with  a  1-1000  salicylic  acid  solution. 


60        HISTORY  AND  CLINICAL  INDICATIONS  OF  GASTRIC   LAVAGE 

Where  there  is  an  immoderate  excretion  of  hydrochloric  acid  (hyper- 
chlorhydria),  and  in  gastric  ulcer,  some  authorities  recommend  spraying 
the  stomach  with  a  1-1000  silver  nitrate  solution.  In  severe,  old,  gastric 
ulcers  particularly,  excellent  results  have  been  obtained,  after  all  internal 
remedies  had  failed,  by  pouring  bismuth  into  the  previously  cleansed  stom- 
ach. With  an  approximately  exact  diagnosis  of  the  seat  of  the  ulcer,  or 
after  a  few  attempts  with  the  patient  in  a  suitable  posture,  it  is  possible 
to  introduce  into  the  adult  stomach,  by  sedimentation,  a  mixure  of  bismuth 
in  suspension  (10  to  20  bismuth  subnitrate  to  200  of  water)  so  that  a 
precipitate  of  bismuth  completely  covers  the  ulcerated  surface.  That  a 
coating  of  bismuth  remains  upon  the  rough  or  sinuous  ulcerated  surface, 
and  irritation  by  the  gastric  contents  is  thus  prevented,  I  have  concluded 
from  numerous  clinical  observations;  for,  after  a  few  applications  of  bis- 
muth in  the  cases  in  question  not  only  the  sensory  but  also  the  secretory 
and  motor  irritative  phenomena  (pains,  hyperchlorhydria  and  hypersecre- 
tion, peristaltic  unrest  and  spasm  of  the  pylorus)  were  lessened,  and  often 
entirely  ceased,  and  with  the  continuance  of  the  bismuth  treatment  of 
the  gastric  ulcer  for  several  weeks  cure  finally  took  place.  In  fresh  gastric 
ulcers  and  in  hemorrhage,  which  do  not  permit  lavage,  I  have  had  good 
results  by  letting  the  patient  drink  bismuth  in  suspension  after  the  stomach 
had  been  cleansed  in  a  natural  manner  by  the  drinking  of  an  alkaline  water 
half  an  hour  previously.  (Here  the  remark  may  be  permissible  that  min- 
eral water  cures,  in  fact,  the  drinking  of  natural  mineral  waters,  may  be 
designated  as  natural  gastric  lavage  in  contrast  to  the  artificial,  that  is, 
gastiic  lavage  performed  with  the  stomach-tube.  For  obvious  reasons  the 
latter  is  much  more  effective  than  the  former.) 

The  best  time  for  gastric  lavage  may  be  seen  from  the  indication:  If 
the  stomach  early  in  the  morning  is  not  empty,  it  must  be  washed  out. 
At  this  time  the  stomach  washing  is  least  exhaustive,  is  completed  most 
rapidly,  and  is  most  useful  to  the  organism.  The  cleansed  stomach-wall, 
refreshed  by  the  washing  with  water,  is  ready  for  new  and  thorough  activity 
(similar  to  the  mouth  after  brushing  the  teeth). 

It  is  true  it  is  very  difficult  for  the  busy  practitioner  so  to  divide  his 
time  that  his  gastric  patients  may  have  regular  treatment  early  in  the 
morning  and  at  the  same  hour  daily.  Yet  it  is  not  right  that  lavage  should 
be  performed  at  any  time  during  the  day  when  our  visiting  list  brings 
us  to  the  patient.  If,  for  example,  we  wash  out  the  stomach  at  a  time 
when  the  labor  of  digestion  is  not  yet  completed,  added  to  the  abrupt 
interruption  of  the  digestive  processes  is  the  disadvantage  that,  besides  the 
digestive  juices,  larger  and  smaller  quantities  of  unused  chyme  are  washed 
out  of  the  stomach. 

Besides,  gastric  lavage  at  an  improper  time  is  much  more  exhausting 
than  when  the  stomach  is  empty.  The  expulsion  of  the  insufficiently  split- 
u]3  food  is  very  difficult,  the  washing,  therefore,  takes  a  long  time,  large 


THE  CLINICAL  EMPLOYMENT  OF   GASTRIC   LAVAGE  61 

quantities  of  fluid  are  necessary  to  cleanse  the  stomach,  much  heat  is  thereby 
withdrawn  from  the  patients  and  they  are  often  exhausted  before  the 
stomach  is  clean;  organ  and  organism  therefore  suffer  injury  by  lavage  at 
an  unsuitable  time.  The  stomach  becomes  worse  instead  of  better,  the  gen- 
eral condition  of  nutrition  falls  instead  of  rises;  in  spite  of  patience  and 
labor  the  treatment  is  unsuccessful,  and  the  criticism  is  made,  "  Even  lavage 
did  not  help  him." 

Moreover,  the  ordering  of  a  test-meal  and  the  later  removal  of  the 
gastric  contents  should  not  occur  at  any  arbitrary  time.  The  stomach  is 
not  a  retort  into  which,  at  any  time,  something  may  be  put,  or  from  which 
something  may  be  taken  to  see  what  process  it  has  undergone  in  the 
meantime. 

I  do  not  deny  that  in  the  treatment  of  diseases  of  the  stomach  our 
adherence  to  the  most  useful  methods  and  to  a  definite  time  is  a  hindrance 
to  the  general  employment  of  gastric  lavage,  and  to  a  certain  extent  limits 
its  utility  in  practice.  It  is  due  to  these  circumstances,  and  not  to  the 
knowledge  of  the  practising  physician,  that  the  results  of  local  treatment 
of  the  stomach  in  well  conducted  institutions  are  usually  better  than  in 
private  practice.  Where  it  is  at  all  possible,  therefore,  if  the  stomach-tube 
is  to  be  employed  for  a  long  time,  the  patient  should  at  once  be  taught 
to  use  it  for  himself. 

Besides,  the  essential  point  in  treatment  of  the  stomach  is  not  alone 
the  correct  use  of  the  stomach-tube:  Much  more  difficult  than  this  is  the 
art  of  nourishing  the  patient.  If  nothing  injurious  is  introduced  into  the 
stomacli,  less  will  be  brought  up  by  lavage;  by  a  proper  diet,  therefore, 
we  may  limit  lavage  and  in  many  cases  maJce  it  unnecessary.  Naturally, 
dietetic  treatment  in  institutions  in  which  food  is  prepared  under  the 
direction  of  the  physician  is  easier  than  in  private  practice. 

Only  definite  symptoms  should  cause  us  to  deviate  from  the  general  rule 
of  washing  out  the  diseased  stomach  early  in  the  morning  when  empty. 
There  are  cases  of  mechanical  insufficiency  of  the  stomach  in  which  secre- 
tion of  hydrochloric  acid  (hypersecretion),  the  formation  of  organic  acids, 
and,  under  some  circumstances,  the  production  of  gas  is  so  great  and  the 
difficulties  arising  from  these  conditions  so  decided  that  by  a  rapid  empty- 
ing of  the  stomach  not  only  are  the  sufferings  of  the  patients  relieved  but 
danger  is  averted. 

If,  in  cases  of  this  kind,  examination  by  the  physician  at  any  hour  of 
the  day  makes  it  appear  that  the  stomach  should  be  emptied  immediately, 
it  is  best  to  choose  for  lavage  a  late  evening  hour;  by  lavage  at  nine  or 
ten  o'clock,  or  even  later  in  the  evening  according  to  the  time  when  food 
was  last  taken,  the  patient  is  relieved  for  the  night  from  his  discomfort, 
and  secures  a  very  necessary  and  grateful  night's  rest.  Evening  lavage, 
however,  if  continued  for  a  long  time,  is  not  well  borne,  not  nearly  so  well 
as  that  of  the  morning,  and  in  cases  in  which  both  morning  and  evening 


62        HISTORY   AND  CLINICAL   INDICATIONS  OF  GASTRIC  LAVAGE 

lavage  are  necessary  the  patient  soon  loses  strength,  the  intestine  no  longer 
receives  sufficient  fluid  and  nourishment  from  the  stomach,  the  require- 
ments of  the  economy  of  the  body  can  no  longer  be  met,  even  although 
we  use  supplementary  rectal  alimentation,  and  unless  an  operation  is  per- 
formed in  such  cases  the  patients  slowly  succumb  to  exhaustion. 


FUNCTIONAL    DISEASES    OF   THE   STOMACH 

By  H.   LEO,  Bonn. 

The  stomach  differs  from  other  organs  in  that  it  frequently  presents 
subjective  and  also  objective  symptoms  of  disease  which  are  not  due  to 
any  organic  change,  or,  at  least,  not  to  any  which  are  recognizable  by  our 
present  methods  of  investigation.  In  this  respect,  only  the  heart,  that 
is,  the  circulatory  apparatus,  and  the  intestines  show  similar  conditions. 
These  clinical  pictures  may  be  grouped  under  the  term,  functional  diseases 
of  the  stomach. 

One  of  these  groups  presents  well-developed  anomalies  of  the  gastric 
contents  which  are  not,  however,  due  to  disease  of  the  stomach  wall,  but 
to  the  ingestion  of  tainted  food,  or  to  the  invasion  of  microbes  which  in 
themselves  cause  the  decomposition  of  the  ingesta  in  the  stomach.  These 
morbid  conditions  have  been  designated  dyspepsia. 

The  second  group  is  distinguished  by  clinical  pictures  which  present 
either  subjective  symptoms  dependent  only  upon  alterations  of  the  stomach 
or,  combined  with  this,  disturbances  of  gastric  activity  which  may  be  ob- 
jectively recognized.  The  majority  unquestionably  depend  upon  abnormal 
functions  of  the  nervous  apparatus,  and  these  affections  are  therefore  desig- 
nated neuroses  of  the  stomach,  in  spite  of  the  fact  that  a  direct  relation 
to  diseases  of  the  nervous  system  does  not  always  exist. 

The  differential  diagnosis  of  individual  diseases  belonging  to  this  group 
from  one  another  and  from  other  organic  diseases  of  the  stomach  is  not 
always  easy.  To  accomplish  this  an  investigation  of  the  entire  organism 
is,  as  a  rule,  necessary,  and  of  the  various  disturbances  which  uncommonly 
often  disturb  the  gastric  activity,  or  may  be  due  to  abnormalities  of  the 
latter.  Naturally  the  chief  stress  is  to  be  laid  upon  the  special  examina- 
tion of  the  stomach,  in  an  anatomical  as  well  as  functional  respect.  On 
account  of  the  increased  importance  of  this  in  the  last  few  years,  it  appears 
advisable  to  discuss  somewhat  minutely  the  best  method  of  examination. 

TO  TEST  THE  FUNCTION   OF  THE  STOMACH 

Of  the  three  functions  of  the  stomach,  the  motor,  the  secretory  and  the 
absorbent,  the  motor,  i.  e.,  the  intimate  admixture  and  mechanical  prepa- 
ration of  the  food  and  its  timely  removal  through  the  pylorus  into  the 
intestine  is  unquestionably  the  most  important.     The  disturbances  of  this 
6  63 


64  FUNCTIONAL   DISEASES   OF  THE  STOMACH 

function,  manifested  by  an  increased  or,  usually,  by  a  decreased  action,  and 
which  appear  in  the  most  varied  diseases,  are  then  conspicuous  to  a  high 
degree.  To  differentiate  them,  besides  other  complicated  and  less  definite 
methods,  it  is  sufficient  to  prove  by  the  Leube-Riegel  test-meal  (see  below) 
or  by  the  Ewald-Boas  test-breakfast  (see  below)  that  the  duration  of 
digestion  deviates  from  the  normal.  As  a  decrease  in  the  motor  function 
{insnificiency  of  the  stomach)  primarily  occurs  in  gastric  dilatation,  I  shall 
forego  a  full  explanation  of  the  test  for  this,  and  instead  refer  the  reader 
to  the  article  by  Riegel.  It  is  sufficient  to  state  here  that  six  hours  after 
a  test-meal,  and,  at  the  latest,  two  hours  after  a  trial-breakfast,  the  stomach 
normally  propels  its  contents  into  the  intestine.  If,  therefore,  at  this  time, 
l)y  sounding  or  by  lavage  ingesta  are  still  found,  the  motility  of  the  stomach 
is  diniinislied.  On  the  other  hand,  experience  teaches  us  that  the  stomach, 
under  normal  circumstances,  three  hours  after  a  test-meal  and  one  hour 
al'tor  a  test-breakfast,  still  contains  remains  of  food.  If,  at  this  time,  it 
is  already  empty,  we  have  proof  of  an  increase  of  its  motility. 

While  a  test  of  the  absorbent  function  of  the  stomach  has,  up  to  the 
present  time,  produced  no  results  which  are  of  value  in  the  diagnosis  of 
gastric  disease,  the  study  of  the  secretory  function  by  an  examination  of 
the  constituents  of  the  gastric  secretion  or  of  the  admixture  of  the  same 
with  the  intaken  ingesta,  and  also  of  the  normal  and  abnormal  products 
of  decomposition,  is  of  great  practical  importance.  Only  since  the  exam- 
'  nation  of  the  gastric  contents  was  incorporated  into  the  diagnosis  of  gas- 
tric diseases  have  certain  well-characterized  clinical  pictures  (hypersecre- 
tion, hyperacidity,  achylia)  become  known.  Their  results  in  many  cases 
determine  the  diagnosis,  either  because  we  find  changes  in  the  gastric  con- 
tents which  are  characteristic  of  certain  diseases,  or  because  changes  of 
this  kind  are  absent;  that  is,  normal  conditions  exist,  and  we  are  thereby 
justified  in  excluding  some  diseases  which  come  into  question  in  the  differ- 
ential diagnosis. 

In  regard  to  the  indications  for  the  examination  of  the  gastric  contents, 
this  procedure,  that  is,  lavage  of  the  stomach,  aside  from  the  contraindica- 
tions to  be  at  once  named,  is  absolutely  harmless  and,  as  a  rule,  may  be 
carried  on  without  difficulty,  but  is  occasionally  unpleasant  to  very  sensi- 
tive patients,  and,  naturally,  not  in  place  when  other  diagnostic  aids  per- 
mit us  to  make  a  positive  diagnosis.  The  artificial  removal  of  the  gastric 
contents  is  now  only  performed  with  a  soft  rubber  tube,  but  is  absolutely 
contraindicated  if  hemorrhages  have  occurred  even  although  a  long  time 
have  elapsed  since  the  last  one.  Otherwise,  a  fresh  hemorrhage  might 
readily  be  produced. 

The  stomach  contents  are  withdrawn  either  when  the  stomach  is  empty, 
therefore,  as  a  rule,  early  in  the  morning,  or  during  the  period  of  diges- 
tion;  if  we  suspect  hypersecretion  (see  below)  it  is  done  at  the  time  first 
named.     In  these  cases,  we  find  a  considerable  amount  of  clear  fluid  while 


TO  TEST  THE   FUNCTION   OF  THE  STOMACH  65 

the  stomach  normally  should  be  empty.  Only  when  ingesta  reach  the 
stomach,  that  is,  when  present  there,  both  in  the  healthy  and  in  the  sick, 
do  we  find  besides  hypersecretion  a  secretion  of  the  gastric  juice.  In  the 
examination  of  the  empty  stomach  the  proof  of  gastritis  may  also  be  valua- 
ble on  account  of  the  mucus  present  in  the  opening  of  the  tube,  and  which 
contains  profuse  amounts  of  leukocytes  and  epithelium.  This  is  also  the 
case  with  the  proof  of  insufficiency  of  the  stomach,  in  which  the  stomach 
that  should  normally  be  empty  in  the  morning  still  contains  ingesta.  In 
all  other  cases,  we  examine  the  gastric  contents  during  the  time  of  digestion. 

During  this  process  two  objects  must  be  borne  in  mind :  First,  the  deter- 
mination of  abnormal  processes  of  decomposition  in  the  gastric  contents, 
and  secondly,  the  determination  of  the  properties  of  the  gastric  secretion. 

To  determine  the  first,  that  is,  the  presence  of  abnormal  products  of 
decomposition  or  causes  of  decomposition,  it  is  often  sufficient  if  we  obtain 
the  gastric  contents  for  examination  upon  the  first  visit  to  the  patient, 
immaterial  when  and  what  the  patient  has  last  eaten.  But  it  is  advisable 
to  do  this  only  when  we  desire  qualitative  proof  of  the  composition  of  the 
gastric  secretion  (hydrochloric  acid  and  pepsin). 

This,  however,  is  unwise  when  an  exact  estimation  of  the  activit}'^  of 
the  gastric  parehchyma  is  to  be  made,  particularly  if  we  wish  to  determine 
the  proportion  of  the  constituents  of  the  secretion,  and,  especially,  of 
hydrochloric  acid.  The  composition  of  the  gastric  contents,  which  repre- 
sent a  mixture  of  the  gastric  secretion  and  the  food  that  has  been  consumed, 
is  dependent  upon  the  amount  and  nature  of  the  ingested  food  and  upon 
the  time  which  has  elapsed  since  the  food  was  eaten.  Therefore,  if  we 
desire  to  ascertain  the  deviations  of  this  composition  from  the  normal, 
these  deviations  not  being  dependent  upon  accidental  variations  in  the 
intake  of  food,  but  upon  anomalies  of  secretion,  we  must  be  sure,  in  the 
first  place,  that  the  composition  and  amount  of  the  introduced  ingesta  are 
always  alike,  and  that  the  stomach  contents  are  always  obtained  after  the 
same  lapse  of  time  following  the  ingestion  of  food. 

For  this  purpose  it  is,  above  all,  necessary  that  the  stomach  be  empty 
before  the  foods  which  are  to  cause  a  secretion  of  gastric  juice  are  eaten. 
The  best  time  for  the  so-called  test-meal  is,  therefore,  early  in  the  morn- 
ing, or  in  the  course  of  the  morning,  several  hours  after  breakfast  has  been 
taken.  When  it  is  doubtful  whether  the  stomach  is  empty  it  must  be 
washed  out  before  the  test-meal  is  given.  Of  the  many  test-meals  which 
have  been  advised  to  stimulate  gastric  secretion,  I  shall  here  mention  only 
the  two  which  are  in  most  common  use,  which  are  the  best,  and  quite  suffi- 
cient for  all  practical  purposes. 

Test-meal  according  to  Leube-Riegel. — Toward  midday  the  patient 
partakes  of  a  plate  of  beef-soup,  150  to  200  grams  of  beefsteak,  50  grams 
of  mashed  potato  and  a  roll.  Four  hours  later,  as  a  rule,  the  stomach  is 
empty,  but  it  is  occasionally  advisable  to  empty  the  stomach  somewhat 


66  FUNCTIONAL   DISEASES  OF  THE   STOMACH 

sooner  or  later.  This  method  has  the  advantage  that  the  gastric  mucous 
membrane  is  stimulated  in  a  normal  manner,  because  all  necessary  foods 
are  contained  in  the  meal.  It  should,  therefore,  always  be  employed  when 
the  sim])ler  Ewald  method  gives  a  negative  result  in  regard  to  hydrochloric 
acid  and  ])epsin.  In  such  cases  we  often  note  that  the  more  intense  and 
prolonged  stimulation  of  Leube's  test-meal  gives  a  conspicuously  positive 
result;  its  disadvantage  lies  in  the  fact  that,  because  of  the  complexity  of 
the  components  of  the  meal,  complete  uniformity  of  the  same  in  every  case 
can  only  be  obtained  with  difficulty,  and  gastric  patients  in  particular  are 
frequently  unable  to  consume  it  entirely.  In  office  practice  it  is  most 
unpleasant,  but  sometimes  necessary,  to  evacuate  the  stomach  a  long  time 
after  the  meal,  at  a  late  afternoon  hour. 

Test-meal  according  to  Ewald  and  Boas. — Early  in  the  morning,  or 
at  another  time  when  the  stomach  is  empty,  the  patient  receives  one  or 
two  rolls  of  wheat  bread  (35  to  70  grams)  and  one  or  two  cups  of  tea 
without  sugar  or  milk.  Water  may  be  taken  instead  of  tea.  After  an 
hour  or  an  hour  and  a  quarter  (according  to  whether  the  single  or  double 
quantity  has  been  taken)  the  stomach  is  evacuated.  This  test-meal  has 
the  advantage  of  great  simplicity,  and  the  masses  which  are  evacuated  do 
not  have  the  smeary  composition  which  they  have  by  Leube's  method.  As 
the  evacuation  may  occur  comparatively  soon  after  the  intake  of  food,  the 
administration  of  the  trial  breakfast  and  the  evacuation  of  the  stomach 
contents  may  be  undertaken  during  the  office  hour. 

[The  shredded  wheat  biscuit  makes  an  excellent  test- meal.  It  is  free 
from  yeast  and  contains  the  entire  food  elements  of  wheat.  Two  biscuits, 
thoroughly  masticated,  and  a  glass  or  two  of  water  form  an  ideal  Ewald 
meal. — Ed.] 

EXAMINATION  OF  THE  GASTRIC  CONTENTS 

A,     MACROSCOPIC    AWD    MICROSCOPIC    EXAMINATION 

The  odor  of  the  gastric  contents  normally  and  also  in  most  pathologic  cases, 
provided  the  stomach  is  empty  before  the  test-meal  is  administered,  is  not  distinc- 
tive. In  stagnation  of  the  ingesta  ( gastrectasis,  dyspepsia,  gastritis)  we  find,  as 
an  expression  of  decomposition,  the  odor  of  fatty  acids,  acetic  acid  or  butyric  acid 
(like  rancid  butter). 

Blood  is  occasionally  admixed  with  the  stomach  contents  as  a  small,  bright  red 
streak;  it  originates  from  retching,  and  is  therefore  of  no  pathognomonic  impor- 
tance. If,  however,  the  entire  contents  have  a  distinct  hemorrhagic  discoloration, 
tlie  presence  of  an  ulcer,  carcinoma,  or  stasis  in  the  portal  vein  system  is  proven, 
and  all  further  sounding  is  to  be  avoided. 

liile.  characterized  by  its  yellow  or  greenish  color,  is  very  frequently  found  in  the 
gastric  contents  and  is  of  no  diagnostic  significance. 

Mucus  in  small  amounts  may  also  be  found  in  the  normal  gastric  contents  if  the 
quantity  of  hydrochloric  acid  present  is  slight.  Larger  amounts,  particularly  thick 
coagula,  denote  gastritis,  unless  the  mucus  originates  from  the  respiratory  passages. 
In  the  case  of  gastritis,  the  microscopic  examination  of  the  mucus  as  well  as  of  the 


EXAMINATION   OF  THE  GASTRIC  CONTENTS  67 

stomach  contents  evacuated  from  the  empty  stomach  is  of  importance.  The  micro- 
scope reveals  numerous  well  retained  leukocytes  and  epithelia;  in  acid  gastritis  in 
which  the  protoplasm  of  the  leukocyte  is  digested,  numerous  cell  nuclei  are  found 
while  these  normally  are  present  in  only  slight  numbers   (A.  Schmidt). 

The  macroscopic  composition  of  the  ingesta  is  of  special  significance.  If,  after 
Leube's  test-meal,  the  particles  of  meat  are  split  up,  the  production  of  hydrochloric 
acid  is  sufficient,  perhaps  even  increased.  On  the  contrary,  if  they  appear  un- 
changed there  is  a  deficiency  of  hydrochloric  acid,  perhaps  of  acidity.  Insufficient 
maceration  of  the  fragments  of  bread  favors  hyperacidity  as  a  greater  amount  of 
HCI  inhibits  the  saccharifying  action  of  the  diastatic  salivary  ferment  which  nor- 
mally occurs  in  the  stomach. 

The  microscopic  examination  of  the  gastric  contents  may  be  of  diagnostic  weight 
on  account  of  the  previously  mentioned  formed  elements  in  gastritis.  The  presence 
of  large  numbers  of  microorganisms  denotes  stagnation  of  the  ingesta,  but  it  must 
be  remembered  that  the  yeast  cells  may  be  due  to  the  ingested  bread. 

B.  CHEMICAL  EXAMINATION 

The  gastric  contents  to  be  examined  must  be  undiluted ;  except  in  an  examination 
for  ferments,  it  is  unnecessary  to  filter  them. 

The  examination  primarily  is  for  the  acids,  particularly  hydrochloric  acid,  vola- 
tile fatty  acids,  and  lactic  acids.  In  most  cases  this  is  sufficient.  Under  some  cir- 
cumstances (if  achylia  be  suspected),  an  examination  of  the  ferment,  perhaps  also 
of  the  products  of  digestion,  is  expedient. 


ACIDS 

(a)  Qualitative  Tests 

Reaction. — The  evacuated  contents  of  the  empty  stomach  may  normally  have  a 
neutral  or  even  an  alkaline  reaction  (the  presence  of  bile  and  intestinal  juices  in 
the  stomach).  If,  after  a  test-meal,  blue  litmus  paper  is  not  reddened,  the  con- 
dition is  one  of  insufficient  or  absent  hydrochloric  acid  secretion. 

Hydrochloric  Acid. — The  test  is  first  made  with  the  Giinzburg  reagent  (two 
grams  of  phloroglucin,  one  gram  of  vanillin,  thirty  grams  of  alcohol)  ;  a  few  drops 
of  this  with  an  equal  quantity  of  gastric  contents  are  placed  in  a  porcelain  dish  and 
heated  over  a  small  fiame.  If  a  beautiful  red  margin  appears,  the  presence  of  hydro- 
chloric acid  is  proven.  If,  however,  the  red  color  does  not  appear,  the  absence  of 
hydrochloric  acid  is  by  no  means  certain,  as  its  presence,  even  in  decided  amounts, 
may  be  obscured  by  other  combinations. 

This  error  cannot  occur  in  the  test  tcith  CaCOi ;  therefore,  this  test  must  always 
be  used  if  the  reaction  with  the  Giinzburg  test  is  negative.  For  this  purpose,  we 
mix  in  a  watch-glass  some  of  the  gastric  contents  with  a  pinch  of  powdered  CaCoj. 
The  reaction  of  the  mixture  is  tested  with  blue  litmus  paper,  and  this  is  compared 
with  the  original  reaction  of  the  gastric  contents.  If  the  redness  of  the  litmus 
paper  after  treatment  with  CaCos  is  less  intense  than  before,  or  if  no  reaction 
occurs,  the  stomach  contents  (in  the  presence  of  volatile  fatty  acids  and  of  lactic 
acid)  contain  hydrochloric  acid.  If  the  reddening  is  the  same,  before  and  after, 
no  hydrochloric  acid  is  present. 

For  further  confirmation  of  this  test  the  digestion  test  may  be  employed  (see 
below ) . 

Volatile  Fatty  Acids. — ^Several  c.c.  of  the  gastric  contents  are  heated  in  a  test- 
tube  to  boiling,  while  a  piece  of  blue  litmus  paper  is  held  over  the  test-tube.     If 


68  FUNCTIONAL  DISEASES  OF  THE  STOMACH 

the  paper  redden,  the  presence  of  volatile  fatty  acids  is  proven:  if  no  redness  appear, 
they  are  absent. 

Lactic  Acid. — About  10  c.c.  of  gastric  contents  are  shaken  up  with  about  the 
same  quantity  of  ether,  and  the  ether  which  has  taken  up  the  greater  part  of  the 
lactic  acid  present  is  poured  off.  To  the  ethereal  fluid  a  few  c.c.  of  a  very  dilute 
ferric  chlorid  solution  are  added  (one  drop  of  an  officinal  ferric  chlorid  solution  to 
a  test-tube  full  of  water).  Even  if  only  minute  quantities  of  lactic  acid  are  present, 
upon  shaking  a  distinct  yellow  color  appears  in  the  ferric  chlorid  solution. 


(b)  Quantitative  Estimation 

We  must  always  remember  that,  in  spite  of  many  methods  for  this  estimation, 
we  do  not  determine  the  absolute  amount  of  acids  excreted  in  a  certain  time  by  the 
quantitative  estimation  of  the  acids,  but  we  measure  relatively  the  secretory  func- 
tion of  the  stomach,  for  the  reason  that  we  never  know  how  much  of  the  gastric 
contents  has  entered  the  intestine  during  the  time  in  which  we  are  evacuating  the 
contents,  and  this,  therefore,  cannot  be  calculated.  As,  normally,  there  is  consider- 
able variation  in  the  secretion  of  hydrochloric  acid  in  the  same  and  in  different 
persons,  we  should  only  regard  marked  and  constant  deviations  as  pathologic. 

If  the  presence  of  HCl  and  the  absence  of  volatile  fatty  acids  and  lactic  acids 
have  been  proven  in  the  manner  described  above  (which  is  the  case  in  the  majority 
of  tests),  this  is  sufficient  to  determine  the  total  acidity  for  practical  purposes.  On 
the  other  hand,  if  we  desire  to  learn  the  exact  proportion  of  acids  present,  their  esti- 
mation must  be  included.  Upon  the  whole,  although  the  qualitative  proof  of  organic 
acids  in  fermentative  processes  is  so  important,  their  quantitative  estimation  is  of 
no  great  practical  utility. 

Total  Acidity. — To  a  definite  quantity  (5  to  10  c.c,  although  we  may  do  with 
less)  of  gastric  contents,  to  which  a  few  drops  of  an  alcoholic  solution  of  phenol- 
phthalein  solution  are  added,  a  decinormal  solution  of  caustic  soda  is  added  drop  by 
drop  from  a  graduated  pipette  until  a  red  color  appears  and  remains.  The  figure 
which  is  expressed  by  the  amount  of  decinormal  soda  solution  used  in  100  c.c.  rep- 
resents the  degree  of  total  acidity  of  the  gastric  contents. 

The  normal  values  of  total  acidity  usually  vary  between  20  and  60.  If  constant 
values  below  20  are  found,  there  is  subacidity.  If  upon  repeated  examination  values 
above  70  are  noted,  we  are  dealing  with  hyperacidity. 

Hydrochloric  Acid. — Of  the  many  methods  advised  for  the  quantitative  estima- 
tion of  HCl  I  shall  describe  only  the  one  proposed  by  myself  which,  among  other 
advantages,  possesses  that  of  great  simplicity,  and  has  shown  itself,  both  in  my 
hands  and  in  those  of  others,  to  be  absolutely  reliable. 

To  10  c.c.  of  gastric  contents,  a  few  c.c.  of  a  concentrated  CaClj  solution  are 
added,  and  after  the  addition  of  a  few  drops  of  an  alcoholic  phenolphthalein  solu- 
tion the  mixture  is  triturated  (as  above)  with  a  decinormal  soda  solution  until  a 
permanent  red  color  appears.  Then,  about  15  c.c.  of  gastric  contents  are  mixed 
in  a  dry  vessel  with  about  1  gram  of  dry  powdered  CaCos,  and,  after  stirring, 
iire  filtered  through  a  dry  filter,  10  c.c.  of  the  filtrate  are  measured  off,  and  the 
CO,  which  has  formed  is  evaporated  by  a  current  of  air,  when  CaClj  solution  and 
some  phenolphthalein  are  again  added,  and  the  acidity  is  calculated  by  means  of  a 
decinormal  soda  solution. 

If  the  sum  of  the  decinormal  soda  solution  obtained  in  this  tritration  (calculated 
upon  tlu-  basis  of  100  c.c.  of  gastric  contents)  be  subtracted  from  the  number  of 
cc.  r((|iiin'(l  in  the  first  tritration,  the  difference  corresponds  to  the  amount  of 
norma!  soda  solution  required  for  the  neutralization  of  free  HCl  present  in  100  c.c. 


DYSPEPSIA  69 

of  gastric  contents.  If  the  reaction  for  volatile  fatty  acids  and  lactic  acids  (see 
above)  is  negative  (as  is  the  case  in  the  overwhelming  majority  of  instances),  the 
figure  obtained  corresponds  to  the  amomit  of  HCl.  This  figure  multiplied  by  0.00365 
gives  the  percentage  in  grams  of  HCl  in  the  gastric  contents. 

If  organic  acids  be  present,  10  c.c.  of  gastric  contents  are  again  measured  and 
shaken  in  a  beaker  with  about  50  c.c.  of  ether;  the  ether  is  then  poured  off,  and 
this  shaking  and  pouring  off  of  ether  is  repeated  five  times.  If  the  acidity  of  the 
residue  of  the  stomach  contents  be  then  determined  the  difference  shows  the  amount 
of  the  organic  acids.  This  is  subtracted  from  the  total  acidity  previously  obtained, 
and  the  remainder  equals  HCl. 

FERMENTS 

The  presence  of  digestive  ferments  (pepsin  and  lab)  may  greatly  assist  us  in  the 
diagnosis  of  achylia   (see  below). 

The  test  for  pepsin  consists  in  placing  10  c.c.  of  filtered  gastric  contents  in 
each  of  two  beakers,  and  also  a  flake  of  washed  blood  fibrin ;  to  one  of  these  a  few 
drops  of  diluted  HCl  is  added,  and  both  beakers  are  placed  in  an  incubator  at  blood 
temperature  (98.6°  F. ).  If,  after  several  hours,  the  flakes  are  still  present,  in 
spite  of  repeated  shaking  of  the  beaker,  pepsin  and  pepsinogen  are  absent  from  the 
gastric  contents. 

To  determine  the  presence  of  the  lab  ferment  about  10  c.c.  of  raw  milk  are 
mixed  with  2  to  5  drops  of  gastric  contents.  Lab  coagulation  either  occurs  at  once, 
or  (at  the  temperature  of  the  body)  after  a  longer  period.  If  the  lab  ferment  is 
eventually  absent,  its  prior  stage,  lab  zymogen,  may  be  recognized  by  adding  2 
c.c.  of  a  CaClj  solution  to  the  previously  mentioned  mixture. 


DYSPEPSIA 

We  employ  the  designation,  dyspepsia,  which  in  common  parlance 
means  "  deficient  digestion,"  to  only  a  limited  extent  in  that  we  restrict 
it  to  gastric  digestion.  But,  even  here,  it  is  still  further  limited  in  that 
we  exclude  from  this  category  organic  diseases  of  the  gastric  walls  which 
give  rise  to  digestive  disturbances. 

In  the  term  "^dyspepsia"  we  include  only  those  alterations  of  the 
stomach  which  are  not  due  to  an  organic  affection.  It  is  true  the  ordi- 
nary conception  of  dyspepsia  is:.decidedly  more  extensive,  for  we  speak  of 
dyspeptic  difficulties.-when  referring  to  abnormal  sensations  in  the  stomach 
without  an  anomaly  of  gastric  activity  being  conjoined  to  them.  This  .is 
especially  true  of  sorcalled  "nervous  dyspepsia"  (see  below),  the  especial 
characteristic  of- which  is  that  gastric  digestion  is  quite  normal.  The  con- 
tradiction in  this  is  quite  obvious,  and  although  the  designation  which  has 
become  firmly  rooted  in  our  language  is  very  difficult  to  displace,  I  never- 
theless believe  it  to  be  correct  in  a  systematic  description  to  speak  only  of 
such  conditions  as  dyspepsia  in  which  gastric  digestion  is,  in  fact,  disturbed. 

By  this  classification,  cases  of  dyspepsia  are  greatly  limited.  Since 
the  gastric  mucous  membrane  is  too  sensitive  to  retain  for  any  length 
of  time  contents  which  have  been   subjected   to   decomposition   without 


70  FUNCTIONAL  DISEASES  OF  THE  STOMACH 

reacting  in  a  short  time  by  irritative  processes,  i.  e.,  by  catarrh,  only  acute 
conditions  belong  in  this  category. 

Under  dyspepsia,  therefore,  and  in  a  restricted  sense,  we  consider  only 
acute  dyspepsia,  i.  e.,  the  digestive  disturbances  which  the  busy  physician 
meets  with  daily,  which  are  due  to  the  ingestion  of  tainted  food  or  to 
generators  of  fermentation.  As  pure  dyspepsia,  without  organic  implica- 
tion, these  disturbances  will  be  considered  only  in  their  initial  stages,  that 
is,  before  a  consecutive  catarrh  has  as  yet  been  produced. 

To  determine  that  only  acute  dyspepsia,  and  not  gastritis,  is  present, 
an  investigation  of  the  gastric  contents  is  always  necessary.  The  presence 
of  products  of  decomposition,  especially  organic  acids,  volatile  fatty  acids, 
and  lactic  acid  is  not  sufficient  for  this  purpose.  For  even  a  primary 
gastritis,  usually  in  consequence  of  anomalies  of  secretions,  causes  an 
abnormal  change  in  the  ingesta  which  become  subject  to  acid  fermentation. 
True  dyspepsia,  however,  is  favored  by  the  absence  of  decided  amounts 
of  mucus,  which,  in  acute  gastritis,  is  always  present  in  the  gastric  con- 
tents, especially  in  the  later  stages;  a  microscopic  examination  permits 
the  recognition  of  numerous  leukocytes  and  epithelial  cells. 

The  effect  also  of  a  single,  thorough  gastric  lavage,  which  is  the  best 
and  most  certain  therapeutic  remedy  in  acute  dyspepsia,  aids  in  the  diag- 
nosis; for  if,  after  this  little  operation,  and  without  other  remedial  meas- 
ures, restoration  to  health  is  immediate,  we  may  feel  assured  that  the 
gastric  mucous  membrane  was  not  implicated,  and  that  the  primary  affec- 
tion consisted  in  a  decomposition  of  the  gastric  contents. 

NEUROSES  OF  THE  STOMACH 

Neuroses  of  the  stomach,  with  comparatively  rare  exceptions,  are  purely 
idiopathic.  As  a  rule,  they  are  caused  by  a  general  anomaly  of  consti- 
tution, or,  reflexly,  are  dependent  upon  disease  of  another  organ.  In  these 
cases,  strictly  speaking,  we  are  therefore  dealing  only  with  a  symptom 
of  another  disease  which  affects  the  stomach;  the  disturbances  of  gastric 
activity  are,  however,  frequently  so  prominent  and  characteristic  that  they 
dominate  the  clinical  picture,  and  for  this  reason  alone  they  merit  a  com- 
prehensive description. 

The  most  important  etiologic  factor  is  neurasthenia,  next  hysteria,  as 
well  as  chlorosis  and  other  anemic  conditions,  diseases  of  the  sexual  ap- 
paratus (especially  in  females),  wandering  kidney  and  affections  of  the 
intestines,  and  these  by  no  means  exhaust  the  series  of  diseases  in  the 
course  of  which  functional  disturbances  of  the  stomach  appear.  As  a  rule, 
they  occur  secondarily  in  cerebral  and  spinal  cord  affections,  in  pulmonary 
tuberculosis,  in  peritonitis,  in  severe  renal  disease,  etc.  Nevertheless,  in 
niakino;  a  diagnosis,  we  must  consider  their  occurrence  in  very  different 
diseases. 


NEUROSES  OF  THE  STOMACH  71 

SEHSORY  NEUROSES 

Anomalies  of  the  Sensation  of  Hunger. — These  consist  in  a  decrease 
(anorexia) ,  an  increase  (bulimia),  and  perversions  of  the  normal  appetite 
(parorexia) . 

Anorexia,  which  is  a  distinguishing  symptom  in  almost  all  gastric  dis- 
eases, may  also  be  autochthonors,  and  here,  above  all,  psychical  influences 
such  as  care,  sorrow,  pain,  disgust,  etc.,  which  dispel  the  sensation  of  hun- 
ger for  a  longer  or  shorter  time,  play  a  part.  Naturally,  before  making 
the  diagnosis,  the  existence  of  an  organic  gastric  affection  must  be  excluded. 

Parorexia,  in  which  there  is  a  tendency  to  eat  impreper  things,  such 
as  sharp  condiments,  vinegar,  iron  filings,  chalk,  etc.,  while  natural  foods 
are  declined,  occurs  particularly  in  women  who  suffer  from  chlorosis  or 
who  are  pregnant,  but  these  abnormalities  may  also  occur  in  other  hysterical 
and  neurasthenic  persons.  The  treatment  is  that  of  the  fundamental  con- 
dition. 

In  bulimia  we  are  dealing  with  a  pathological  augmentation  of  the 
normal  sensation  of  hunger.  This  varies  extraordinarily  under  different 
physiologic  conditions,  and,  particularly  in  growing  persons,  is  frequently 
intensified;  and,  since  food  not  only  serves  to  maintain  the  healthy  condi- 
tion of  the  body  but  also  to  promote  growth,  we  can  only  regard  excessive 
increase  of  the  appetite  as  pathologic.  This  is  shown  by  an  abnormal 
hunger  which  appears  soon  after  profuse  amounts  of  food  have  been  taken, 
and,  besides  the  unconquerable  desire  to  eat,  it  is  accompanied  by  numer- 
ous distressing  symptoms.  Among  these  are  lassitude,  numbness  of  thie 
head,  sometimes  actual  headache,  specks  before  the  eyes,  tinnitus  aurium, 
general  sweating,  and  tremor  as  well  as  general  weakness.  In  some 
patients  local  abnormal  sensations,  as  in  the  region  of  the  stomach,  are 
prominent ;  these  are  sometimes  designated  as  pressure,  sometimes  as  actual 
pain. 

As  the  sensation  of  hunger  is  produced  by  direct  action  upon  the  hun- 
ger center  (central  disease  and  chemical  irritation  of  the  center  by  an 
abnormal  condition  of  the  blood)  as  well  as  by  reflex  causes  which  may 
originate  from  the  periphery,  it  is  evident  that  the  causes  of  bulimia  may 
be  extremely  numerous.  Besides  neurasthenia  the  following  must  be  men- 
tioned: Organic  diseases  of  the  brain  and  psychoses,  Graves's  disease,  diar- 
rhea, helminthiasis,  menorrhagia,  pregnancy,  diabetes  mellitus,  etc.  Those 
cases  of  bulimia  are  especially  interesting  which  depend  upon  other  func- 
tional diseases  of  the  stomach,  particularly  upon  hyperacidity  (see  below) 
and,  above  all,  upon  hypermotility  (see  below) ;  in  the  former  case  it  is 
apparently  the  abnormal  irritation  of  the  hyperacid  gastric  juice,  in  the 
latter  the  abnormally  rapid  emptying  of  the  stomach  after  the  inges- 
tion of  food,  whereby  a  stimulation  of  the  hunger  center  is  caused  cen- 
tripetally. 


72  FUNCTIONAL  DISEASES  OF  THE  STOMACH 

The  therapy  of  bulimia,  on  account  of  the  great  difference  in  the 
etiologic  factors,  must  naturally  be  adapted  to  the  underlying  affection. 
The  measures  in  the  individual  case  are  indicated  in  what  has  been  pre- 
viously said;  in  fact,  in  the  case  of  helminthiasis,  diarrhea,  diabetes  mel- 
litus,  and  menorrhagia,  a  rational  treatment  of  the  underlying  affection 
will  in  most  instances  suppress  the  bulimia,  or,  at  least,  decrease  it.  In 
hypermotility  of  the  stomach  it  is  wise  to  administer  small  quantities  of 
food  very  frequently,  and  to  alternate  with  fluid  and  solid  food.  In  all 
cases  in  which  there  is  hyperirritation  of  the  nervous  system,  and  these 
form  the  majority,  besides  the  general  regime  suited  to  this,  the  adminis- 
tration of  preparations  of  bromin  as  well  as  belladonna  and  similar  reme- 
dies is  of  value. 

Gastralgia  {cardialgia,  gastrodynia) . — This  affection  which,  under  the 
picture  of  gastric  crises,  forms  such  a  prominent  symptom  in  tabes  dorsalis 
and  other  central  diseases,  may  also  appear  in  consequence  of  the  above 
mentioned  affections  as  a  substantive  disease.  Yet,  upon  the  basis  of  my 
experiences,  the  cases  in  which  typical  and  marked  attacks  of  pain  in  the 
gastric  region  are  observed,  may  only  in  an  insignificant  percentage  be 
considered  as  gastric  neuroses;  even  then  the  diagnosis  is  extremely  ques- 
tionable, for  the  positive  exclusion  of  cholelithiasis  and  gastric  ulcer  (some- 
times also  pancreatic  calculi)  is  very  difficult,  and  when  we  consider  the 
great  frequency  of  the  two  first  mentioned  affections,  we  had  better,  in 
a  doubtful  case,  incline  to  these,  and  adjust  the  treatment  in  conformity. 

Gastralgias  of  moderate  degree,  which  cannot  be  referred  to  an  organic 
affection,  are,  on  the  other  hand,  quite  frequent.  In  these  cases  the  pain 
or  sensitiveness  is  referred  to  the  entire  epigastrium,  and  this  circumstance, 
as  well  as  the  patient's  frequent  statement  that  the  pains  are  lessened  by 
pressure,  is  of  value  in  the  differential  diagnosis  between  ulcer  and  chole- 
lithiasis; in  regard  to  ulcer,  the  independence  of  the  quality  of  the  food 
and  of  the  time  elapsed  since  the  last  ingestion  of  food  also  aids  in  the 
diagnosis. 

Gastralgia  is  not  infrequently  combined  with  hyperesthesia  of  the  gas- 
tric walls,  which  is  particularly  observed  in  anemic  and  nervous  individuals, 
and  which  shows  itself  by  a  more  or  less  decided  sensitiveness  directly 
associated  with  the  intake  of  food.  This  sensitiveness  may  reach  a.  very 
high  degree,  and  cause  severe  irritative  83miptoms,  such  as  convulsions  and 
cataleptic  spasms.  

The  main  point  in  the  treatment  is  to  quiet  the  nervous  system.  Be- 
sides other  measures,  the  constant  current  may  be  usefvd. 

MOTOR   NEUROSES 

The  disturbances  of  motility  of  the  stomach  consist  in  an  increase  or 
diminution  of  this  function,  affecting  the  entire  stomach,  or  only  the  cardia 
or  the  pylorus.     There  are,  however,  pathologic ,  pictures  which  are  diffi- 


NEUROSES   OF  THE   STOMACH  73 

cult  to  explain  otherwise  than  as  a  combination  of  irritative  and  depress- 
ing influences. 

Atony  (insufficiency)  of  the  stomach,  which  appears  so  frequently  in 
organic  disease  of  the  stomach  (dilatation  and  gastrectasis),  is  one  of 
the  most  important  functional  disturbances ;  it  often  occurs  in  anemia  and 
other  nutritive  disturbances  without  demonstrable  anatomic  change  in  the 
gastric  walls.  In  this  condition  we  are  dealing  with  atony  of  the  muscu- 
lature as  well  as  a  decrease  in  its  elasticity  and  consequent  impairment 
of  the  property  of  propelling  the  ingesta  from  the  stomach  at  the  proper 
time.  As  the  abnormal  tension  of  the  gastric  walls  which  results  is  usually 
only  a  transitory  extension  of  the  organ,  I  shall  omit  its  consideration  at 
this  point,  and  refer  the  reader  to  the  excellent  article  by  Kiegel. 

Insufficiency  of  the  Cardia. — While  flaccidity  of  the  musculature  of 
the  pylorus,  causing  an  insufficiency  of  the  pylorus,  has  only  been  described 
in  isolated  cases  as  a  neurogenous  affection  (Ebstein),  insuMciency  of  the 
cardia  is  an  anomaly  which  may  frequently  show  itself  under  different  clin- 
ical pictures. 

Where  there  is  a  moderate  degree  of  atony  and  a  simultaneous  tendency 
to  voluminous  collections  of  gas  which  are  sometimes  increased  by  decided 
swallowing  of  air  (Quincke),  we  also  observe  eructation  (ructus,  eructatio) 
of  gases,  which  may  vary  in  intensity,  and  be  transitory  or  habitual;  in 
the  latter  case  this  becomes  very  distressing  to  the  patient.  As  the  same 
symptom  is  conspicuous  in  almost  all  organic  gastric  affections,  errors  in 
diagnosis  can  only  be  avoided  with  care.  Besides  hysteria,  a  circumstance 
in  favor  of  the  purely  nervous  character  of  the  affection  is  that  the  gas 
which  is  discharged  is  odorless  and  tasteless,  and  the  eructation  may  volun- 
tarily be  suppressed  by  the  impulse  of  the  will.  Besides  general  tonics,  the 
treatment  must  be  designed  to  influence  the  psychical  element,  and  we 
must  endeavor  to  strengthen  the  will  power.  Occasionally  gastric  lavage 
is  of  use. 

Another  typical  clinical  picture,  which  is  attributable  to  incontinence 
of  the  mouth  of  the  stomach,  due  not  only  to  atony  of  the  cardia  but  also 
to  a  flaccidity  in  opening  and  to  antiperistalsis  of  the  esophagus,  consists 
in  rumination  (ruminatio,  merycism).  In  persons  affected  by  this  con- 
dition, the  ingested  food  rises  from  the  stomach  a  short  time  after.it  has 
been  swallowed,  and  returns  to  the  mouth  {regurgitation) ,  where  it  is 
again  chewed  and  swallowed.  This  process  usually  occasions  no  disgust, 
and  since  regurgitation,  as  a  rule,  occurs  soon  after  eating  (rarely  later 
than  an  hour),  the  food  has  no  sour,  or  even  unpleasant,  taste.  Many 
patients  are  unconscious  of  any  disagreeable  sensation,  while  others  are 
keenly  alive  to  their  repulsive  condition.  Not  rarely  they  are  able  to  sup- 
press the  regurgitation  which  they  have  voluntarily  produced,  but  only 
temporarily,  for  this  afterward  recurs  to  an  increased  extent.  I  know  sev- 
eral patients  who  have  had  this  affection  for  decades,  and  who  can  pre- 


74  FUNCTIONAL  DISEASES  OF  THE   STOMACH 

vent  regurgitation  by  lying  down  immediately  after  their  meals,  but  if, 
after  some  time,  they  rise,  the  regurgitation  at  once  appears.  The  cir- 
cumstance that  psychical  alterations,  fatigue,  menstruation,  etc.,  cause  an 
increased  and  more  frequent  appearance  of  the  affection  is  in  favor  of 
its  nervous  character. 

The  treatment,  in  the  main,  must  be  directed  toward  increasing  the 
energy  of  the  will  and  suppressing  the  pathologic  process.  Gastric  lavage 
should  be  tried  as  well  as  preparations  of  bromin.  Unfortunately,  we  rarely 
succeed  in  bringing  about  a  cure. 

So-called  nervous  vomiting  may  also  be  included  in  this  class  of  affec- 
tions. Vomiting  is  caused  by  increased  muscular  activity,  but  a  paroxysmal 
contraction  of  the  diaphragm  and  of  the  abdominal  muscles  only  causes 
immediately  a  compression  of  the  stomach,  that  is,  an  expulsion  of  its 
contents,  and  it  is  unquestionably  true  that  the  forcing  of  the  stomach 
contents  upward  occurs  all  the  more  readily  the  less  resistance  there  is 
on  the  part  of  the  cardia.  Nervous  vomiting  is  characteristic  because  of 
the  particular  ease  with  which  it  appears  (prodromes,  especially  nausea, 
are  frequently  absent),  and  it  is  obvious  that  flaccidity  of  the  cardia  plays 
an  important  role.  This  affection  is  prone  to  occur  in  hysterical  persons, 
also  in  chlorotics,  more  rarely  in  neurasthenics.  The  idiopathic  form  of 
nervous  vomiting  described  by  v.  Leyden,  which  is  characterized  by  its 
periodic  appearance  (periodical  vomiting),  must  be  here  included.  Nerv- 
ous vomiting  may  exist  for  years  without  the  nutritive  condition  of  the 
patient  suffering. 

[Regurgitation  of  food  due  to  stenosis  of  the  esophagus,  especially  at 
the  cardia,  may  be  mistaken  for  vomiting.  This  is  especially  true  of  cardio- 
spasm. General  nervous  conditions  may  be  the  cause  of  the  cardiospasm, 
and  at  the  same  time  a  nervous  dyspepsia  or  a  gastric  ulcer  may  exist. 
A  close  attention  to  the  character  of  the  symptoms,  especially  of  the  act 
of  so-called  vomiting  and  an  examination  of  the  expelled  food,  will  make 
the  case  plain. — Ed.] 

In  tlie  diagnosis,  an  unusually  large  number  of  general  affections  and 
diseases  of  the  most  varied  organs,  intoxications  and  autointoxications,  as 
well  as  organic  gastric  affections  in  which  vomiting  is  a  symptom,  must  be 
excluded,  and  furthermore,  particular  stress  must  be  laid  upon  the  etiologic 
factor  of  hysteria.  Besides  combating  hysteria,  local  treatment  of  the 
stomach  by  lavage  or  irrigation  and  electricity  are  in  place. 

Hypemiotility. — Hypermotility  is  a  condition  in  which  the  motor  ac- 
tivity of  the  stomach,  by  means  of  which  its  contents  are  propelled  into 
tlio  intestine,  is  increased.  In  consequence  the  stomach  is  empty  during 
a  time  in  which,  normally,  ingesta  should  still  be  present.  Whether  in- 
suHicioncy  of  the  pylorus  also  plays  a  causative  role  cannot  be  determined. 
Hy [xTinotility  is  by  no  means  rare.  It  occurs  particularly  in  neuras- 
iIuMiirs.  and  shows  itself  by  the  appearance  of  bulimia  (see  above).     In 


NEUROSES   OF  THE   STOMACH  75 

the  diagnosis,  the  proof  that  the  stomach  one  hour  after  the  Ewald,  or 
three  hours  after  a  Leube,  test-meal  is  empty  or  contains  but  few  particles 
of  food  is  necessary.     In  regard  to  treatment,  see  that  indicated  for  bulimia. 

Peristaltic  "Unrest  (tormina  ventriculi). — This  anomaly  is  distinguished 
by  increased  peristaltic  movement  of  the  stomach  (and  frequently  also  of 
the  intestine),  and  is  accompanied  by  more  or  less  loud  rumbling  which, 
with  a  thin  abdominal  wall,  is  distinctly  audible.  In  making  a  diagnosis 
stenosis  of  the  pylorus,  above  all,  must  be  excluded.  The  treatment 
consists  in  the  use  of  sedatives;  occasionally  lavage  of  the  stomach  acts 
favorably. 

Spasm  of  the  Cardia. — In  contrast  to  the  descriptions  of  this  occurrence 
which  are  variously  given,  we  must  fully  understand  that  the  isolated  spastic 
closure  of  the  cardia  may,  primarily,  cause  difficulty  in  deglutition.  We 
therefore  have  the  symptoms  of  a  deeply  situated  stenosis  of  the  esophagus. 
This  anomaly  is  purely  functional,  particularly  in  hysteria,  but  it  also 
occurs  in  marked  anemia  without  other  nervous  irritative  phenomena.  It 
may  run  its  course  with  or  without  pain,  it  may  occur  paroxysmally,  par- 
ticularly in  connection  with  the  act  of  deglutition,  or  be  permanent.  Cases 
have  been  described  in  which  the  spasm  had  existed  for  years,  and  had  given 
rise  to  a  sac-like  dilatation  of  the  esophagus  above  the  stenosis  (Leichten- 
stern.  Dinkier).  Whether,  however,  in  these  cases  an  ulcer  of  the  cardia 
did  not  originally  exist  would  be  very  difficult  to  decide.  For  the  diagnosis, 
examination  with  the  gastric  sound  is  decisive.  Upon  its  introduction,  if 
a  spasm  at  the  height  of  the  cardia  exists,  resistance  is  met  with  which,  as 
a  rule,  is  readily  overcome.  This  procedure  may  be  accompanied  by  pain  or 
occur  without  it.  In  the  absence  of  pain  the  diagnosis  is  easy.  In  a  dif- 
ferentio-diagnostic  respect,  carcinoma,  in  the  usually  youthful  patient,  need 
scarcely  be  considered.  But  with  a  painful  course  of  the  affection,  care 
must  be  taken  not  to  confound  the  condition  with  ulcer  of  the  cardia.  The 
successful  introduction  of  the  sound  would  exclude  the  latter,  while,  on 
the  other  hand,  treatment  similar  to  that  for  ulcer  is  to  be  instituted. 

Besides  general  remedial  measures,  sounding  the  esophagus  is  indi- 
cated. Sometimes  a  single  sounding  is  sufficient.  If  this  is  not  the  case 
it  is  well  to  apply  cocain  by  moistening  the  lower  end  of  the  tube  with  a 
solution;  or,  still  better,  after  introducing  the  gastric  tube  to  the  depth 
of  the  cardia,  a  few  cubic  centimeters  of  a  not  too  concentrated  cocain 
solution  may  be  poured  into  the  tube,  which  is  allowed  to  remain  in  situ 
for  a  few  minutes. 

Spasm  of  the  Pylorus. — This  frequently  occurs  in  organic  diseases  of 
the  stomach,  and  is  said  to  be  also  purely  functional,  particularly  in  hyper- 
acidity. The  consequences  are  stagnation  of  the  ingesta  and  tympany  of 
the  stomach,  and  the  latter  may  be  particularly  severe  wlien  combined  with 
spasm  of  the  cardia.  Asthma  dyspepticum,  so  designated  by  Henoch,  is 
due  to  a  combination  of  this  kind. 


76  FUNCTIONAL  DISEASES  OF  THE  STOMACH 

NEUROSES   OF  SECRETION 

The  anomalies  of  secretion  are  less  numerous  than  those  of  sensation 
and  motion.     They  consist  in  a  decrease  or  increase  of  the  secretion. 

Achylia  Gastrica. — While  the  achylia  observed  in  connection  with  car- 
cinoma and  chronic  gastritis  depends  upon  an  atrophy  of  the  gastric  mucous 
membrane,  we  observe  in  neurasthenic,  and  especially  in  anemic,  persons, 
a  decrease  or  complete  absence  of  the  secretory  activity  of  the  stomach  with- 
out a  causative  anatomical  change,  and  whether  or  not  due  to  a  purely 
functional  disturbance  is  doubtful.  Martins  quite  properly  states  that  the 
ready  vulnerability  of  the  mucous  membrane,  so  obvious  in  cases  of  this 
kind  upon  the  introduction  of  the  tube,  raises  the  suspicion  of  the  exist- 
ence of  slight  degenerative  or  inflammatory  processes.  Besides,  the  sub- 
jective symptoms  of  achylia  affecting  the  stomach  are,  as  a  rule,  few,  and 
their  action  upon  the  entire  nutritive  condition  is  slight,  or  may  be  wholly 
absent,  for  the  absence  of  gastric  digestion  with  intactness  of  the  motor 
function  is  not  of  importance  in  utilizing  the  ingesta. 

A  diagnosis  of  achylia  can  only  be  made  when  repeated  examination  of 
the  gastric  contents,  possibly  after  a  previous  irritation  of  the  mucous  mem- 
brane by  the  introduction  of  a  salt  solution,  shows  an  absence  of  acid 
reaction  or  only  very  low  values  of  the  total  acidity  (at  most  ten  or  less). 
In  the  differential  diagnosis  carcinoma  and  gastritis  must  be  excluded. 
In  the  treatment,  besides  general  strengthening  therapy,  the  absent  secre- 
tion must  be  substituted  for  by  the  administration  of  hydrochloric  acid  and 
pepsin  at  every  meal,  and  the  maintenance  of  the  motor  activity  of  the 
stomach  must  be  provided  for.  The  former,  as  has  been  remarked,  is 
unnecessary  for  the  sufficient  utilization  of  the  ingesta.  There  is,  however, 
no  doubt  that  by  the  absence  of  hydrochloric  acid  in  the  stomach  there  is 
danger  of  the  further  development  of  pathogenic  microorganisms  which 
have  gained  entrance  there,  and  this  danger  may  be  averted  by  the  admin- 
istration of  hydrochloric  acid. 

Hyperacidity  {hyperchlorliydria,  gastroxynsis) . — Hyperacidity  repre- 
sents one  of  the  most  important  disturbances  of  function  of  the  stomach, 
and  it  may  also  be  combined  (see  below)  with  hypersecretion  (gastrorrhcea 
acida).  It  is  chiefly  noted  in  young,  anemic  individuals,  particularly 
chlorotics,  and  also  in  neurasthenics,  but  by  no  means  exclusively  in  these 
conditions.  Psychical  irritation  is  unquestionably  an  important  etiologic 
factor,  but  it  is  also  observed  in  persons  whose  nervous  system  is,  in 
general,  quite  normal.  Of  organic  gastric  affections,  which  we  shall  not 
minutely  consider  here,  the  anomaly  is  most  often  associated  with  ulcer. 
We  find  it,  too,  in  motor  insufficiency  of  the  stomach,  in  gastrectasis,  in 
gastroptosis  and  purely  functional  atony  (see  above),  probably  due  to  the 
abnormally  long  presence  in  the  stomach  of  the  ingesta  which  causes  the 
secretion.     Cases  of  hyperacidity  have  also  been  described  (acid  gastritis) 


NEUROSES   OF  THE   STOMACH  77 

in  chronic  gastritis  which,  as  a  rule,  runs  its  course  with  a  decrease  in 
gastric  secretion,  and  in  the  amount  of  acid.  On  account  of  the  extreme 
difficulty  of  excluding  these  organic  affections,  we  must  admit  that  abso- 
lutely certain  cases  of  purely  functional  hyperacidity  are  by  no  means 
frequent. 

The  subjective  symptoms,  combined  with  a  normal  appetite,  are  pyrosis, 
which  may  be  increased  to  gastric  pain,  pressure  in  the  gastric  region,  and 
acid  eructations.  Vomiting  of  decidedly  acid  masses  is  rare;  thirst  and 
bulimia  are  frequent.  These  symptoms  appear  in  very  different  degrees 
without  a  parallel  degree  in  the  amount  of  acid.  The  sensitiveness  of 
the  gastric  mucous  membrane  to  the  irritative  action  of  hydrochloric  acid 
is  apparently  very  variable  in  the  same  and  in  different  individuals,  and 
the  relation  in  time  of  these  difficulties  to  the  intake  of  food  shows  many 
variations.  Sometimes  they  are  nearly  continuous  with  occasional  exacer- 
bations attributed  to  the  food  consumed,  at  other  times  they  occur  only 
paroxysmally  after  meals.  Sometimes  also  certain  foods  which  are  invar- 
iably not  well  borne  are  responsible  for  the  difficulty. 

The  diagnosis  of  hyperacidity  depends  upon  an  examination  of  the 
gastric  contents.  If,  upon  repeated  examination,  we  find  an  amount  of 
0.25  per  cent,  of  HCl  or  more,  hyperacidity  is  proven.  If  upon  the  ab- 
sence of  organic  acids  the  total  acidity  is  more  than  70,  the  same  condition 
is  proven.  The  circumstance  that  particles  of  bread  are  less  broken  up 
than  normally  is  also  characteristic  of  a  high  degree  of  acid.  It  must  also 
be  borne  in  mind  that,  just  as  under  physiologic  conditions,  variations  in 
the  amount  of  acid  frequently  occur,  yet  the  diagnosis  of  hyperacidity  is 
not  superseded  by  the  fact  that  occasionally  normal  amounts  of  acid  are 
found. 

While  the  proof  of  hyperacidity,  as  a  rule,  is  simple,  the  exclusion  of 
an  organic  disease  of  the  stomach  and  the  proof  of  a  purely  functional 
disturbance  combined  with  hyperacidity  may  be  most  difficult.  Here,  in 
the  first  place,  gastric  ulcer  must  be  mentioned.  On  account  of  its  great 
frequency,  and  that,  as  a  rule,  it  runs  its  course  with  hyperacidity,  and 
also  that,  in  this  affection,  the  symptoms  usually  appear  some  time  after 
eating,  we  cannot  be  too  careful  in  the  differential  diagnosis.  When  there 
is  well  developed  gastric  pain  besides  the  other  mentioned  s3nnptoms,  in 
my  experience  a  purely  functional  hyperacidity  should  be  excluded  and 
the  treatment  should  be  based  upon  the  hypothesis  of  a  gastric  ulcer.  If 
positive  factors  for  the  development  of  an  acid  gastritis  have  been  proven, 
in  the  differential  diagnosis  we  must  also  consider  this  affection.  Contrary 
to  the  reports  of  some  authors,  the  absence  of  mucus  in  the  evacuated  masses 
favors  the  assumption  of  the  purely  nervous  character  of  the  malady,  if 
the  evacuation  have  occurred  at  the  usual  time  after  the  test-meal,  for  the 
mucus  secreted  in  consequence  of  catarrh  is  very  rapidly  digested  by  the 
acid  gastric  juice,  which  has  a  strong,  peptonizing  action.     More  signifi- 


78  FUNCTIONAL  DISEASES  OF  THE  STOMACH 

cant,  on  the  other  hand,  is  the  fact  that  toward  the  end  of  digestion,  upon 
microscopic  examination  of  the  remnants  in  the  opening  of  the  tube,  large 
numbers  of  cell  nuclei  are  found,  since,  normally,  but  few  nuclei  of  this 
kind  are  present.  Another  circumstance  that  favors  an  existing  catarrh 
is  that  upon  withdrawal  of  the  tube  from  an  empty  stomach  adherent  par- 
ticles of  mucus  containing  large  numbers  of  leukocytes  are  found. 

The  views  in  regard  to  the  best  treatment  of  hyperacidity  have  under- 
gone decided  change.  The  fact  that  an  increased  amount  of  HCl  in  the 
gastric  contents  unquestionably  disturbs  the  saccharification  of  the  food- 
containing  starch  by  the  salivary  ferment  which  is  swallowed  made  it 
appear  rational  to  limit  starchy  food  in  the  diet  of  the  patients  suffering 
from  hyperacidity  (to  the  utmost),  and  to  place  them  upon  animal  food. 
Experience  has,  however,  shown  that  a  diet  of  this  kind  does  not  always 
lessen  the  difficulties,  but  not  infrequently  they  increase,  and  this  coincides 
with  the  fact  that  objective  investigations  of  the  gastric  contents  show  no 
decrease  in  the  amount  of  acid.  In  the  first  place,  a  meat  diet  is  generally 
not  well  borne  by  patients  with  gastric  disease,  and,  above  all,  a  diet  rich 
in  albumin  causes  a  greater  secretion  of  acid  (Hemmeter,  Fleiner,  Jiir- 
gensen  and  others).  It  is,  therefore,  rational  to  prescribe  for  the  patient 
a  mixed  diet  which  possesses  the  property  of  combining  acids,  which  in- 
creases acid  secretion  to  the  slightest  degree,  and  is  as  little  irritating  as 
possible.  These  indications  are  best  fulfilled  by  milk,  and  by  milk  rich  in 
fat,  since  fats  have  an  extremely  slight  influence  upon  the  gastric  juice.  If 
milk  is  declined,  or  not  well  borne,  as  is  unfortunately  often  the  case  with 
these  patients,  lime  water  may  be  added  to  it.  Sbft,  pappy  rice,  maizena, 
stewed  calves'  brains,  sweetbreads,  etc.,  are  given.  Toasted  wheat  bread, 
and  tea  with  a  plentiful  addition  of  cream,  are  likewise  permitted.  We 
also  prescribe  soda  bicarbonate,  magnesia  (hydrated),  Carlsbad  salt  and 
other  alkalies,  besides  narcotics  (especially  belladonna).  In  some  cases 
there  is  a  favorable  influence  from  takadiastase,  whose  saccharifying  prop- 
erty is  less  disturbed  by  hydrochloric  acid  than  that  of  ptyalin.  In  addi- 
tion, stimulating  measures  are  not  to  be  neglected. 

Hyperacidity  is  a  very  stubborn  disorder,  and  we  must,  therefore,  be 
guarded  in  the  prognosis. 

Hypersecretion  {flow  of  gastric  juice) . — This  affection  is  characterized 
by  an  abnormally  profuse  secretion  of  the  gastric  juice,  which  occurs  with- 
out the  stimulation  of  the  ingesta.  It  may  be  continuous  or  periodic,  and 
may  run  an  acute  or  chronic  course.  The  amount  of  HCl  of  the  secre- 
tion may  be  increased  (gastrorrhoea  acida)  or  normal.  In  the  former 
case  the  symptoms  are  those  of  hyperacidity;  but,  even  when  HCl  is 
not  increased,  the  patients  complain  of  pyrosis  and  acid  eructations. 
Vomiting  of  a  more  or  less  profuse,  watery,  acid  fluid  while  the  stomach 
is  empty  of  food  is  characteristic  of  the  condition. 

The  diagnosis  depends  upon  the  last  mentioned  symptom  and  upon 


NEUROSES   OF  THE   STOMACH  79 

the  results  obtained  by  the  stomach-tube  while  the  stomach  is  empty; 
that  is,  whether  by  this  procedure  large  amounts  (100  c.c,  to  1  liter) 
of  an  almost  clear  fluid  having  an  acid  reaction  and  containing  HCl  and 
pepsin  are  evacuated. 

The  treatment  must  be  directed  to  the  removal  of  the  probable  under- 
lying affection,  neurasthenia,  anemia,  etc. ;  the  preparations  of  bromin, 
narcotics  (codein,  belladonna,  cocain,  etc.),  are  in  place  as  well  as  irriga- 
tion of  the  gastric  mucous  membrane. 


NERVOUS   DYSPEPSIA   (GASTROSIS) 

Among  the  gastro-neuroses,  so-called  "  nervous  dyspepsia "  occupies  a 
peculiar  position.  Leube,  who  accurately  portrayed  the  clinical  picture 
after  it  had  been  described  by  others,  particularly  by  English  authors 
(Beard  and  Eockwell),  defines  it  as  a  pathologic  condition  in  which  sub- 
jective symptoms  of  chronic  dyspepsia,  analogous  to  those  of  chronic  gas- 
tritis are  present,  but  in  which  objectively  demonstrable  anomalies  of 
activity,  as  well  as  organic  changes  of  the  stomach,  are  absent. 

It  is  evident  that,  in  a  pathological  condition  the  basis  of  which  is 
subjective  difficulties,  the  negative  results  of  investigations  of  the  anatomi- 
cal and  functional  disturbances  of  the  stomach  create  a  difference  of 
opinion  among  authors  in  regard  to  the  definition  and  the  limitation  of 
the  affection,  and  that  many  deny  that  there  is  any  justification  for  con- 
sidering a  symptom-complex  of  this  kind  as  a.  disease,  sui  generis.  In 
fact  the  number  of  authors  who  are  opposed  to  the  pathologic  conception 
of  "  nervous  dyspepsia,"  in  Leube's  sense,  is  quite  considerable.  We  would 
digress  too  far,  and  in  entire  opposition  to  the  character  of  this  article, 
were  we  minutely  to  consider  the  comprehensive  literature  of  this  subject. 
Some  of  these  explanations  bear  a  remote  date,  and  it  may  be  assumed 
that  not  a  few  of  the  opponents  of  "  nervous  dyspepsia  "  have,  in  the  course 
of  time,  made  subsequent  ob^rvations,  and  have  changed  their  former 
opinions. 

According  to  my  experience  which  coincides  with  that  of  others,  there 
is  no  doubt  of  the  existence  of  a  clinical  picture  as  described  by  Leube 
and  others.  Far  be  it  from  me  to  maintain  that,  in  such  cases,  an  organic 
change  can  always  be  excluded.  We  are  unable,  however,  to  demonstrate 
it,  and  we  may  often  convince  ourselves  that  no  organic  disease  known 
to  us  is  the  cause  of  the  affection.  Shall  we  therefore  deny  the  existence  of 
this  clinical  picture?  With  as  much  right  as  we  could  eliminate  many  other 
affections,  such  as  migraine,  neuroses  of  the  heart  and  of  the  intestines, 
flittering  scotoma,  pruritis,  etc.,  from  pathology.  For  in  these  conditions 
also  we  are  unable  at  present  to  detect  any  anatomical  anomaly  which  is 
certainly  the  cause  of  the  symptoms  or  to  exclude  it.  The  justification 
and   the  necessity   of   limiting   "  nervous    dyspepsia "    as    a   disease,   sui 


80  FUNCTIONAL   DISEASES  OF  THE  STOMACH 

generis,  as  well  as  the  previously  mentioned  functional  disturbances,  simply 
depend  upon  experience,  in  consequence  of  which  the  symptoms  mentioned 
and  those  still  to  be  discussed  appear,  and  must  be  considered,  as  the 
expression  of  this  affection  of  the  stomach. 

Objections  have  been  raised  to  the  description  of  the  clinical  picture, 
as  well  as  to  its  name.  This  is  quite  reasonable.  Since  objective  dis- 
turbances of  digestion  are  absent  in  the  disease  it  would  naturally  follow 
that  the  name  "nervous  dyspepsia"  would  provoke  discussion.  It  might 
also  be  added  that  the  nomenclature  does  not  correspond  to  the  actual 
conditions,  since  the  dyspeptic  difficulties  are,  without  exception,  to  be 
attributed  to  an  implication  of  the  nervous  apparatus.  In  many,  perhaps 
in  a  majority  of  the  cases,  this  origin  may  be  at  once  admitted;  namely, 
for  those  in  which  the  disease  depends  upon  neurasthenia,  hysteria  or 
organic  disease  of  the  nervous  system,  or  where  it  appears  as  a  reflex 
neurosis,  particularly  from  the  sexual  apparatus.  Even  where  the  causa- 
tive factor  is  looked  for  in  intoxications  or  infections,  such  as  the  abuse 
of  nicotin,  alcoholism  (here  it  is  true  there  is  usually  chronic  gastritis), 
syphilis,  malaria,  etc.,  which  usually  exert  a  damaging  influence  upon 
the  peripheral  nerves,  we  are  justified  in  ascribing  to  the  primary  cause 
the  development  of  the  gastric  symptoms.  On  the  other  hand,  it  must 
bo  remembered  that  the  symptom-complex  peculiar  to  this  group  also 
appears  in  consequence  of  anemic  and  general  debilitative  conditions,  such 
as  chlorosis,  the  puerperium,  improper  and  insufficient  food,  etc.  It 
would  seem  far-fetched  to  look  for  the  cause  of  the  morbid  sensations 
in  "the  nervous  system.  This  would  be  more  obvious  in  an  insufficient 
nutrition  of  tlie  parenchyma  of  the  stomach  which  is  undoubtedly  present, 
which,  however,  as  the  actual  causal  factor,  has  as  yet  shown  no  gross 
patliologico-anatomical  changes  of  the  organ.  For  this  reason,  the  desig- 
nations neurasthenia  dyspeptica  orvgastrica  (Burkart,  Ewald)  are  not  to 
be  regarded  as  improvements;  for,  as  v.  Leyden  quite  properly  remarks, 
the  chief  disturbances  are  not  in  the  stomacji,  as  should  be  the  case.  Of 
the  other  names  which  have  been  proposed,  the  beet  appears  to  be  "  com- 
bined gastroneurosis,"  which,  it  is  true,  is  somewhat  complicated,  and 
does  not  emphasize  the  sometimes  non-nervous  nature  of  the  affection. 

Perhaps  it  would  be  wise  to  choose  a  more  indifferent  designation, 
which  would,  however,  permit  us  to  recognize  that  we  are  dealing  with 
a  functional  anomaly  of  the  stomach.  As  such  I  propose  the  name: 
Gastrosis.  The  designation  nervous  dyspepsia  has  become  so  firmly  rooted 
in  our  minds  that  it  will  not  readily  be  eradicated,  but  the  name  is  of 
subordinate  significance  provided  we  are  unanimous  as  to  what  it 
signifies. 

Among  the  etiologic  factors  which  have  been  mentioned  there  is  one 
whicli  is  important  because  of  its  comparative  frequency.  This  is  an 
aliiiorinal  state  of  nutrition  due  to  the  fact  that  the  periods  between  the 


NEUROSES  OF  THE  STOMACH  81 

individual  meals  are  too  long.  There  are  some  persons  who,  like  dogs, 
take  only  once  a  day  a  meal  which  really  deserves  the  name,  and  yet  they 
continue  in  the  best  of  health.  In  spite  of  the  latter  circumstance,  there 
can  be  no  doubt  that  this  habit  is  irrational.  It  is  contrary  to  the  laws 
regulating  the  function  of  the  stomach  as  a  reservoir  of  food,  and  it 
cannot  be  an  advantage  to  the  stomach  to  remain  empty  for  several  hours 
during  the  day  and  then  suddenly  to  become  excessively  loaded.  The 
effect  of  this  is  particularly  noticeable  in  persons  who  do  not  voluntarily 
or  from  habit  make  these  long  pauses  between  meals,  but  are  forced  to 
it  by  the  stress  of  circumstances.  This  occurs  in  very  busy  physicians, 
particularly  surgeons,  in  merchants,  in  lawyers,  etc.  According  to  my 
experience,  this  category  of  occupations  furnishes  the  main  contingent  of 
the  cases  of  gastrosis.  The  circumstance  that  the  digestive  disturbances 
of  the  patients  improve  when  they  change  their  mode  of  life  and  take 
more  frequent  but  smaller  meals,  is  proof  of  the  etiologic  importance  of 
this  improper  mode  of  nutrition. 

The  symptoms  of  nervous  dyspepsia,  as  already  stated,  are  in  the  main 
subjective.  The  patients  complain  chiefly  of  a  feeling  of  pressure  and 
distention  in  the  gastric  region,  and  of  eructations  which  sometimes  become 
exceedingly  severe  and  loud.  The  appetite,  as  a  rule,  is  disturbed.  The 
patients  have  more  or  less  repugnance  to  food,  and  not  rarely  complain 
of  nausea.  Tendency  to  vomit  and  actual  vomiting  also  occur,  but  not 
so  frequently  as  in  gastritis.  The  loss  of  appetite  in  some  cases  depends 
upon  autosuggestion.  The  patients  fear  that  by  eating  their  distress  will 
be  increased,  and  therefore  refrain  from  food  as  far  as  possible.  On  the 
other  hand,  even  bulimia  occurs;  the  patients  then  are  tormented  by  a 
voracious  appetite  which  causes  them  to  crave  food.  As  a  rule,  as  soon 
as  they  begin  to  eat,  the  bulimia  not  only  disappears,  but  also  all  desire 
for  food.  They  can  only  -take  small  amounts,  and  are  unable  to  satisfy 
the  existing  hunger.  Perverse  anomalies  of  taste  are  also  frequently  ob- 
served. Acids  and  other  foods  difficult  of  digestion  are  especially  pre- 
ferred, and  in  the  circumstance  that,  after  their  use,  the  preceding  dis- 
comfort often  lessens,  this  clinical  picture  differs  from  other  organic 
affections. 

Among  the  abnormal  sensations  which  originate  from  the  gastric 
region,  besides  fulness  and  eructation,  pyrosis  must  be  mentioned.  This 
symptom,  which  is  an  almost  invariable  accompaniment  of  actual  dyspepsia, 
of  "  sour  stomach,"  is  not  always  found  hand  in  hand  with  an  increase 
in  the  acidity  of  the  gastric  contents,  nor  need  this  be  the  case  in  nervous 
dyspepsia.  There  are,  however,  instances  in  which  the  degree  of  acidity 
exceeds  the  normal  limits. 

Actual  pain  in  the  stomach  is  but  rarely  complained  of,  and,  even  then, 
it  is  not  the  pain  upon  pressure  which  is  so  characteristic  of  ulcer.  The 
gastric  region  may  be  sensitive  to  the  pressure  of  palpation,  but  often  this 


82  FUNCTIONAL  DISEASES  OF  THE  STOMACH 

is  only  an  indefinite,  disagreeable  feeling,  which  is  also  observed  in  other 
sensitive  patients  whose  stomach  and  other  abdominal  organs  are  perfectly 
normal. 

The  condition  of  the  bowels  varies.  Constipation  exists  in  many  cases, 
as  in  other  chronic  gastric  affections.  Diarrhea  is  rare,  and  often  no 
anomaly  is  present. 

The  disturbances  of  the  general  condition  may  be  manifold  and  corre- 
spond to  the  varied  etiologic  bases  of  the  affection.  From  the  symptoms 
of  neurasthenia  (such  as  numbness  in  the  head,  lassitude,  depression, 
hypochondriasis,  even  melancholia,  on  the  other  hand  frequently  slight 
irritability,  cardiac  palpitation,  vertigo,  etc.)  it  is  not  always  easy  to  de- 
cide whether  we  arc  dealing  with  coordinated  symptoms  of  the  same  cause 
of  the  disease  or  with  the  sequels  of  the  gastric  affection. 

The  general  nutrition  may  also  vary  according  to  the  causal  factor. 
In  most  cases  the  patients  are  well  nourished,  and  there  is  no  external 
sign  of  suffering.  But  we  also  see  patients  who  are  hollow-eyed  and  more 
or  less  emaciated  with  no  malady  save  one  of  the  stomach  to  account 
for  the  distur])ance.  The  history  then  reveals  that  the  emaciation  is  due 
to  insuHicient  food.  These  patients,  partly  from  fear  of  distress,  partly 
in  obedience  to  unwise  professional  advice,  have  for  a  long  time  taken 
only  a  minimum  of  food,  and  have  actually  undergone  a  starvation  cure. 
It  cannot  be  wondered  at  that,  in  consequence  of  tiiis  limited  diet  and 
the  resulting  loss  of  resistance  of  the  walls  of  the  stomach,  the  symptoms 
instead  of  decreasing  have  been  decidedly  aggravated.  These  are  the  most 
hopeful  cases  for  treatment;  the  physician  who  clearly  recognizes  the 
a  fleet  ion  and  acts  upon  this  knowledge,  helped  by  the  previous  error,  may, 
with  ease,  bring  about  what  seems  a  miraculous  cure. 

In  the  diagnosis  of  nervous  dyspepsia,  which  should  be  made  with  great 
care,  we  must  first  decide  whether  the  complaints' of  the  patient  are  actually 
attributable  to  gastric  activity,  or  whether  the  difficulties  referred  to  the 
stomach  are  not  due  to  a  disease  of  other  parts  of  the  organism,  or  whether 
they  do  not  at  least  owe  to  it  their  origin.  In  this  connection  we  cannot 
be  too  skeptical,  since  such  so-called  dyspeptic  symptoms  as  were  empha- 
sized above  may  occur  in  a  number  of  different  affections  which  cannot 
be  minutely  described  at  this  point. 

The  presence  of  well  developed  neurasthenia  or  hysteria,  and  the  proof 
that  these  anomalies  existed  prior  to  the  dyspeptic  symptoms,  are  of 
inijwrtance  in  the  diagnosis.  It  is  obvious  that  these  will  aid  us  only  in 
the  diagnosis,  as  neurasthenic  and  hysterical  persons  may  also  suffer  from 
ori^anic  disease  of  the  stomach,  and  as  gastrosis  also  occurs  in  persons  who, 
in  the  main,  sliow  no  functional  disturbances  of  the  nervous  system. 

Tlie  coincidence  of  dyspeptic  disturbances  belonging  to  the  symptom- 
coiiiiilcx  of  nejvous  dyspepsia,  with  functional  disturbances  of  the  heart 
without  organic  disease,  is  also  important  in  diagnosis.     Cardiac  palpita- 


NEUROSES  OF  THE  STOMACH  83 

tion  and  irregularity  of  the  cardiac  action  in  connection  with  gastric  affec- 
tions are,  therefore,  symptoms  which  must  be  considered  in  the  diagnosis. 

The  report  of  the  patient  that  the  digestive  symptoms  vary,  that,  in- 
stead of  the  usual  disturbances,  there  are  times  when  the  disease  seems 
to  have  almost  disappeared,  particularly  when  the  mind  is  diverted  by 
pleasant  company,  may  be  of  value.  With  Rosenheim  I  admit  this  fact, 
but  it  rarely  occurs,  and  is  not  absolute  proof  that  other  gastric  patients, 
for  example,  those  suffering  from  chronic  gastritis,  occasionally  will  forget 
their  dyspeptic  disturbances  when  in  interesting  society,  at  the  theatre,  etc. 
Nevertheless  this  occurs,  although  less  frequently. 

The  objective  examination  of  the  stomach  is  chiefly  important  because 
conspicuous  anomalies  are  not  found.  I  am  of  the  opinion  that  the  mod- 
erate grades  of  gastroptosis  which  prevail  so  commonly  in  women  without 
giving  rise  to  symptoms,  cannot  annul  the  diagnosis:  Nervous  dyspepsia. 

In  regard  to  the  functional  test,  Leube,  as  remarked  above,  has  laid 
special  stress  upon  the  fact  that  the  motor  function  is  intact.  According 
to  my  experience,  we  must  in  general  agree  with  him,  and  the  cases  in 
which  there  is  a  well  developed  slowing  of  motion  should  not  be  consid- 
ered as  nervous  dyspepsia.  Moderate  grades  of  atony,  or  the  presence  of 
small  remains  of  food  two  hours  after  a  test  breakfast  and  seven  hours 
after  a  test-meal,  belong  to  the  same  clinical  picture,  particularly  if  this 
condition  is  not  constant.  In  testing  the  functions  of  the  stomach  these 
frequently  great  variations  are  characteristic,  and  this  is  true  of  a  higher 
degree  of  secretion.  In  this  respect  I  entirely  agree  with  Boas  and  Rosen- 
heim. It  is  true  that  while  the  degree  of  acid  is  usually  within  normal 
limits  we  occasionally  note  surprising  variations  of  the  acidity  below  and 
above  the  normal. 

On  account  of  this  variability  of  the  symptoms,  and  the  difficulty  of 
limiting  exactly  the  clinical  picture,  we  should  never  fail  to  consider  the 
possibility  of  organic  disease  of  the  stomach  before  we  make  a  positive 
diagnosis. 

The  condition  may  be  mistaken  for  gastric  ulcer,  for  this  affection  does 
not  always  present  the  well  known  classical  symptom  of  typical  pain 
occurring  a  short  time  after  the  intake  of  food,  but  it  may  develop  with- 
out any  pain,  and  an  examination  of  the  gastric  contents  may  reveal  no 
characteristic  differences.  If  there  is  actually  well  developed  pain,  the 
case  is  not  one  of  nervous  dyspepsia.  Marked  tenderness  and  a  drawing 
sensation  in  the  gastric  region,  however,  are  observed,  and  the  report  that 
these  sensations  are  not  increased  by  external  pressure  but  are  rather  re- 
lieved is  decidedly  against  ulcer.  The  manner  in  which  the  sensitiveness 
of  the  gastric  region  shows  itself  upon  palpation  is  important.  If  it  be 
localized  to  a  circumscribed  area  this  favors  ulcer,  while  a  diffuse,  painful 
sensitiveness  of  the  entire  epigastric  region  points  to  the  nervous  character 
of  the  affection.     If  hysteria  is  present  we  not  rarely  observe,  especially 


84  FUNCTIONAL   DISEASES   OF  THE   STOMACH 

in  thin  patients,  painful  pressure  areas  upon  both  sides  of  the  vertebral 
column.  But  a  confusion  of  this  previously  mentioned  pain  upon  pressure 
with  simultaneous  gastroptosis  is  not  impossible. 

Even  if  there  is  no  marked  sensitiveness  of  the  gastric  region,  we  can- 
not at  once  exclude  ulcer,  particularly  when  dealing  with  young  anemics. 
As  the  examination  of  the  gastric  contents  permits  no  positive  conclu- 
sions, it  is  wise  in  cases  of  this  kind  to  proceed  as  if  ulcer  were  present, 
therefore,  to  prescribe  absolute  rest,  fluid  diet,  and  silver  nitrate.  If  by 
tliis  means  the  affection  is  not  favorably  influenced,  the  assumption  of 
gastrosis  is  justified. 

Gastric  carcinoma  may  be  excluded  with  certainty  provided  the  dys- 
peptic difficulties  have  existed  for  a  long  time  without  any  diminution  of 
tlie  body-weight.  We  must,  however,  remember  that  carcinoma  may  run 
a  very  slow  course  without  producing  symptoms  other  than  those  of  dys- 
pepsia, anemia,  and  slight  emaciation.  In  elderly  individuals  we  must 
be  very  cautious  in  the  diagnosis  of  an  affection  of  this  character,  existing 
for  a  short  time,  perhaps  only  for  a  few  months.  If  well  developed  symp- 
toms of  neurasthenia  or  hysteria  have  preceded,  they  favor  the  diagnosis 
of  nervous  dyspepsia,  although,  of  course,  patients  of  this  kind  may  be 
attacked  by  carcinoma.  A  normal  hydrochloric  acid  reaction  and  the  ab- 
sence of  lactic  acid  in  the  stomach  contents  are  factors  which  decidedly 
favor  nervous  dyspepsia.  Absolute  certainty,  however,  can  only  be  attained 
when  regular  weighings  of  the  body,  under  sufficient  nourishment,  show  no 
loss  in  weight. 

Well  developed  gastrectasis  presents  such  a  characteristic  clinical  pic- 
ture that  this  disease  can  scarcely  be  mistaken  for  another.  But  this  may 
readily  occur  when  the  symptoms  depend  upon  a  simple  atony  of  the  gas- 
tric walls.  Here  definite  conclusions  are  reached  by  the  examination  of 
the  motor  function.  The  proof  that  there  is  no  stagnation  of  the  ingesta, 
that,  on  the  contrary,  the  stomach  discharges  its  contents  normally,  ex- 
cludes this  anomaly.  Naturally,  we  should  not  be  content  with  a  single 
examination,  for,  as  has  been  stated,  variations  in  the  motor  function  occur 
in  nervous  dyspepsia.  But  the  existence  of  this  affection  is  not  disproven 
if,  transitorily,  a  prolonged  retention  of  the  ingesta  in  the  stomach  is 
observed. 

Chronic  gastritis  must  be  specially  borne  in  mind  in  the  differential 
(lia;j:nosis.  as  the  subjective  symptoms  of  this  condition  completely  coincide 
with  those  of  nervous  dyspepsia.  The  absence  of  a  coated  tongue,  and  the 
non-appearance  of  mucus  in  the  vomit  and  evacuated  gastric  contents, 
particularly  when  the  stomach  is  empty  (see  above),  favor  the  latter.  If 
gastritis  is  present,  upon  microscopic  examination  of  the  contents  of  the 
tube  we  find  profuse  formed  elements,  leukocytes  and  epithelium.  The 
chemical  examination  of  the  gastric  contents  after  a  test-meal  is  not  unim- 
portant, for,  as  a  rule,  the  secretion  of  HCl  is  deficient  in  gastritis.     This 


NEUROSES  OF  THE  STOMACH  85 

is,  of  course,  not  always  the  case,  for  in  so-called  acid  gastritis,  which 
is  rare,  it  may  even  be  increased.  Therefore,  in  cases  of  this  kind,  the 
circumstance  that  the  affection  occurs  in  neurasthenics  or  hysterical 
persons,  as  well  as  the  modification  of  the  disease  by  treatment,  is  of 
significance. 

The  prognosis  is  always  doubtful.  By  proper  treatment  many  cases 
are  favorably  influenced  and  even  complete  recovery  ensues.  But  it  some- 
times happens  that,  at  the  onset,  decided  improvement  takes  place,  and 
the  easily  excited  patients  are  enthusiastic  regarding  the  result ;  then,  how- 
ever, relapses  occur  which  affect  the  entire  nervous  system,  and  reproduce 
the  former  gastric  disturbances.  In  other  cases  all  endeavors  favorably  to 
influence  the  condition  are  without  avail.  These  cases  test  the  patience  of 
the  sufferer  and  the  physician. 

In  therapy  the  psychical  treatment  is  hardly  less  important  than  the 
somatic.  It  is  true  we  will  only  rarely  be  successful  if  we  represent  to 
the  patients  that  the  affection  is  a  very  slight  one,  which  may  yield  to  a 
little  exercise  of  the  will.  As  a  rule  the  patients  resent  a  suggestion  of 
this  kind.  It  is  in  crass  contrast  to  their  discomfort,  and,  as  a  matter  of 
fact,  the  mere  determination  not  to  be  ill  rarely  suffices  to  cure  the  disease. 

But  there  are  instances,  as  stated  before,  in  which  a  mere  change  in 
the  diet,  i.  e.,  a  return  to  the  usual  home  living,  is  sufficient  to  restore  the 
patient  to  health.  These  are,  however,  not  cases  due  to  neurasthenia  or 
hysteria,  but  those  which  at  the  onset  were  very  insignificant  gastric  diffi- 
culties, but  excessive  carefulness  and  a  fear  of  the  injurious  effect  of  whole- 
some and  plentiful  food  has  limited  the  diet  to  such  uniform  and  insuffi- 
cient food  that  it  has  not  conduced  to  improvement;  hence,  in  consequence 
of  imperfect  nutrition  of  the  walls  of  the  stomach  and  of  the  entire  organ- 
ism, a  steady  aggravation  of  the  dyspeptic  symptoms  has  been  brought  about. 

A.,  a  manufacturer,  aged  45,  as  a  young  man  had  disease  of  the  left  pulmonary 
apex,  which,  however,  entirely  disappeared  and  there  is  no  trace  of  it  at  present. 
After  this  illness,  the  patient  became  extraordinarily  careful  and  anxious  about  his 
health.    The  slightest  deviation  from  the  normal  made  him  fear  the  onset  of  disease. 

According  to  report,  several  years  ago  he  began  to  have  a  sensation  of  fulness 
and  pressure  in  the  epigastrium  after  his  principal  meal,  accompanied  by  eructa- 
tions and  constipation.  Gastritis  was  diagnosticated,  and  the  patient,  whose  appe- 
tite was  always  normal,  limited  to  an  extreme  the  quantity  and  quality  of  his  food. 
By  this  means  and  the  use  of  Carlsbad  water,  his  condition  is  said  to  have  at  first 
improved,  but  gradually  there  Avas  an  aggravation,  and,  although  pressure  in  the 
region  of  the  stomach  was  no  longer  especially  noticeable,  the  eructations  continued, 
and  to  these  vertigo,  headache  and  palpitation  of  the  heart  were  added.  Appetite 
was  lost,  and  not  infrequently  the  monotonous  diet  caused  repugnance.  Neverthe- 
less, the  patient  continued  upon  this  diet  through  fear  of  injuring  himself  by  a 
change. 

The  examination  of  the  powerfully  built,  but  pale  and  poorly  nourished  patient, 
revealed  no  anomaly  of  the  stomach  (total  acidity  upon  repeated  examination  30 
to  60,  Giinzburg's  test  positive,  motility  normal)   or  any  other  part  of  the  organism. 


86  FUNCTIONAL   DISEASES   OF  THE  STOMACH 

I  explained  to  the  patient  that  there  was  no  disease  of  the  stomach,  nor,  in  fact, 
any  organic  affection,  and  that  his  symptoms  were  due  to  an  injudicious  mode  of 
life,  particularly  to  monotonous  and  insufficient  food.  I,  therefore,  advised  him  not 
only  to  take  the  "  easily  digested  foods  "  but  to  return  to  his  former  favorite  foods. 
No  restrictions,  whatever,  in  diet  were  necessary.  The  patient  at  first  was  some- 
what incredulous  but  followed  my  advice  and  at  once  ate  some  peas  with  sour  kraut 
and  pickled  meat.  As  the  symptoms  which  he  looked  for  did  not  appear  he  gained 
confidence,  again  ate  and  drank  like  a  healthy  man,  and  after  three  weeks  presented 
himself  to  me  completely  cured.  His  weight  steadily  increased  (about  21.9  pounds) 
and  except  for  constipation,  which  still  existed,  all  symptoms  had  disappeared. 

Cases  of  this  kind  are,  however,  infrequent,  and,  particularly  when 
dealing  with  nervous  persons,  treatment  such  as  above  described  is  not 
in  order.  Here,  above  all,  it  is  necessary  to  tone  up  the  entire  nervous 
system.  Bodily  and  mental  rest,  removal  from  the  ordinary  occupation, 
are  usually  the  first  requirements,  but  by  no  means  always.  Patients  who 
have  previously  passed  their  time  in  idleness,  with  hypochondriac  thoughts 
dwelling  upon  their  stomach  affection,  should  be  advised  to  take  up  a  stimu- 
lating occupation,  strengthening  and  even  fatiguing  bodily  exercises.  But 
the  diet  jnust  be  regulated.  In  severe  cases,  particularly  in  debilitated 
women,  complete  isolation  and  rest  in  bed,  at  least  for  the  greater  part 
of  the  day,  and  forced  feeding,  will  be  beneficial. 

In  other  cases  a  change  of  air,  i.  e.,  residence  in  pure  fresh  air  (medium 
altitude  in  the  woods)  is  sufficient.  Special  stress  must  be  laid  upon  the 
stimulation  of  the  skin  by  baths,  massage  and  electricity.  Above  all,  the 
diet  must  be  regulated.  Food  difficult  of  digestion,  and  particularly  that 
which  causes  flatulence,  must  be  avoided,  but  the  fact  should  be  emphasized 
that  the  diet  should  be  varied  as  much  as  possible,  and  the  intervals  be- 
tween the  meals  are  not  to  be  too  long. 

Drug  treatment,  compared  with  these  general  dietetic  rules,  is  of  de- 
cidedly secondary  importance,  but  it  is  frequently  necessary  to  support  the 
latter  mode  of  treatment.  Here  stomachics  such  as  rhubarb,  tincture  of 
quinin  and  bitters,  iron  and  Fowler's  solution,  perhaps  also  quinin  as  a 
tonic,  then  sodium  bromid  and  valerian,  as  well  as  various  remedies  for 
the  usually  stubborn  constipation,  are  beneficial. 


THE    DIAGNOSTIC    AND    THERAPEUTIC    SIG- 
NIFICANCE   OF    SECRETORY    DISTURB- 
ANCES   OF    THE    STOMACH 

By  H.   STRAUSS,  Berlin 

The  significance  in  diagnosis  and  therapy  of  the  secretory  disturbances 
of  the  stomach  is  unquestionable,  and  is  important  from  a  scientific  as  well 
as  a  practical  standpoint.  This  will  be  admitted  even  by  those  who  hold 
the  certainly  justifiable  view  that  the  nosological  significance  of  disturb- 
ances of  secretion  was  greatly  over-estimated  in  the  first  few  years  of 
the  new  departure  in  functional  diagnosis  of  the  stomach.  But  there 
is  no  reason  for  under-estimating  it  to-day.  Though  we  must  acknowl- 
edge from  actual  observation  that  a  person  absolutely  without  secretion  in 
the  stomach  may  not  only  live  for  years  but  even  decades  without  showing 
noteworthy  disturbance  of  nutrition,  we  know,  nevertheless,  that  the  result 
of  marked  secretory  insufficiency  of  the  stomach — as,  for  instance,  diar- 
rhea— may  damage  nutrition  to  a  marked  extent,  and  that,  on  the  con- 
trary, excessive  secretion — continuous  secretion  of  the  gastric  juice — by 
causing  chronic  under-nutrition,  drjmess  of  the  tissues,  and  perhaps  also 
withdrawal  of  chlorin  may  induce  conditions  which  threaten  life.  It  is 
not  my  object  to  describe  in  detail  these  conditions  in  which  disorders  of 
secretion  play  a  role,  but  I  shall  consider  secretory  disturbances  only  in  so 
far  as  they  represent  subjects  for  diagnostic  and  therapeutic  consideration. 
If  this  manner  of  presenting  the  subject  is  a  priori  unfamiliar  to  the  reader 
accustomed  to  regard  definite  clinical  pictures  as  nosological  entities,  it  cer- 
tainly will  facilitate  the  description,  and  the  physician  who  understands 
also  other  disturbances  of  the  stomach,  their  importance,  and  the  methods 
for  their  recognition,  will  not  be  led  by  such  a  description  to  a  too  one-sided 
conception  of  the  subject,  or  allow  himself  as  a  therapeutist  to  drift  into 
errors  of  omission.  As  a  rule,  the  careful  physician  will  have  already 
grasped  the  knowledge  that,  as  a  basis  for  the  erection  of  pathologic  pictures 
in  gastric  pathology,  the  clinical  s}Tnptom-complexes  which  we  meet  to-day 
in  gastric  pathology  frequently  do  not  equal  the  pathologico-anatomical 
changes  mth  which  we  have  long  been  familiar.  Following  0.  Rosenbach, 
almost  all  investigators  in  this  realm  have  come  to  the  conclusion  that  for 
the  purpose  of  treatment  the  interests  of  our  patient  demand  not  only  a 
thorough  investigation  of  the  symptoms  of  anatomical  change  (position, 
form,  and  size  of  the  stomach,  production  of  mucus  and  pus,  superficial 

87 


88  SECRETORY   DISTURBANCES   OF  THE  STOMACll 

lesions),  but,  in  every  case  also  an  accurate  study  of  the  individual  disturb- 
ances in  function.  In  many  instances  our  method  of  treatment  will  only 
enable  us  to  reach  the  goal  by  a  test  of  function  (secretion,  motility,  etc.). 


GASTRIC   SECRETIONS 

Among  the  different  secretions  of  the  stomach  (hydrochloric  acid,  pep- 
sin, lab-ferment,  steapsin,  water)  the  secretion  of  hydrochloric  acid  occu- 
pies tlie  first  place  in  our  present  clinical  description,  as  the  disturbance 
of  other  secretions,  such  as  pepsin  and  lab-ferment,  the  secretion  of  steap- 
sin, and  of  the  diluting  secretions,  either  is  so  far  parallel  with  disturb- 
ances in  the  production  of  hydrochloric  acid  that  for  clinical  purposes  it 
requires  special  consideration  only  in  particular  cases,  or,  according  to 
the  existing  state  of  our  knowledge,  it  is  to  be  regarded  as  of  so  little 
practical  value  that,  for  our  present  purpose,  we  need  not  enter  upon  its 
detailed  description. 

A\'hen  we  refer  to  a  disturbance  of  secretion  as  an  object  for  diagnosis 
and  treatment,  the  first  question  that  arises  is  in  regard  to  the  normal  or 
pathologic  limits  of  the  secretion.  This  question  can  be  no  more  accurately 
answered  than  we  can  determine  by  a  simple,  fixed  formula  the  boundary 
between  health  and  disease;  for  the  relation  of  gastric  juice  secretion  in 
individual  persons  not  only  varies  within  wide  limits  but  also  in  one  and 
the  same  individual  at  different  times;  just  as  in  every  other  function, 
this  has  an  intimate  connection  with  the  nervous  system.  This  has  been 
shown  conclusiyely  by  the  clinical  study  of  cases  and  by  experimental 
physiology — I  refer  here,  above  all,  to  the  classical  investigations  of  Paw- 
low.  Moreover,  investigation  of  the  gastric  contents  in  the  individual  case 
may  reveal  an  extreme  increase  or  diminution  of  gastric  juice  secretion 
without  the  person  in  question  presenting  the  slightest  subjective  sign  of 
disease.  Regional  differences  in  the  realm  of  gastric  juice  secretion  may  also 
1)0  recognized,  as  I  demonstrated  some  years  ago  in  my  experiments  at  Gies- 
sen  and  Berlin.  If  the  production  of  hydrochloric  acid  be  taken  as  a  test 
object  for  gastric  juice  secretion,  in  a  stomach  acting  normally,  one  hour 
nfior  taking  a  test  breakfast,  that  is,  three  to  four  hours  after  the  ingestion 
of  a  test-meal,  we  may  expect  to  determine  free  hydrochloric  acid  in  the 
pistric  contents,  and  that  in  a  test  breakfast,  as  a  rule,  the  total  acidity  will 
lit'  not  liiglicr  than  about  60,  and  in  a  test-meal  not  higher  than  about  100. 
'I' lie  lowest  computation  of  total  acidity  in  a  trial  breakfast  under  normal 
circumstances  will  rarely  exceed  from  35  to  40,  and  in  a  test-meal  from 
()0  to   70.^     I  have  here  quoted  figures,  but,   in  spite  of  this,   I  must 

'  From  wliat  has  been  said  it  is  at  once  evident  that,  if  we  desire  to  form  an  opin- 
ion rcirardiiijf  tlie  secretory  activity  of  a  case,  a  single  examination  is  insufficient,  but 
ropoatod  examination  of  the  gastric  contents  is  necessary. 


GASTRIC  SECRETIONS  89 

premise  that  the  determmation  of  the  total  acidity  represents  only  the 
final  act  in  the  test  of  the  secretion  of  the  stomach.  We  do  not  begin  the 
examination  of  the  heart  with  auscultation,  neither  do  we  introduce  the 
test  of  the  secretion  with  titration,  but  we  necessarily  assign  the  first  place 
to  close  inspection  of  the  gastric  contents. 

As  I  do  not  desire  to  become  involved  to  any  great  extent  with  the 
question  as  to  which  tests  are  to  be  preferred  for  daily  practice,  I  shall  only 
state  here  that  many  roads  lead  to  Eome.  I,  myself,  am  of  the  opinion  that 
although  the  introduction  of  the  test-meal  has  deepened  our  insight  into 
the  mechanism  of  gastric  digestion,  and  that  in  many  respects  and  even 
to-day,  in  a  concrete  case,  it  is  sometimes  calculated  to  enlarge  our  knowl- 
edge, nevertheless,  in  the  majority  of  cases,  the  test  breakfast  suffices  for 
a  practical  test  of  function,  provided  it  is  carried  out  lege  artis,  and  its 
results  are  subjected  to  examination  from  all  points  of  view.  The  last 
requirement  must,  however,  be  particularly  emphasized  if  we  assign  to  the 
test  breakfast  the  position  just  indicated;  and  here  it  must  be  remembered 
that  in  some  cases  of  hyperacidity,  and  under  some  circumstances  after  ad- 
ministering the  test  breakfast,  a  comparative  test  with  a  test-meal  may  be  de- 
sirable, and  also  that  there  are  rare  cases  of  "perverted  secretion ''(Riegel). 

Inspection. — On  inspection  of  the  test  breakfast,  the  consistency  of  the 
sediment,  which  resembles  flour  soup,  or  puree  without  the  appearance  of 
coarser  particles  in  the  expressed  contents,  shows  normal  or  increased  gas- 
tric juice  secretion,  while  a  gross,  fragmentary  appearance  in  the  evacuated 
gastric  contents  leads  us  to  suspect  insufficiency  of  gastric  juice  secretion. 
The  "  amylorrhexis,"  so  designated  by  me  (in  contrast  to  amylolysis),  is 
only  a  function  of  proteolysis,  and,  as  such,  an  indication  which  may  be  well 
utilized  in  studying  the  secretion  of  tMfe  gastric  juice.  Any  one  accus- 
tomed systematically  to  regard  the  test  breakfast  from  the  point  of  view 
of  the  degree  of  "  amylorrhexia  "  may,  even  from  the  macroscopic  examina- 
tion of  the  evacuated  contents,  determine  the  presence  of  subacidity  and — 
although  with  less  certainty — also  assume  the  existence  of  hyperacidity. 
Under  certain  circumstances,  the  microscopic  examination  of  the  secretion 
may  give  us  valuable  aid.  Thus,  as  a  rule,  in  extreme  subacidity,  net-like 
formations  are  found  which  I  some  time  ago  described  as  "  structure  sub- 
stance," because  they  consist  of  the  adhesive  structure — giving  the  histo- 
chemical  reaction  of  albumin — in  which  granules  of  starch  are  embedded. 
Such  structures  are  found  particularly  in  "  apepsia  gastrica."  Further- 
more, in  those  cases  in  which  leukocytes  are  admixed  with  the  gastric  con- 
tents, a  high-graded  secretory  insufficiency  may  also  show  the  retention 
of  the  protoplasm  ring  of  the  leukocytes  which  is  absent  in  all  those  in- 
stances in  which  a  more  marked  production  of  acid  is  present — according 
to  my  experience,  even  the  presence  of  free  hydrochloric  acid  may  be  un- 
necessary. 

For  practical  purposes  the  methods  which  are  to  be  considered  in  the 


90  SECRETORY   DISTURBANCES   OF  THE   STOxMACH 

investigation  of  the  products  of  secretion  of  the  gastric  mucous  membrane 
have  been  detailed  to  a  great  extent  in  the  article  by  Professor  Leo,  "  Func- 
tional Diseases  of  the  Stomach  "  (page  66).  I  shall  not  consume  time  with 
their  description,  but  shall  allow  myself  only  a  few  critical  remarks  based 
upon  personal  experience.  At  the  close  of  this  article  I  shall  enumerate  a 
few  methods  not  given  in  the  previously  mentioned  treatise. 

Test  for  Hydrochloric  Acid. — For  the  test  of  free  hydrochloric  acid  I 
see  no  reason  to  reject  Congo  paper,  since  this  permits  in  the  simplest  man- 
ner the  sufficiently  positive  recognition  of  its  presence.  The  dimethyl- 
amidoazol)cnzol  paper  recently  advised  for  this  purpose  by  Einhorn  I  did 
not  find  superior  to  Congo  paper  when  I  conducted  investigations  about 
eight  years  ago  in  RiegeFs  Clinic.  Only  when  Congo  paper  gives  indefinite 
results,  should  the  Giinzburg  reagent  be  employed.  For  the  quantitative 
estimation  of  free  hydrochloric  acid  I  still  advise  dipping  with  Congo  paper 
according  to  the  processes  of  Riegel,  Morner  and  others — perhaps  also  the 
utilization  of  diniethylamidoazobenzol  as  an  indicator.  With  Linossier's 
reagent,  which  also  contains  phenolphthalein  and  dimethylamidoazobenzol, 
1  have  not  always  obtained  a  definite  result.  The  question  in  which  cases 
free  hydrochloric  acid  should  be  determined  quantitatively  can,  in  my  opin- 
ion, only  be  decided  in  practice  in  the  individual  case,  since  the  physician 
who  frequently  investigates  the  gastric  contents  learns  in  the  course  of 
time,  from  the  combination  of  values  for  total  acidity,  from  the  Congo 
reaction,  as  well  as  from  other  signs  in  the  gastric  contents,  what  practical 
conclusions  are  to  be  drawn  in  the  majority  of  cases.  From  my  own  expe- 
rience I  maintain  this  in  regard  to  the  determination  of  combined  hydro- 
cliloric  acid,  and  I  have  only  rarely  foUnd  a  strict  necessity  for  its  quanti- 
tative estimation — at  least  for  practical  purposes.  In  the  overwhelming 
majority  of  cases  in  which  there  is  a  deficiency  of  free  hydrochloric  acid 
and  the  absence  of  lactic  acid,  the  comparative  estimation  of  the  propor- 
tion of  total  acidity  and  the  degree  of  digestion  in  the  evacuated  contents 
onal)le  us  to  form  an  opinion  sufficiently  clear  for  practical  purposes  as  to 
the  amount  of  secretion  and  the  measure  of  the  peptic  labor  of  the  stomach, 
provided  wo  start  with  the  assumption  that  when  large  quantities  of  com- 
bined hydrochloric  acid  are  present  in  the  evacuated  contents,  a  good  degree 
of  digestion  may,  as  a  rule,  be  recognized,  while  this  is  absent  when  there 
are  only  slight  quantities  of  combined  hydrochloric  acid.  I  cannot,  however, 
strongly  recommend  the  complicated  methods  which  are  advised  for  deter- 
mining combined  hydrochloric  acid,  as  their  adoption  into  practice  is  beset 
with  great  difficulty,  and  the  exactness  of  their  results  is  often  not  com- 
mensurate with  the  complexity  of  their  use.  If  we  desire  to  know  the 
amount  of  secretion  while  excluding  the  phosphates,  we  may  titrate  with 
jilicnoljilithalein  and  tincture  of  cochineal  (see  later),  or  Leo's  process  may 
be  om])loyed,  or  a  trial  may  eventually  be  made  with  a  method  recently 
advised  by  Cohnheim  and  Kriiger.     In  my  experience,  however,  the  latter 


GASTRIC  SECRETIONS  91 

necessitates  the  utmost  care,  and  gives  only  approximate,  not  always  abso- 
lutely exact,  values  for  combined  hydrochloric  acid  if,  as  I  found  when 
working  with  Dr.  Cahn,  at  the  same  time,  investigations  are  made  of  the 
gastric  juice  for  free  hydrochloric  acid,  utilizing  Leo's  process.  The  pre- 
vious method,  advised  by  v.  Noorden  and  Honigmann,  for  "  hydrochloric ' 
acid  deficit,"  is  simple  but  does  not  always  give  similar  values  in  regard 
to  the  amount  of  combined  hydrochloric  acid  in  a  test-meal  at  the  height  of 
digestion,  as  I  determined  after  numerous  investigations  of  the  gastric  con- 
tents for  free  hydrochloric  acid  with  Leo's  process,  and  with  Congo  titra- 
tion; Ehrmann  determines  it  at  from  0.05-0.07  HCl — particularly  in  cases 
of  stagnation  with  good  secretion — and  also  higher  values  are  observed. 

Total  Acidity. — The  total  acidity  of  the  gastric  contents,  as  is  well 
known,  is  determined  by  the  aid  of  phenolphthalein  which  reacts  upon  all 
three  of  the  acid  components  of  the  normal  gastric  contents  (free  and  com- 
bined hydrochloric  acid  as  well  as  acid  phosphates).  For  the  determina- 
tion of  the  "  physiologically  active  "  hydrochloric  acid  alone  this  property 
of  phenolphthalein  is  unsatisfactory,  especially  in  the  cases  in  which,  by  a 
diminution  of  the  production  of  hydrochloric  acid,  the  amount  of  acid 
phosphate  in  proportion  to  the  total  quantity  of  the  "  physiologically 
active "  hydrochloric  acid  increases.  The  acid  phosphates,  as  I  am  in  a 
position  to  prove,  form  no  inconsiderable  part  of  the  total  acids.  In  14 
investigations  (according  to  Leo's  process)  I  found  that  the  total  quan- 
tity of  acid  phosphates  in  the  empty  stomach,  that  is,  in  the  secretion  free 
from  food,  amounted  in  value  to  7.5  (maximum  10,  minimum  5) ;  in  19 
test  breakfasts  with  free  hydrochloric  acid,  an  average  value  of  11  (maxi- 
mum 15,  minimum  8) ;  and  in  14  test-meals  with  free  hydrochloric  acid, 
an  average  value  of  22  (maximum  38,  minimum  9).  Therefore,  another 
indicator  would  be  desirable  which,  without  reacting  upon  the  phosphates 
in  the  absence  of  lactic  acid,  would  show  exactly  what  acid  factors  of  the 
gastric  contents  might  be  referred  to  hydrochloric  acid  production.  With 
this  in  view  I  have  attempted  the  comparative  titration  of  about  30  gastric 
contents  with  methylene  orange  and  tincture  of  cochineal,  and  in  the  inves- 
tigation of  7  cases  of  typical  "  apepsia  gastrica  "  with  phenolphthalein,  I 
found  upon  an  average  an  increase  of  about  16  in  the  value  of  the  total 
acidity  in  comparison  with  the  values  obtained  with  cochineal  tincture. 
In  15  cases  in  which  stagnation  was  present  the  differences  were  even 
greater;  they  amounted  to  between  18  and  21.  In  about  half  the  cases 
these  differences  were  compensated  for  by  the  values  which  I  obtained  with 
Leo's  process,  in  the  other  half  this  difference  was  increased  to  a  slight 
extent,  and  therefore  we  may  say  that  among  the  conditions  found  in  the 
stomach  the  cochineal  tincture  does  not  reveal  acid  phosphates.  In  my 
opinion,  the  influence  of  acid  phosphates  also  deserves  mention  because  of 
the  values  for  total  acidity  which  we  obtain  after  administering  a  test 
breakfast  and  test-meal  at  tlie  hoig-ht  of  digestion,  and  because,  as  I  was 


92  SECRETORY   DISTURBANCES   OF  THE   STOMACH 

able  to  demonstrate  by  special  investigations,  the  acid  phosphates  of  meat 
present  in  the  evacuated  contents  at  a  test-meal  may  have  caused  an  in- 
crease in  the  total  acidity.  I  have  permitted  myself  these  brief  remarks  in 
order  to  show  that  some  of  the  findings  in  gastric  pathology  which  we  have 
been  accustomed  to  look  upon  as  conclusive,  in  some  points  still  admit  of 
critical  investigation. 

Pepsin. — In  definite  cases  of  extreme  subacidity,  the  quantitative  esti- 
mation of  pepsin  may,  under  some  circumstances,  serve  a  practical  purpose 
in  diagnosis  notwithstanding  the  fact,  according  to  my  own  experience, 
that  a  strict  parallelism  between  the  production  of  pepsin  and  hydrochloric 
acid  does  not  exist.  Nevertheless — as  I  have  seen  in  numerous  investiga- 
tions— with  complete  absence  of  hydrochloric  acid  secretion,  appreciable 
(luantities  of  pepsin  are  so  rare — their  entire  absence  is  exceedingly  rare — 
(hat  in  practice  we  will  hardly  fall  into  error  if,  in  cases  of  high-graded 
subacidity  in  which  the  pepsin  value  of  the  gastric  contents  is  but  slightly 
above  zero,  we  assume  an  "  apepsia  gastrica."  From  my  own  knowledge 
of  the  various  methods  employed  to  determine  pepsin  I  advise  only  Mett's 
method,  which  for  simplicity  and  exactness  is  preferable  to  all  others,  and 
whicli  I  myself  used  for  more  than  three  years.  Even  Hlimmerschlag's 
method,  a  modification  of  which  I  employed  to  increase  the  amount  of 
iilhumin  of  the  solution — using  a  Puro-solution  in  order  to  prepare  a  test- 
fluid — and  the  employment  of  specially  chosen  Esbach  tubes  which  exactly 
('((ual  one  another,  I  have  found  neither  more  simple  nor  more  exact.  As 
the  preparation  of  Mett's  tubes  as  practised  by  me  differs  somewhat  from 
the  method  given  in  the  last  publication  on  this  subject,  it  is  detailed  some- 
w  liat  more  minutely  in  the  footnote.^ 

Lab-Ferment. — Quantitative  estimations  of  lab-ferment  are  very  rarely 
necessary  in  practice,  after  making  an  examination  for  pepsin.  Never- 
theless, they  serve  a  certain  purpose  (see  later)  and  thus  acquire  some  im- 
portance. Lab- ferment  is  either  estimated  according  to  the  well  known 
methods  or,  in  the  absence  of  an  incubation  oven — at  least  one  suitable  for 


'  A  part  of  the  white  of  an  egg  is  filtered  through  a  piece  of  gauze  into  a  small 
heaker  glass  or  into  a  short,  wide-mouthed  test-tube,  after  which  glass  tubes  about 
2VL,  ccm.  in  length  and  about  2  mm.  in  breadth  are  slowly  dipped  into  the  filtered 
albumin.  Air  bubbles  which  rise  in  the  glass  tubes  are  permitted  to  disappear;  this 
may  be  facilitated  by  slight  tapping  with  the  point  of  the  finger  upon  the  glass, 
which  causes  the  air  bubbles  to  rise.  Then  the  beaker  or  test-tube  with  the  tubes 
containing  the  albumin  solution  are  placed  in  a  perpendicular  position  in  a  large 
vessel  of  boiling  water,  and  allowed  to  boil  from  five  to  ten  minutes  to  coagulate  the 
albumin.  Tlie  flame  is  then  removed  and  the  glasses  are  permitted  to  cool  slowly 
ffir  a  few  hours.  Now  the  test-tube  is  broken,  or  the  coagulated  albumin  is  cut  out 
of  tlip  beaker  glass,  the  tubes  are  freed  from  the  albumin  which  adheres  externally, 
and  are  preserved  either  in  glycerin  or  in  chloroform  water.  Prior  to  use  the  tubes 
are  wasliod  with  water.  After  use  the  remainder  of  the  albumin  is  removed,  and  the 
lubes  may  be  filled  as  before  with  albumin. 


GASTRIC  SECRETIONS  93 

the  purpose — in  the  following  manner:  The  patient  is  permitted  to  drink 
half  a  liter  of  milk,  this  is  removed  from  the  stomach  one-half  to  three- 
quarters  of  an  hour  later,  when  the  evacuated  contents  will  show  whether 
or  not  the  milk  is  coagulated. 

Steapsin. — The  test  for  steapsin  is  up  to  the  present  of  no  practico- 
diagnostic  importance;  I  can,  however,  absolutely  confirm  Volhard's  re- 
sults from  my  own  researches.  The  test  of  the  diluting  secretion  proposed 
by  Both  and  myself  is  as  yet  of  no  value  in  practice.  The  method  I 
proposed  for  employing  Gerber's  acidbutyrometric  test  in  the  quantitative 
investigation  of  the  diluting  secretions  and  of  resorption  is  only  suitable 
for  extreme  grades  of  subacidity  of  the  gastric  contents.  In  regard  to  the 
method  recently  proposed  by  Sahli  for  testing  the  function  of  the  stomach, 
V.  Koziczkowski,  under  my  direction,  has  shown  sources  of  error,  a  fact 
which  has,  in  the  meantime,  been  confirmed  by  Lang  and  by  Boeniger. 

Other  constituents  of  the  gastric  contents  dependent  upon  the  condi- 
tion of  the  secretion  have  more  of  theoretic  than  practical  interest,  and, 
although  not  accurately  developed  in  each  individual  case,  are  nevertheless 
worthy  of  brief  mention.  I  have  shown  by  means  of  systematic  investi- 
gations that  in  high-graded  subacidity  the  filtrate  on  the  addition  of  a 
solution  of  iodin  usually  shows  no  change  in  color,  or  at  most  turns  slightly 
to  a  yellowish-brown  color,  while  in  hypersecretion  or  h)rperacidity  the  mass 
not  rarely  turns  to  a  bluish-violet  or  blue  color.  Normal  conditions  are 
indicated  by  a  Burgundy-red  color  which,  in  extreme  cases,  may  have  more 
of  a  violet,  at  times  more  of  a  brownish-red,  tint.  These  peculiarities  of 
the  gastric  contents  have  lately  been  confirmed  by  Bakman.  The  specific 
gravity,  as  I  have  shown  in  cases  of  subacidity,  is  usually  increased — 
although  not  invariably — while  in  cases  of  hyperacidity  and  hypersecretion 
it  as  a  rule — but  by  no  means  constantly — shows  a  decrease.  According 
to  my  experience — and  even  with  some  reserve  which  is  especially  empha- 
sized because  exceptions  occur — this  is  also  true  of  the  presence  in  the 
gastric  contents  of  a  dextro-rotary  substance  which  may  be  determined 
with  Pulfrich's  refractometer  called  "refraction  difference."  I  shall  not 
enter  here  upon  a  discussion  of  the  osmotic  concentration  of  the  gastric 
contents,  although  it  has  certain  relations  to  secretion.  In  the  meantime, 
I  have  also  made  numerous  tests  of  the  electric  conduction  of  the  gastric 
contents,  and  will  only  remark  that  these,  as  was  to  be  expected,  denoted 
a  close  relation  to  the  amount  of  chlorin  therein. 

Passing  from  these  preliminary  remarks  to  the  clinical  consideration 
of  disturbances  of  gastric  secretion,  we  deal  either  with  a  decrease,  that 
is,  a  loss,  or  an  increase  of  secretion.  In  referring  to  hydrochloric  acid 
secretion  we  speak  of  subacidity.  that  is  anacidity  (hypochlorhydria  or 
aehlorhydria).  of  hyperchlorhydria  (hyperacidity^),  and  of  hypersecretion 

'  From  usage  this  term  is  applied  especially  to  hyperaciditaa  anorganica. 


94  SECRETORY   DISTURBANCES   OF  THE  STOMACH 

(gastiosiKconliea).  Expressions  such  as  hypochylia  and  hyperchylia,  which 
are  formed  from  achylia,  as  little  convey  the  true  meaning  as  does  the  word 
achylia,  since  chyle  is  entirely  different  from  the  gastric  juice.  The  term 
lioterochylia  is  quite  misleading  as  it  does  not  describe  a  substantive  patho- 
logic i)icture.  On  the  other  hand,  it  would  be  well  to  retain  expressions 
like  hypo])epsia,  apepsia  and  hyperpepsia  for  the  reason  that  they  clearly 
express  the  effect  of  gastric  digestion  without  revealing  more  in  regard  to 
tlio  nature  of  the  secretory  disturbance  than  terms  which  denote  the  state 
of  liydroehloric  acid  secretion.  This  is  self-evident  when  we  reflect  that 
tlie  amount  of  hydrochloric  acid  contained  in  the  gastric  juice  is  the  impor- 
tant and  decisive  factor  for  gastric  digestion,  because  even  a  gastric  juice 
rich  in  pepsin  is  incapable  of  producing  a  corresponding  digestive  activit}' 
without  a  large  amount  of  hydrochloric  acid.  These  designations  are  also 
suitable  for  the  reason — as  I  have  already  remarked — that  special  disturb- 
ances of  pepsin,  lab-ferment,  steapsin  and  the  diluting  secretion  have  as 
yet  not  been  so  fully  recognized  as  to  evoke  any  special  therapeutic  interest. 

SUBACIDITY  (APEPSIA   GASTRICA) 

In  occupying  ourselves  first  with  cases  of  hypochlorhydria  and  achlor- 
hydria,  tliat  is,  hypopepsia  and  apepsia,  we  observe  that  they  portray  no 
comprehensive  clinical  picture,  but,  instead,  a  series  of  peculiarities  com- 
mon to  the  gastric  contents.  Among  these  the  absence  of  free  hydrochloric 
acid  is  tlie  most  important.^  Other  peculiarities,  such  as  the  coarse,  frag- 
mentary character  of  the  evacuated  gastric  contents  which,  in  cases  of 
aj)e})sia,  reveals  only  traces  of  oral  cavity  digestion — not  gastric  digestion — 
showing  low  values  for  total  acidity,  usually  a  high  specific  gravity,  high 
values  for  the  dextro-rotary  substance,  the  absence  of  staining  products 
of  amvlolysis  as  well  as  the  appearance  of  shreds  of  structure  substance 
upon  microscopic  examination  of  the  gastric  contents,  are  as  consequences 
of  the  decreased  secretion  merdy  of  symptomatic  importance,  but  may 
occasionally  be  of  value  in  a  clinico-diagnostic  sense.  Of  pepsin  and  lab- 
ferment  production  we  may  say  in  general  that  they  are  more  permanent 
llian  hydrochloric  acid  secretion,  but,  like  the  steapsin  production  in  com- 
plete insufficiency  of  secretion,  these  may  also  be  decidedly  decreased  or 


'  Xaturallj'  tliere  are  also  cases  with  abnormally  low  total  acidity  in  which  free 
hydiooliloiie  acid  is  still  present,  and  also  cases  (rare)  with  normal  total  acidity 
iuul  absence  of  free  hydrochlpric  acid  without  lactic  acid.  As  in  the  latter  cases — 
tbey  are  usually  associated  with  disturbances  of  motility  in  patients  whose  secre- 
tion is  dooreased  to  only  a  slight  degree — the  secretory  energy  of  the  stomach  is 
iiisullKient  for  the  production  of  the  physiologic  plufi  of  free  hydrochloric  acid, 
those  cases  are  looked  upon  a.s  instances  of  "relative"  subacidity.  because  every 
normal  stomach  at  the  height  of  digestion  must  show  a  physiologic  plus  of  free 
livdrochloric  aciJ. 


SUBACIDITY   (APEPSIA  GASTRICA)  95 

entirely  absent.  According  to  Glaessner,  only  in  carcinoma  of  the  pylorus 
with  complete  or  almost  complete  absence  of  pepsin  may  the  distinct  pres- 
ence of  lab-ferment  be  observed.  That  we  miss  a  constantly  recurring 
parallelism  between  acid  values  and  pepsin  is,  in  my  opinion,  explained 
from  the  fact  that,  besides  other  causes — according  to  the  experimental 
investigations  of  Pawlow,  Schiff,  Herzen  and  others,  there  are  various 
stimuli  which  promote  in  a  one-sided  way  hydrochloric  acid  or  pepsin 
production — in  examining  the  total  acidity  we  have  considered  too  little 
the  influence  of  phosphates,  whose  amount  depends  only  partially  upon 
the  energy  of  secretion  of  the  affected  stomach.  To  this  may  be  added 
that  in  former  researches  with  the  Hammerschlag  process,  the  inac- 
curacy of  the  method  has  not  been  sufl&ciently  taken  into  account  in 
judging  the  results.  In  apepsia  gastrica,  at  a  time  in  which  individ- 
ual authors  found  different  values  for  pepsin,  I  employed  the  Hammer- 
schlag process  with  my  own  modifications,  and  in  4  instances  I  twice 
found  the  peptonizing  ferment  positively  absent,  and  twice  a  property  of 
peptonization  of  from  10  to  12  per  cent.,  while  on  using  the  Mett  process 
in  8  cases  of  apepsia  gastrica,  I  found  the  property  of  peptonization  only 
twice  and  then  respectively  2  and  4  mm.  In  regard  to  the  "  diluting  secre- 
tion," I  proved  in  earlier  investigations  of  the  specific  weight,  and  in  more 
prolonged  studies  of  the  osmotic  pressure  of  the  gastric  contents,  as  well 
•as  in  quantitative  estimations  of  the  excretion  of  water  by  the  gastric 
walls,  that  even  in  extreme  secretory  insufficiency,  and  especially  in  apepsia 
gastrica,  it  was  still  present,  although  apparently  in  diminished  amounts. 

In  regard  to  the  degree  of  total  acidity  in  apepsia  gastrica,  I  must 
reiterate  what  I  have  previously  stated  of  the  importance  of  phosphates  in 
an  estimation  of  the  total  acidity  of  the  gastric  contents.  Although,  as 
a  rule,  the  majority  of  my  cases  of  apepsia  gastrica  showed  values  for  total 
acidity  between  3  and  7 — in  a  few  cases  I  found  the  gastric  juice  neutral 
with  phenolphthalein — I  have,  nevertheless,  repeatedly  observed  cases  with 
an  acidity  of  10  and  12,  which  possessed  no  property  of  peptonization,  and 
at  most  showed  only  traces  of  combined  hydrochloric  acid  (Leo's  process). 
I  have,  therefore,  made  it  a  rule  in  suspicious  cases  of  apepsia  always 
to  titrate  with  litmus  and  with  tincture  of  cochineal. 

As  apepsia  gastrica  represents  the  highest  grade  of  subacidity,  so  this 
affection  distinctly  demonstrates  the  clinical  expressions  of  subacidity,  its 
effects  upon  gastric  and  intestinal  digestion,  and  upon  metabolism;  hence, 
in  this  description,  I  shall  enumerate  the  causative  factors  and  also  the 
therapeutic  indications  which  arise  when  a  secretory  insufficiency  of  the 
stomach  is  determined. 

SYMPTOMS 

The  clinical  signs  which  we  observe  in  the  higher  grades  of  subacidity 
vary  greatly.     Often  symptoms  are  entirely  absent.     At  other  times  we 
8 


96  SECRETORY   DISTURBANCES  OF  THE  STOMACH 

meet  with  indefinite  complaints  of  sensations  of  pressure  or  fulness,  or 
of  eructation,  partly  of  loss  of  appetite,  partly  of  intestinal  disturbance — 
particularly  of  diarrhea — or  of  more  or  less  painful  sensations  in  the 
abdomen.  The  great  variety  of  clinical  pictures  in  which  we  find  sub- 
acidity  as  a  symptom  is  not  surprising  when  we  consider  that  subacidity 
in  a  mild  or  severe  degree  accompanies  or  follows  in  the  train  of  many 
maladies.  Thus  we  find  it  not  only  in  numerous  local  gastric  affections 
among  which  carcinoma  and  alcoholic  gastritis  are  probably  the  most  fre- 
quent, but  also  not  rarely  in  nervous  and  organic  general  affections,  par- 
ticularly in  cardiac  and  renal  disease,  in  pulmonary  tuberculosis,  and  in 
the  various  disturbances  of  metabolism.  For  example,  in  the  clinical  his- 
tory of  30  cases  of  persistent  and  "  uncomplicated  "  apepsia  gastrica  which 
I  observed  for  a  long  time,  and  of  which  I  possess  accurate  notes,  there 
were  8  cases  of  chronic  alcoholism,  4  of  pernicious  anemia,  5  of  advanced 
pulmonary  tuberculosis,  3  of  chronic  nephritis,  1  of  Graves'  disease,  2  of 
well-developed  chronic  hysteria,  1  of  trauma,  2  of  severe  erosion  of  the 
gastric  mucous  membrane  (in  both  cases  there  were  simultaneously  symp- 
toms of  stenosis  of  the  esophagus  leading  to  a  "  stenosed  "  form  of  gastritis) . 
In  5  cases  no  especial  etiology  could  be  discovered.  I  have  also  observed 
transitory  forms  of  apepsia  gastrica  in  neurasthenics,  above  all,  in  a  series 
of  cases  of  delirium  tremens.  When  I  refer  to  an  "  uncomplicated  "  form 
of  apepsia  gastrica,  in  contrast  to  a  "  complicated  "  form,  I  have  particu-  * 
larly  in  mind  that  prognostically  ominous  form  which  is  an  accompaniment 
of  malignant  neoplasm. 

DIAGNOSIS 

As  it  is  especially  important  in  the  absence  of  a  recognizable  tumor 
and  metastasis  (if  necessary,  palpation  per  rectum  and  X-ray  examination 
of  the  mediastinum)^  to  base  the  differential  diagnosis  on  the  condition  of 
the  gastric  contents,  I  shall  briefly  include  in  this  description  the  different 
diagnostic  criteria,  above  all,  the  significance  of  an  admixture  of  blood 
with  the  stomach  contents,  and  the  possibility  of  evacuating  blood  by  lavage 
when  the  stomach  is  empty.  In  more  than  6  cases  which,  by  prolonged 
observation,  were  positively  recognized  as  non-carcinomatous  apepsia  gas- 
tnca,  I  found  blood  in  the  stomach  empty  of  food,  and  in  some  cases  I 
detected  shreds  of  tissue;  therefore,  I  maintain  that  only  the  combination 
of  blood  and  pus  indicates  carcinoma.  As  to  the  diagnostic  inferences  from 
the  presence  of  shreds  of  tissue,  I  agree  with  Kuttner.  In  several  cases 
in  which  I  repeatedly  found  shreds  of  tissue  upon  lavage  of  the  empty 
stomach,  the  patients  complained  of  a  gnawing  sensation,  sometimes  of 
pain,  and,  upon  taking  food,  of  even  more  severe  s3miptoms.     I  have  con- 

'  (rlaTidular  tumors  of  the  mediaBtinum  have  been  actinographically  detenninea 
by  Weinberger  (see  his  Atlas)  and  others. 


SUBACIDITY   (APEPSIA  GASTRICA)  97 

sidered  hemorrhagic  erosions  which,  in  common  with  Ewald  and  Boas, 
and  in  opposition  to  Einhorn,  Parish,  and  others,  I  found  in.  various  gastric 
conditions,  but  I  am  not  inclined  to  believe  in  the  uniformity  of  a  special 
clinical  condition  in  hemorrhagic  erosions.  An  increased  vulnerability  of 
the  gastric  mucous  membrane  I  have  quite  often  observed  in  cases  of 
apepsia  gastrica  as  a  consequence  of  chronic  nephritis,  or  as  an  accom- 
paniment of  chronic  alcoholic  intoxication.  As  apepsia  gastrica  may  also 
be  observed  as  a  secondary  accompaniment  of  true  pernicious  anemia,  the 
differentiation  of  the  forms  of  apepsia  gastrica  occurring  in  connection 
with  carcinoma  may,  under  some  circumstances,  be  of  practical  significance. 
Here  it  must  be  borne  in  mind  that  pernicious  anemia  going  hand  in  hand 
with  apepsia  gastrica,  in  contrast  with  carcinoma  ventriculi,  will,  in  spite 
of  the  severe  anemia,  usually  present  a  well  maintained  panniculus  adiposus, 
and  that  a  thorough  examination  of  the  blood  will  generally  reveal  decided 
differences  between  these  affections.  For  those  cases  of  pernicious  anemia 
in  which  there  is  no  profusion  of  megaloblasts  in  the  blood,  I  especially 
advise  the  minute  observation  of  the  leukocytes ;  for,  in  my  numerous  stud- 
ies of  pernicious  anemia,  I  have  found  that  with  a  diminution  in  the  total 
number  of  leukocytes,  which  is  quite  usual,  there  is  a  relative  increase  of 
the  mononuclear  cells,  while  in  the  majority  of  cases  of  carcinoma,  leuko- 
penia is  more  rare,  and  the  multinuclear  cells  are  perceptible  in  normal 
or  even  increased  amounts.  Anemia  without  severe  cachexia — it  is  true 
this  is  scarcely  ever  observed  with  the  typical  blood  picture  of  pernicious 
anemia — may  also  occur  in  carcinoma  of  the  lesser  curvature  which  leaves 
both  ostia  of  the  stomach  intact.  In  cases  of  this  kind  the  nutrition  of 
the  patient  is  often  but  little  disturbed,  although  hemorrhage  from  the 
ulcerating  tumor  may  produce  the  picture  of  anemia  (often  to  only  a  slight 
extent  the  picture  of  cachexia).  In  my  experience  cases  of  this  kind  are 
by  no  means  so  rare  as  we  might  suppose  from  the  reports  of  various 
authors;  for,  among  the  cases  of  carcinoma  which  for  several  months  I 
had  opportunities  of  examining  in  the  Clinic, — in  the  majority  of  cases, 
up  to  the  time  of  death  or  of  the  operation, — more  than  one-third  ran  their 
course  without  symptoms  of  stenosis,  and  especially  without  the  finding 
of  lactic  acid. 

Practical  interest — particularly  therapeutic — is  also  elicited  by  those 
chronic  intermittent  diarrheas  which,  in  my  experience,  are  noted  in  about 
one-third  of  all  cases  of  apepsia  gastrica.  We  have  long  been  familiar 
with  these  diarrheas,  as  well  as  with  their  relation  to  severe  forms  of  sub- 
acidity,  the  condition  having  been  lately  described  by  Einhorn,  Oppler,  and 
others.  In  some  instances  they  represent  the  most  striking  and  unpleas- 
ant expression  of  the  secretory  disturbance,  and  they  chiefly  require  ob- 
servation for  the  reason  that  they  may  decidedly  damage  the  nutrition. 
In  my  opinion,  the  tendency  to  diarrhea  depends  to  a  great  extent  upon 
the  fact  that  the  coarse  ingesta,  on  which  the  stomach  exerts  no  digestive 


98  SECRETORY  DISTURBANCES  OF  THE  STOMACH 

effect  whatever,  mechanically  irritate  the  intestine,  and  also  upon  the  fact 
that  a  larger  number  of  bacteria  with  noxious  influence  upon  the  intestine 
have  reached  this  organ  than  is  the  case  with  a  normal  secretion  in  which 
the  virulence  of  one  or  the  other  of  these  bacteria  has  been  attenuated. 
Moreover,  the  diarrhea  may  cause  an  injury  to  the  general  nutrition,  since 
a  disturbance  of  motility  is  associated  with  apepsia  gastrica,  and  makes 
the  ingestion  of  food  insufficient  because  of  vomiting,  etc.  The  effect  of 
a  disturbance  of  motility  combined  with  apepsia  gastrica,  that  is,  with  a 
high  degree  of  subacidity,  becomes  apparent  when  we  examine  the  gastric 
contents  from  the  fact  that  lactic  acid  may  appear  in  such  great  amounts 
as  to  be  easily  recognized  by  the  method  I  have  indicated,  with  which,  as 
is  well  known,  we  can  only  determine  pathological  amounts  of  lactic  acid 
in  the  test  breakfast  or  in  the  residue  of  the  stomach  before  food  is  taken. 
That  the  absence  of  pepsin,  as  was  first  maintained  by  Hammerschlag,  is 
necessary  for  the  development  of  lactic  acid,  besides  the  combination  of 
subacidity  and  motor  insufficiency,  I  regard  as  not  only  unproven  at  the 
present  time,  but  as  most  unlikely ;  for,  under  my  direction,  v.  Aldor  showed 
that  in  the  artificial  conditions  of  experiment,  and  under  circumstances 
otlierwise  favorable  for  the  production  of  lactic  acid,  pepsin  by  no  means 
inliibits  the  appearance  of  lactic  acid  fermentation.  Only  lately  I  have  had 
an  opportunity  of  observing  three  cases  of  apepsia  gastrica  with  temporary 
but  undoubted  lactic  acid.  Two  of  these  cases  occurred  in  perigastritis 
following  cholelithiasis,  and  were  confirmed  by  operation.  The  third  case 
occurred  in  an  elderly  colleague  who,  since  he  was  first  examined  two 
years  ago,  has  continued  in  the  best  of  health.  I  formerly  made  similar 
observations  in  a  case  of  complete  erosion  of  the  stomach  with  the  forma- 
tion of  numerous  cicatrices  and  "  stenosing  pyloric  hypertrophy,"  in  a 
case  of  duodenal  stenosis  in  consequence  of  tubercular  peritonitis,  as  well 
as  in  a  case  of  fat  necrosis  of  the  pancreas.  Notwithstanding  this,  I  am 
quite  ready  to  admit  that  the  finding  of  lactic  acid  in  non-malignant  con- 
ditions is  so  rare  that,  if  continuously  found  for  weeks,  I  consider  an  ex- 
ploratory laparotomy  to  be  not  only  justified  but  sometimes  even  absolutely 
necessary,  provided  we  cannot  certainly  exclude  carcinoma.  In  fact,  my 
own  observations  of  the  frequent  occurrence  of  lactic*  acid  in  carcinoma 
differ  from  the  ordinary  in  that  I  succeeded  in  demonstrating  its  presence 
in  only  about  60  per  cent,  of  my  cases  of  gastric  carcinoma,  and  I  must 
particularly  emphasize  that  among  these  cases  were  a  large  number  in  which 
an  autopsy  was  conducted. 

In  regard  to  the  cases  in  which  an  absolute  cessation  of  hydrochloric 
acid  secretion  did  not  occur,  the  presence  of  combined  hydrochloric  acid, 
even  williout  a  quantitative  estimation  as  I  have  previously  remarked,  may 
be  assumed  in  all  cases  in  which  the  total  acidity,  without  lactic  acid  being 
present,  reaches  a  certain  amount;  i.e.,  with  the  employment  of  phenol- 
phthalein  it  exceeds  20,  and,  at  the  same  time,  the  gastric  contents  reveal 


\ 


SUBACIDITY   (APEPSIA   GASTRICA)  99 

positive  signs  that  gastric  digestion  is  present.  If,  after  a  test  breakfast, 
the  gastric  contents  without  free  hydrochloric  acid  show  an  acidity  which 
exceeds  30,  and  if  the  examination  for  lactic  acid,  which  should  never  be 
omitted  in  any  case  of  subacidity,  gives  a  negative  result,  we  are  probably 
right  in  assuming  the  presence  of  combined  hydrochloric  acid.  As  I  have 
repeatedly  observed  in  cases  of  stagnation  combined  with  slight  subacidity, 
in  rare  cases  without  the  presence  of  lactic  acid,  higher  values  of  total 
acidity — values  from  50  to  60 — may  be  found.  I  noted  this  particularly 
in  cases  in  which  ulcer  of  the  pylorus  gradually  underwent  carcinomatous 
degeneration,  but  also  in  non-carcinomatous  cases  of  pyloric  stenosis  with 
a  secretion  which  was  not  quite  sufficient.  In  these  cases,  the  gastric  con- 
tents did  not  show  the  symptomatologic  and  simultaneous  increase  of  the 
long  bacilli  which  indicates  lactic  acid.  Cases  of  this  kind  have  not  only 
confirmed  my  view  that  combined  hydrochloric  acid  may  inhibit  lactic  acid 
fermentation,  but  by  their  excellent  chymification,  as  well  as  by  their 
amount  of  erythrodextrin,  they  have  proven  that  where  large  amounts  of 
combined  hydrochloric  acid  are  present,  notwithstanding  the  absence  of 
free  hydrochloric  acid,  we  have  the  objective  signs  of  proteolysis  and  of 
disturbed  amylolysis.  In  regard  to  chymification,  I  must  here  remark  that 
occasionally,  even  when  large  amounts  of  lactic  acid  were  present,  I  suc- 
ceeded in  recognizing  a  slight  degree  of  chymification  in  the  gastric  contents. 

TREATMENT   OF   SUBACIDITY 

Since  it  is  my  intention  in  describing  the  treatment  of  subacidity  to 
consider  the  diminution  of  the  secretory  energy  of  the  stomach  only  as  a 
symptom  of  definite  affections,  I  shall  not  fully  discuss  the  treatment  of 
these  maladies,  but  shall  limit  myself  in  the  main  to  the  therapeutic  indi- 
cations necessary  to  combat  this  condition. 

Diet. — Beginning  with  the  dietetic  treatment,  we  find,  fortunately,  en- 
tire unanimity  between  theory  and  practice.  This  is  first  shown  by  the 
requirement  that  the  food  be  finely  divided,  and  of  such  a  character  that 
it  will  pass  the  pylorus  as  under  normal  circumstances.  The  importance 
of  this  therapeutic  principle,  so  long  established  in  practice,  we  can  appre- 
ciate after  we  understand  that  the  reduction  of  bread  and  pastry  to  a  fine, 
pappy  mass  is  not  only  the  function  of  mastication  in  the  oral  cavity,  but 
also  that  of  proteolysis  in  the  stomach.  As  I  have  demonstrated  by  micro- 
scopic investigations,  a  small  portion  of  bread  (consisting  of  gluten  albu- 
min) may  be  compared  to  tissue  or  a  sponge  in  whose  meshes  the  starch 
granules  are  deposited.  To  secure  this  reduction  of  food  with  defective 
proteolysis,  good  teeth  are  absolutely  necessary,  therefore  in  many  cases 
of  extreme  subacidity  the  examination  of  the  teeth  by  a  dentist  and  the 
correction  of  defects  form  the  first  part  of  the  treatment.  The  thorough 
cleansing  of  the  oral  cavity  is  also  necessary,  for  the  reason  that  the  stomach 
of  the  patient  in  question  can  offer  but  slight  resistance  to  the  bacteria 


100  SECRETORY   DISTURBANCES   OF  THE  STOMACH 

descending  from  the  mouth.  In  patients  suffering  from  subacidity  thor- 
ough mastication  is  also  necessary  for  another  reason.  Kecent  investiga- 
tions (Pawlow,  Schiile,  Troller,  Kiegel  and  Schreuer,  as  well  as  the  ex- 
periments conducted  by  Martin  Cohn  under  my  direction)  have  shown  that, 
in  cases  in  which  the  property  of  secretion  has  not  been  entirely  lost  but 
is  capable  of  increase  upon  decided  stimulation,  thorough  chewing  will, 
in  fact,  increase  the  production  of  acid.  Therefore,  slow  eating  and  thor- 
ough mastication  are  to  be  especially  insisted  upon  with  those  patients  who 
suffer  from  subacidity.  As  a  rule,  crisp  bread  and  pastry  which  are  well 
ground  up  by  the  te^th,  such  as  crackers,  zwieback,  toast,  etc.,  are  the  best. 
The  more  tender  varieties  of  meat  are  given,  such  as  poultry,  veal,  etc.,  in 
place  of  that  containing  coarse  fibers  held  together  by  a  tough  connective 
tissue  network  (beef,  lamb),  and  we  should  see  that  the  food  is  so  prepared 
in  the  kitchen  as  to  facilitate  its  mastication.  According  to  the  investiga- 
tions of  A.  Schmidt,  in  which  I  entirely  concur,  too  thorough  cooking  of 
meat,  that  is,  broiling  which  hardens  the  connective  tissue  which  is  not 
subsequently  dissolved  in  the  intestine  in  apepsia  gastrica,  may  irritate  the 
intestinal  wall  and  thus  produce  diarrhea.  Raw  meat  should  not  be  given 
to  the  patient  suffering  from  subacidity.  Gelatinous  foods  (gelatin)  are 
very  useful  since  gelatin  dissolves  into  fluid  in  the  stomach.  In  those  cases 
in  which  it  is  impossible  to  administer  sufficient  nourishment  in  the  manner 
described,  as  well  as  by  the  contingent  use  of  artificial  foods,  the  employ- 
ment of  means  for  disintegrating  food,  for  example,  Collin's  apparatus,  or 
masticators,  or  small  meat  choppers,  are  advisable,  and  it  is  well  for  the 
patient  to  use  the  apparatus  himself  since  food  brought  upon  the  table  in 
a  broken-up  condition  is  less  stimulating  to  the  appetite  than  that  served 
in  its  original  form  and  then  finely  divided  by  the  patient  himself.  This 
point,  in  my  opinion,  is  all  the  more  worthy  of  consideration  because  the 
preparation  of  food  and  its  appetizing  appearance  are  important  matters 
to  a  patient  suffering  from  subacidity.  Pawlow  has  shown  that  the  appear- 
ance of  food  has  a  stimulating  or  depressing  effect  upon  the  appetite  which 
materially  influences  the  intensity  of  the  secretion  of  gastric  juice.  We 
may  truly  say  that  the  sight  of  appetizing  food  not  only  makes  the  mouth 
water,  but  also  causes  the  gastric  juice  to  flow,  and  to  the  joy  of  every 
j^ourmand,  we  maintain  that  food  eaten  with  zest  is  half  digested.  For  this 
reason,  in  all  cases  of  subacidity  in  which  the  glandular  parenchyma  still 
reacts  to  stimulation  by  a  secretion  of  gastric  juice,  great  weight  must  be 
attached  to  the  attractive  and  appetizing  preparation  of  the  food,  which  is 
obvious  from  the  fact  that  many  of  these  patients  already  suffer  from  loss 
of  ap])etite.  Therefore  spices,  meat  sauces,  and  the  other  condiments  of 
tlie  kitchen — within  certain  limits — are  just  as  necessary  here  as  the 
stomachics  of  the  apothecary.  In  regard  to  the  latter,  I  must  mention  in 
passing  that  they  act  upon  the  nerves  of  smell  and  taste  and  thus  produce 
a  feeling  of  desire  which  reflexly  influences  gastric  secretion.     It  is  evi- 


SUBACIDITY   (APEPSIA   GASTRICA)  101 

dent  from  the  foregoing  that  not  only  bouillon  but  even  the  so-called  appe- 
tizers should  be  advised  as  overtures  to  a  meal  in  all  cases  of  this  kind. 
When  the  auxiliary  measures  here  mentioned  do  not  sufficiently  break  up 
the  ingesta,  and  also  stimulate  the  gastric  secretion,  we  must  at  the  onset 
dissolve  or  very  finely  pulverize  the  greater  part  of  the  food.  As  to  albu- 
min, milk  and  eggs  are  to  be  utilized  in  different  ways  prior  to  or  simul- 
taneously with  artificial  foods.  In  the  use  of  milk,  it  is  true  that  great 
care  is  necessary  in  patients  who  show  a  tendency  to  diarrhea,  and  the  advice 
of  A.  Schmidt  to  administer  to  such  patients  only  the  salicylated  milk — 
particularly  in  summer — is  especially  valuable.  In  cases  in  which  there 
is  a  tendency  to  diarrhea  I  have  repeatedly  seen  favorable  results  from 
well-sterilized  diabetic  milk  (almost  free  from  sugar),  which  I  used  chiefly 
in  cases  of  diarrhea.  Of  artificial  food  preparations — thanks  to  the  zeal 
of  busy  manufacturers — a  large  number  are  at  our  disposal,  so  that  in  the 
choice  in  a  given  case  we  pay  more  attention  to  the  taste,  or,  in  other  cases, 
to  the  price  of  the  article.  These  food  preparations  are  best  given  in  soups, 
in  milk,  or  in  puree.  The  various  meals  should  not  be  large,  and  we  should 
rather  adhere  to  the  law,  "  Little  and  frequently "  than  to  "  Much  and 
rarely."  Of  fats  I  prefer  the  easily  digested  milk  fats  (milk,  cream,  but- 
ter), whose  secretory,  inhibitive  influence  in  severe  forms  of  secretory  in- 
sufficiency is  no  longer  of  much  importance. 

Physical  Treatment. — Physical  treatment  generally  aids  us  but  little 
in  controlling  subacidity.  In  so  far  as  my  own  experience  and  investiga- 
tions permit  an  opinion,  neither  hydrotherapeutic  measures,  nor  massage, 
nor  electricity  of  the  stomach  can  claim  a  positive  influence  upon  the  secre- 
tion of  gastric  juice.  Gastric  lavage  may  also  be  tried  in  subacidity  when 
there  are  large  quantities  of  mucus  in  the  empty  stomach,  although  in  the 
majority  of  such  cases  the  use  of  alkaline  mineral  waters  upon  an  empty 
stomach  is  sufficient  (washing  in  the  direction  of  the  pylorus),  and  also 
when  a  disturbance  in  motility  is  combined  with  subacidity.  In  regard 
to  the  balneotherapeutic  treatment  of  subacidity,  I  prefer  the  waters  con- 
taining sodium  chlorid  (Kissingen,  Homburg,  Wiesbaden,  etc.),  but  ex- 
periments to  demonstrate  the  relation  in  such  spa  cures  of  the  sodium 
chlorid  in  the  organism  to  the  secretion  of  hydrochloric  acid  lack  a  satis- 
factory scientific  basis.  The  secretion  of  hydrochloric  acid  can  nowise  be 
increased  by  the  rectal  introduction  of  sodium  chlorid,  as  I  have  proven  in 
a  number  of  patients  suffering  from  subacidity.  This  is  the  result  I  ex- 
pected inasmuch  as,  in  the  patients  who  here  come  into  question,  the  secre- 
tory insufficiency  is  to  be  attributed  more  to  the  pathological  condition  of 
the  secreting  cells  and  the  nerves  which  stimulate  them  than  to  a  deficiency 
of  sodium  chlorid  in  the  organism.  In  cases  in  which  a  general  neurosis 
is  the  cause  of  subacidity,  the  elements  of  physical  treatment  may,  under 
certain  circumstances,  indirectly  act  favorably  upon  the  production  of 
hydrochloric  acid. 


102  SECRETORY  DISTURBANCES  OF  THE  STOMACH 

Drug  Treatment. — Drug  treatment  of  subacidity  represents  on  the  one 
hand  a  substitution  therapy,  and  on  the  other  hand  an  attempt  to  increase 
the  diminished  secretion.  Substitution  therapy  aims  to  supply  hydrochloric 
acid  and  the  ferments  which  have  been  lost — particularly  pepsin — from 
without,  and  probably  represents,  so  far  as  the  introduction  of  pepsin  is 
concerned,  the  oldest  form  of  organotherapy  upon  an  exact  basis  in  man. 
If  we  study  the  consequences  of  subacidity  from  the  introduction  of  hydro- 
chloric acid  and  of  pepsin,  a  critical  judge  will  not  place  a  high  estimate 
upon  the  effect  of  such  treatment;  for,  as  the  investigations  of  Pfungen, 
Schiile  and  others  have  demonstrated,  the  amount  of  hydrochloric  acid 
combined  by  the  proteids  compared  with  the  quantity  of  hydrochloric  acid 
therapeutically  administered  by  the  mouth  is  so  great  that  the  introduced 
hydrochloric  acid  can  hardly  be  looked  upon  as  a  substitute  for  the  secre- 
tion which  has  been  lost.  Moreover,  in  regard  to  pepsin  it  must  be  stated 
that,  v/ith  adequate  quantities  of  hydrochloric  acid,  even  slight  amounts 
of  pepsin  are  enough  to  produce  a  satisfactory  proteolytic  effect ;  that,  how- 
ever, the  introduction  of  pepsin  is  useless  if,  during  the  entire  duration  of 
digestion,  a  sufficient  quantity  of  hydrochloric  acid  is  simultaneously  present 
in  the  stomach.  Benefit  from  the  various  wines  of  pepsin,  therefore,  is  prob- 
ably because  of  the  stomachics  they  contain.  In  cases  with  complete  loss 
of  secretion  it  is  far  wiser  to  use  the  pancreas  preparations  which  act  upon 
a  neutral  or  alkaline  floor  and  permit  digestion  of  the  small  intestine  to 
begin  in  the  stomach;  that  is,  where  gastric  digestion  is  lacking,  intestinal 
digestion  is  aided  by  the  administration  of  proper  preparations.  Among 
these  preparations  pankreon  has  been  most  serviceable  in  my  hands,  while 
from  papain,  which  is  said  to  be  active  in  an  acid  media,  I  have  seen  no 
remarkable  results  nor  have  Grote,  Hirsch  and  others.  In  regard  to  a 
special  form  of  substitution  therapy,  the  administration  of  canine  gastric 
juice,  which  was  first  advised  by  Pawlow  and  subsequently  by  Russian  and 
French  investigators — in  Germany  this  has  only  been  employed  by  Paul 
Meyer — I  have  no  personal  experience.  I  do  not  believe,  however,  that  this 
method  is  often  absolutely  necessary,  nor,  the  material  being  so  difficult  to 
obtain,  that  it  will  come  into  general  use. 

Great  value  was  formerly  attached  to  certain  products  that  increased 
secretion,  and  Pawlow  by  masterly  investigation  and  technic  has  now  made 
it  possible  for  us  accurately  to  study  this  question  experimentally.  Pawlow 
found  that  raw  meat,  meat  juice,  meat  broth,  Liebig's  meat  extract,  milk, 
gelatin,  certain  peptones  and  large  quantities  of  water  stimulate  the  gastric 
juice.  Herzen  compared  dextrin  (not  chemically  pure)  and  Liebig's  meat 
extract,  and  found  that  the  combination  of  large  doses  of  these  (25  to  50 
grams)  in  a  dog  with  gastric  fistula  stimulated  the  gastric  secretion  and 
formed  pepsin.  Employed  alone,  dextrin  particularly  influenced  pepsin 
formation,  while  Liebig's  meat  extract  chiefly  acted  upon  the  gastric  juice. 
Alcohol  proved  a  mighty  stimulant  to  the  gastric  secretion  but  had  abso- 


HYPERACIDITY  103 

lutely  no  effect  upon  the  production  of  pepsin.  Alcohol  administered  per 
rectum  also  showed  itself  a  stimulant  to  the  gastric  juice,  as  Metzger  deter- 
mined in  Riegel's  Clinic.  Herzen  reports  that  he  produced  favorable  re- 
sults in  man  with  a  mixture  of  Liebig's  meat  extract  and  dextrin  in  a  pala- 
table form.  Another  preparation,  inulin,  after  the  administration  of  which 
Herzen  found  a  marked  amount  of  pepsin  in  the  gastric  Juice  if  he  simul- 
taneously administered  alcohol,  I  have  employed  in  a  few  cases  in  the  form 
of  a  tea  containing  inulin  ( 25  grams  in  300  c.c.  of  the  tea  for  a  trial  break- 
fast). Although  I  have  in  a  few  cases  seen  a  slightly  stimulating  effect 
upon  the  gastric  juice,  yet,  considering  the  expense  of  inulin,  this  was  not 
so  marked  as  to  tempt  me  to  make  very  extensive  experiments. 

It  may  be  urged  in  opposition  to  the  explanations  given  here  that  there 
are  cases  of  apepsia  gastrica  which  run  their  course  for  years  and  even 
decades  without  any  marked  disturbance,  and  we  may  conclude  from  this 
that  it  is  not  always  necessary  in  cases  of  subacidity  to  follow  the  outlined 
treatment  here  suggested.  In  reply  it  may  be  maintained  that  no  proof 
has  yet  been  furnished  that  the  persistent  functional  over-exertion  of  those 
glands  of  the  intestine  which  furnish  the  proteolytic  ferments  and  their 
combinations  will  never  produce  injurious  effects.  What  we  have  stated  of 
the  relation  of  certain  forms  of  diarrhea  to  apepsia  gastrica,  and  the  favor- 
able influence  upon  them  of  measures  hqre  described,  by  no  means  strength- 
ens the  arguments  of  those  who  declare  these  measures  to  be  unnecessary; 
and  even  if  we  could  adduce  no  positive  facts  in  support  of  the  fundamental 
principles  here  developed,  the  purely  theoretical  assumption  that  prophy- 
laxis is  the  best  therapy  is  sufficient  reason  and  justiification.  This  is  par- 
ticularly true  of  the  suggestion  of  small  and  frequent  meals,  since  these, 
more  than  any  other  means,  conserve  the  motility  of  the  stomach,  the  weak- 
ening of  which  at  once  disturbs  the  equilibrium  of  the  patient's  metabolism. 
A  disturbance  of  motility  in  cases  of  apepsia  gastrica  soon  changes  the 
stomach  from  a  natural  disinfectant  apparatus  into  an  incubation  apparatus 
for  various  microorganisms — under  some  circumstances,  also  the  pathogenic 
— and,  from  a  teleologic  point  of  view,  a  reason  may  be  discerned  in  the 
facts  that  the  stomach  in  apepsia  gastrica  usually  empties  itself  more 
rapidly  than  under  normal  circumstances,  that  it  is  unable  to  digest  its 
contents,  and  also  that  it  has  no  power  upon  micro-parasites,  but  rapidly 
propels  them  into  the  small  intestine,  in  which  a  great  number  of  micro- 
organisms appear  to  perish. 

HYPERACIDITY 

In  the  description  of  an  immoderate  secretion  of  acid  we  must  sharply 
differentiate  those  conditions  in  which  gastric  juice  abnormally  rich  in 
hydrochloric  acid  is  excreted  only  by  the  stimulation  of  the  ingesta  from 
those  in  which  gastric  juice  is  excreted  with  a  permanent  secretion — one 
independent  of  the  introduction  of  food.     We  must,  therefore,  sharply  dia- 


104  SECRETORY   DISTURBANCES   OF  THE  STOMACH 

• 

tinguish  hyperacidity  (superacidity,  peracidity)  from  hypersecretion  (su- 
persecretion,  parasecretion,  gastrosuccorrhea).  As  in  the  former  the  stom- 
ach reacts  only  to  the  stimulation  of  the  ingesta  present,  and  produces  a 
secretion  powerful  in  digestion,  in  the  second  case  a  secretion  takes  place 
without  stimulation,  and,  as  to  cause  and  effect,  the  stomach  in  the  former 
case  bears  the  same  relation  to  the  latter  as  a  pump  or  open  well  to  an 
artesian  well.  But  since  it  is  not  my  purpose  here  to  discuss  the  ques- 
tion in  how  far  hyperacidity  is  a  substantive  disease  or  is  merely  a  symptom 
of  other  affections,  I  shall  at  once  define  our  chemical  conception  of  hyper- 
acidity. To  express  this  in  figures  is  very  difficult,  for,  on  the  one  hand, 
tlie  amount  of  secretion  varies  greatly  under  physiological  conditions  in 
one  and  the  same  individual  as  well  as  in  different  persons,  and,  on  the 
other  hand,  the  sensibility  of  individual  persons  to  an  excess  of  hydro- 
cliloric  acid  in  the  stomach  shows  extraordinary  variations.  In  practice, 
tliis  latter  factor  merits  special  consideration  because  only  that  patient 
sufi'ering  from  hyperacidity  seeks  a  physician  who  suffers  discomfort  on 
account  of  his  disturbance  in  secretion.  In  my  opinion,  therefore,  a  de- 
scription of  hyperacidity  necessitates  the  simultaneous  delineation  of  all 
those  factors  which  produce  a  more  or  less  marked  acid  hyperesthesia.  Be- 
sides, our  conception  of  the  condition,  that  is,  whether  we  base  the  chem- 
ical conception  of  hyperacidity  on  the  total  acidity,  or  make  free  hydro- 
chloric acid  most  prominent,  varies  greatly.  Among  those  who  adhere  to 
the  first  theory,  Ewald  estimates  hyperacidity  in  a  total  acidity  between 
GO  and  70,  and  Rosenheim  above  60;  Johnson  and  Behm  consider  a  gastric 
juice  with  a  total  acidity  of  70  as  hyperacid,  and  Boas  regards  in  the  same 
light  a  gastric  juice  with  an  acidity  of  over  2  per  thousand.  Riegel,  besides 
laying  much  stress  upon  the  total  acidity,  also  attaches  great  significance 
to  the  proportion  of  free  hydrochloric  acid.  "  The  most  important  point 
is  the  free  hydrochloric  acid.  Only  where  this  is  increased  are  we  justified 
in  speaking  of  an  actual  hyperaciditas  hydrochlorica.  Values  of  60,  70, 
80  and  more  after  a  test-meal,  of  50  to  60  and  upwards  after  a  test  breakfast 
are  frecjuently  found  here."  Schiile  considers  the  gastric  juice  to  be  hyper- 
acid when  it  reaches  a  height  of  0.22  per  cent,  more  than  free  hydrochloric 
acid,  and  shows  a  total  acidity  of  more  than  70.  Schneider  maintains  that 
a  <,^astric  juice  with  more  than  0.25  per  cent,  of  free  hydrochloric  acid  is 
to  1)0  looked  upon  as  hyperacid,  and  that  we  may  also  regard  as  hyperacid 
a  gastric  juice  which  still  gives  a  reaction  for  free  hydrochloric  acid  with 
a  dilution  of  more  than  ten  times  its  bulk.  Although  it  must  be  admitted 
without  more  ado  that  gastric  contents  which  with  a  total  acidity  of  70 
give  an  intense  reaction  for  HCl  may  be  called  hyperacid,  yet,  in  doubtful 
cases  I  should  be  reluctant  to  diagnosticate  hyperacidity  of  the  gastric  juice 
upon  this  single  symptom  of  the  gastric  contents,  but  only  upon  the  sum 
of  peculiarities  which  the  test  breakfast  or  the  test-meal  enable  us  to  recog- 
nize.    For  we  may  examine  gastric  juice  in  which  titration  shows  no  ab- 


HYPERACIDITY  105 

normally  high  degree  of  total  acidity,  while,  notwithstanding  this,  certain 
peculiarities  of  the  gastric  contents  and  also  the  clinical  symptoms  of  the 
patient  may  correspond  to  the  condition  which  we  are  accustomed  to  find 
in  hyperacidity.  Cases  of  this  kind  which  Schiile  under  my  direction  de- 
scribed by  the  name  of  hyperaciditas  larvata  or  hyperaciditas  occulta  are 
not  extremely  rare  and,  in  a  certain  sense,  are  the  antitheses  of  those  cases 
of  hyperacidity  running  their  course  without  symptoms  in  which  the  exam- 
ination of  the  gastric  contents  reveals  the  distinct  characteristics  of  hyper- 
acidity while  the  patient  presents  absolutely  no  symptoms. 

The  typical  peculiarities  of  the  gastric  contents  in  hyperacidity  are 
the  following: — 

The  thin  fluidity  of  the  gastric  contents,  the  tendency  rapidly  to  form 
two  layers,  an  upper  one  consisting  of  fluid  and  a  lower  one  of  a  finely  pul- 
verized, starchy  sediment,  and,  especially  prominent,  its  conspicuous  chymi- 
fication.  In  regard  to  the  layers,  we  find  that  if  the  gastric  juice  is  placed 
in  a  graduated  test  tube  for  two  hours  after  its  withdrawal,  and  spontane- 
ous sedimentation  is  permitted,  the  "  layer  quotient,"  i.  e.,  the  figure  which 
the  height  of  the  sediment  shows  divided  by  the  total  amount  of  gastric 
contents  collected  for  sedimentation,  is  frequently — although  not  invariably 
— ^below  50  per  cent.  Sedimentation — contrasted  with  that  of  many  sub- 
acid gastric  contents — not  only  occurs  very  rapidly  but  most  completely. 
Besides  amylorrhexis  of  the  hyperacid  gastric  contents,  amylolysis  also 
merits  some  consideration.  As  I  showed  years  ago  in  a  large  number  of 
cases  of  hyperacidity,  relatively  low  values  for  the  dextro-rotary  substance 
were  found  in  the  majority,  and  (particularly  dependent  upon  this)  also 
a  low  specific  gravity  of  the  gastric  contents,^  as  well  as  frequently  a  Bor- 
deaux red  or  violet — in  rare  cases  also  a  blue — reaction  of  the  iodin  test. 
In  some  cases  I  detected  an  abnormally  low  molecular  concentration  of  the 
gastric  contents.  As  to  the  proportion  of  free  hydrochloric  acid  to  total 
acidity,  in  a  comprehensive  examination  of  my  cases  of  hyperacidity  in 
which  the  total  acidity  amounted  to  more  than  60,  more  frequently  than 
otherwise  I  found  the  free  hydrochloric  acid  equalled  two-thirds  and  more 
of  the  total  acidity.  In  nine  cases  of  hyperaciditas  larvata  in  which  the 
total  acidity  did  not  exceed  50,  I  only  twice  saw  the  acidity  value  of  free 
hydrochloric  acid  fall  below  50  per  cent,  of  the  total  acidity,  while  in  other 
cases  in  which  the  total  acidity  was  not  over  50  the  value  for  free  hydro- 
chloric acid  was  more  often  below  than  above  50  per  cent,  of  the  total 
acidity.  These  conditions,  however,  are  not  so  characteristic  in  the  indi- 
vidual case  as  to  be  of  direct  diagnostic  use.  The  relation  of  the  total 
amount  of  the  gastric  contents  here  calls  for  consideration,  and  all  the 
more  so  because  in  various  places  erroneous  views  have  been  promulgated 

1  I  am  unaware  that  either  Schiile  or  I  have  given  a  specific  gravity  of  over  1.020 
as  a  "  positive  "  sign  of  subacidity,  as  has  recently  been  alleged  by  lUoway,  nor  can 
this  statement  be  proven. 


106  SECRETORY   DISTURBANCES   OF  THE  STOMACH 

as  to  the  influence  of  motility  in  hyperacidity.  For  a  long  time  it  was 
remarked  that  one  hour  after  administering  the  test-breakfast  in  cases  of 
hyperacidity,  and  upon  the  evacuation  of  the  gastric  contents,  an  increased 
amount  was  not  rarely  evacuated.  This  fact  was  long  known  to  those  who 
only  recently  relinquished  the  antiquated  method  of  estimating  the  total 
amount  of  gastric  contents  solely  by  expression,  that  is,  by  aspiration,  with- 
out subsequent  lavage.  For  more  than  eight  years,  after  every  investiga^ 
tion  of  the  gastric  contents  I  have  made  an  exact  estimation  of  the  residue 
of  the  gastric  contents  by  the  aid  of  a  mathematical  formula  which  is  based 
on  the  relation  of  the  specific  gravity  of  the  undiluted  gastric  juice  to  that 
of  the  gastric  juice  diluted  with  100  c.c.  of  water,  this  principle,  as  I 
learned  subsequently,  having  been  previously  employed  by  Jaworski  in  his 
scientific  investigations.  I  still  employ  this  mode  of  calculation  because 
the  estimation  of  acidity  according  to  the  method  of  Mathieu  and  Remond 
in  cases  of  anacidity  leaves  us  in  the  lurch ;  that  is,  only  by  the  employment 
of  a  complicated  modification  given  by  Cohnheim  are  we  enabled  to  reach 
a  conclusion.  It  may  be  interesting  to  note  here  that  the  amount  of  gastric 
contents  I  have  obtained  in  a  great  number  of  investigations  in  normal 
persons  one  hour  after  a  test  breakfast  reached  on  an  average  the  figure 
of  150  c.c,  Avhile  in  40  cases  of  hyperacidity  I  obtained  an  average  figure 
of  210  c.c.  (the  lowest  being  124  c.c,  and  the  highest  400  c.c).  Con- 
trary to  numerous  authors,  I  do  not  believe  this  increase  in  the  amount 
of  gastric  contents  one  hour  after  the  administration  of  the  test  breakfast — 
at  least  in  uncomplicated  cases — to  be  the  consequence  of  a  so-called 
"  atony  "  (an  expression  which  had  best  be  eliminated  from  the  nomencla- 
ture of  gastric  pathology  since  it  is  not  only  superfluous  but,  in  consequence 
of  the  dissimilar  significance  attached  to  it  by  different  authors,  is  liable 
to  cause  confusion)  but  to  be  the  product  of  an  increase  in  the  secretion  of 
the  gastric  juice  of  a  hyperacid  stomach.  In  numerous  researches  in  un- 
complicated cases  of  hyperacidity  I  was  unable  to  detect  any  sign  of  motor 
insufficiency  either  by  the  currant  test,  by  the  fermentation  test,  or  by  micro- 
scopic examination  of  the  evacuated  gastric  contents.  Perhaps  the  fact, 
which  has  already  been  alluded  to,  that  the  "  layer  test "  of  hyperacidity 
usually  gives  a  lower  layer  quotient  than  in  subacidity,  and  that  occasion- 
ally a  conspicuously  low  value  for  the  molecular  concentration  of  the  gastric 
contents  is  found  ("  hydrorrhoea  gastrica")  may  be  utilized  in  the  same 
sense  as  my  explanation.  The  view  that  the  increase  of  the  gastric  contents 
in  hyperacidity  is  to  a  great  extent  the  consequence  of  an  increased  secre- 
tion is  somewhat  favored  by  the  experience  that,  in  contrast  to  the  condi- 
tion, just  described,  of  the  test  breakfast  (rich  in  starch),  upon  utilizing 
the  test-meal  relatively  rich  in  albumin  and  poor  in  carbohydrates,  an 
extremely  rapid  emptying  of  the  stomach  may  frequently  be  observed;  this 
phenomenon  may  be  satisfactorily  explained  by  the  theory  that  the  test 
breakfast,  by  the  too  early  interruption  of  amylolysis  ("  Secretio  celer  et 


HYPERACIDITY  107 

alta"),  and  the  disturbed  liquefaction  of  the  introduced  starches,  promotes 
an  increase  of  secretory  stimulation.  Johannes  Miiller  admits  that  the 
digestion  of  bread  is  generally  delayed  by  a  decidedly  acid  secretion,  and 
that  the  inhibition  of  amylolysis  appears  to  be  influenced  more  by  the  rapid- 
ity than  by  the  intensity  of  the  acid  secretion. 

SYMPTOMS 

As  already  indicated,  the  clinical  manifestations  of  hyperacidity  vary 
in  individual  cases  to  an  extraordinary  degree.  One  case  will  run  its  course 
without  symptoms,  and  another  with  excessive  pain  which  occasionally 
reaches  such  a  degree  and  is  so  frequent  that  signs  of  chronic  under-nutri- 
tion  and  loss  of  strength  may  appear.  Complications  such  as  erosions, 
fissures  with  consecutive  pylorospasm,  ulcer  of  the  stomach,  and  especially 
ulcer  of  the  pylorus,  may  in  isolated  instances  impress  their  stamp  upon 
the  case.  However,  except  for  such  "  complications,"  in  the  great  majority 
of  cases  of  hyperacidity  we  may  construct  a  clinical  picture  which,  although 
not  applicable  to  all  cases,  nevertheless  applies  in  a  great  many.  The 
patients  are  usually  thin — but  not  always — are,  as  a  rule,  between  20  and 
40  years  of  age,  the  majority  of  them  belong  to  the  erethismic  type,  they 
complain  of  gnawing,  painful  sensations  of  pressure  in  the  gastric  region, 
and  state  that  these  unpleasant  symptoms  occur  as  a  rule  several  hours  after 
eating — after  the  midday  meal,  or  in  the  late  afternoon  hours — they  con- 
tinue for  a  time  and  then  disappear.  The  mechanical  state  of  the  food  is 
said  to  be  unimportant,  and  the  pains  to  disappear  frequently  by  the  in- 
gestion of  milk  or  by  a  large  dose  of  sodium  bicarbonate.  The  appetite  is 
good,  but  the  patients  refrain  from  eating  through  fear  of  pain  (cibo- 
phobia).  Vomiting  is  rare,  but  eructations  are  frequent,  as  well  as  nausea 
and  retching.  The  patients  usually  complain  of  chronic  constipation. 
Provided  complications  or  other  diseases  which,  according  to  experience, 
play  a  role  in  the  etiology  of  hyperacidity  (pyloric  stenosis,  gastroptosis, 
hernia  epigastrica,  etc.)  are  not  present,  objective  investigation  in  most 
cases  reveals  only  slight  diffuse  sensitiveness  on  pressure.  Frequently  even 
this  is  absent. 

Hyperacidity  is  observed  in  different  countries  in  varying  frequency. 
According  to  Jaworski  it  occurs  in  Lemberg  in  51.8  per  cent.,  according 
to  Einhorn  in  New  York  in  51  per  cent.,  according  to  Johnson  and  Behm 
in  Stockholm  in  36.4  per  cent.,  according  to  Kovesi  in  Budapest  in  30.4 
per  cent.,  according  to  Mathieu  and  Eemond  in  Paris  in  29  per  cent.,  accord- 
ing to  Bouveret  in  Lyons  in  25  per  cent,  of  all  cases  of  gastric  disease  which 
come  under  observation.  In  my  own  experience  it  is  noted  in  Berlin  in 
scarcely  more  than  one-third  of  all  gastric  cases.  At  all  events,  among 
the  clinical  cases  received  at  the  Charite  in  Berlin,  the  disease  is  decidedly 
less  frequent  than  it  was  in  the  Clinic  in  Giessen,  as  I  had  an  opportunity 
of  observing. 


108  SECRETORY  DISTURBANCES  OP  THE  STOMACH 


ETIOLOGY 

The  causes  of  hyperacidity  also  vary  in  the  individual  cases,  and  are 
partly  of  a  local,  partly  of  a  general,  nature.  Among  the  local  factors 
chemic,  thermal  and  mechanical  irritants  play  a  role  which,  upon  prolonged 
action,  may  perhaps  also  lead  to  parenchymatous  changes  in  the  gastric 
mucous  membrane.  I  believe  it  very  likely  that  the  constant  use  of  food 
rich  in  spices  and  the  generous  consumption  of  alcohol — especially  of  sour 
Rhine  wine — play  a  role  in  the  etiology  of  hyperacidity,  and  I  also  take 
cognizance  of  the  thermic  factors  because  hyperacidity  is  relatively  com- 
mon among  bakers,  who,  as  is  well  known,  frequently  eat  hot  pastry. 
Moreover  it  is  by  no  means  certain  that  the  frequent  drinking  of  ice  cold 
fluids  upon  an  empty  stomach  does  not  predispose  to  hyperacidity.  In 
addition  there  is  a  large  group  of  local  and  general  neuroses — essential, 
toxic  (tobacco!),  or  arising  reflexly  ^ — and,  what  I  believe  to  be  worthy 
of  serious  discussion,  the  chronic  constipation  so  often  noted  in  hyperacidity. 
With  their  removal  the  symptoms  of  hyperacidity  frequently  disappear. 
By  some  authors  (Hemmeter)  continuous  over-stimulation  with  a  meat  diet 
is  considered  of  special  etiologic  importance,  and  Westphalen  even  discrim- 
inates a  congenital  predisposition  attributable  to  the  predominant  meat 
diet  of  preceding  generations.  Cloetta  has  also  shown  that  in  dogs  of  the 
same  litter,  those  nourished  with  meat  show  free  hydrochloric  acid  after 
a  meal  while  in  dogs  fed  with  milk  it  is  absent.  Although  Cloetta  could 
find  no  absolute  difference  in  the  histologic  structure  of  the  mucous  mem- 
brane of  these  dogs  on  different  foods,  I  believe  it  at  least  possible  that 
organic  changes  may  be  produced  in  the  gastric  mucous  membrane  by 
hyperacidity.  There  is,  as  I  have  proven  in  several  of  my  cases,  a  true 
acid  gastritis,  i,  e.,  a  combination  on  the  part  of  the  stomach  of  the  pro- 
duction of  mucus  with  that  of  hyperacidity.  Such  cases  upon  lavage  of 
the  empty  stomach  not  only  show  more  mucus  than  in  the  norm — the  lavage 
water  of  a  normal  stomach  before  food  is  taken  is  grey,  has  a  turbid  appear- 
ance, and  resembles  the  water  after  cleansing  the  mouth — but  the  micro- 
scopic examination  of  the  peculiar  mucus  plugs  from  the  test- breakfast  also 
shows  a  conspicuous  number  of  glistening  nuclei  of  leukocytes  with  com- 
pletely digested  protoplasm.  The  conclusion  is  obvious  that  the  increase 
of  acid  production  in  such  cases  is  not  only  functional  but,  perhaps,  also 
anatomical,  especially  in  the  cases  of  hyperacidity  running  their  course 
with  motor  insufficiency,  and  in  which  the  autopsy  reveals  proliferation  of 
the  glandular  parenchyma. 

^  Some  cases  of  hyperacidity  and  gastroptosis,  hernia  epigastrica,  and  local  peri- 
tonitis may  also  be  of  more  or  less  neurogenic  origin. 


HYPERACIDITY  109 


TREATMENT   OF    HYPERACIDITY 

In  the  treatment  of  hyperacidity  diet  occupies  the  first  place.  Its  im- 
portance is  evident  from  the  fact  that,  probably,  in  no  branch  of  the  treat- 
ment of  gastric  affections  are  the  fundamental  laws  of  nutrition  so  warmly 
disputed  as  in  this  instance.  The  question  chiefly  resolves  itself  into  this, 
whether  preference  should  be  given  to  albumin  which  readily  combines 
acids,  or  to  starches  which  are  less  stimulating  to  the  production  of  hydro- 
chloric acid  in  the  patient  suffering  from  hyperacidity.  To-day,  when  the 
waves  of  discord  have  become  somewhat  smoother,  we  may  say  that  occa- 
sionally in  this  discussion  the  point  of  view  has  been  too  one-sided,  inas- 
much as  it  has  been  overlooked  that  in  the  dietetic  treatment  of  the  patient 
the  entire  organism  is  to  be  considered  as  well  as  the  stomach,  and  that 
in  the  consideration  of  dietetic  experiments  and  experiences,  meat  and 
albumin  have  often  been  regarded  as  synonymous  with  carbohydrates  and 
vegetables.  In  some  of  the  earlier  researches,  too,  the  importance  of  the 
employment  of  "  equicaloric "  amounts  of  ingested  food,  and  differences 
in  the  composition  of  the  food,  have  not  been  sufficiently  taken  into  account 
in  the  individual  experiment,  as  is  apparent  from  the  special  preparation 
of  the  food,  its  volume,  and  the  labor  necessary  in  masticating  it.  Finally, 
in  my  opinion,  the  varying  etiology  of  hyperacidity  from  the  basis  of  nutri- 
tion has  been  too  little  considered  in  the  individual  cases.  A  certain  bias 
of  observation  has  until  recently  been  manifest,  for,  in  the  question  under 
discussion  the  cry  has  almost  always  been  "  here  albumin  "  or  "  here  carbo- 
hydrates "  while  of  fat  we  have  only  been  told  that  patients  suffering  from 
hyperacidity  "  may  "  have  good  butter,  or  that  large  quantities  of  fat  should 
be  avoided  for  the  reason  that  they  readily  disturb  intestinal  digestion  by 
the  hyperacidity  of  the  gastric  juice.  Fat,  at  the  present  time,  not  only 
occupies  a  position  of  equal  importance  with  the  two  other  nutritive  prod- 
ucts in  the  diet  of  the  person  suffering  from  hyperacidity  but  even  a  pre- 
ferred position,  for  the  reason — as  we  know  from  the  pioneer  experiments 
of  Pawlow  upon  the  dog,  and  those  which  I  simultaneously  carried  out  with 
Akimow  Perez,  and  the  subsequent  ones  of  Backman  and  others  in  man — 
that  fat  inhibits  gastric  juice  secretion,  and  therefore  is  utilized  normally 
in  the  intestinal  canal  of  the  patient  with  hyperacidity,  yet  does  not  inhibit 
the  motility  any  more  than  an  equal  quantity  of  other  caloric  food  prod- 
ucts. The  curative  power  of  large  quantities  of  milk  fat  in  the  dietary 
of  hyperacidity  thus  appears  to  be  proven,  accordingly  fat,  especially  milk 
fat,  has  been  accorded  a  permanent  place  in  the  treatment  of  hyperacidity. 
In  earlier  investigations  which  I  made  regarding  the  relation  of  the  dextro- 
rotary  substance  in  the  human  gastric  contents.  I  found  in  concentrated 
solutions  of  sugar  another  dietetic  measure  to  diminish  gastric  juice  secre- 
tion. Similar  researches  have  recently  been  made  by  v.  Aldor  in  man,  and 
by  Clemm  in  the  dog,  with  gastric  fistula,  and  the  results  have  been  con- 


110  SECRETORY   DISTURBANCES   OF  THE  STOMACH 

firmed.  For  the  removal  of  the  acid  symptoms,  concentrated  sugar  solu- 
tions are  most  effective  if  administered  to  the  patient  only  upon  their 
appearance.  Instead  of  sugar  solutions  we  may  use  honey,  although,  as 
Clemm  has  shown,  levulose  lacks  the  powerful,  inhibiting  secretory  effect 
of  dextrose.  For  the  rational  treatment  of  hyperacidity,  however,  dietetic 
measures  to  diminish  gastric  juice  secretion  are  by  no  means  sufficient,  but 
we  must  simultaneously  remove  from  the  diet  all  those  articles  which  in 
themselves  possess  the  property  of  increasing  the  secretion  of  the  gastric 
juice.  As  food  and  dainties  in  this  respect  have  already  been  discussed 
in  the  description  of  subacidity,  I  desire  only  to  urge  the  utmost  care  in 
the  free  use  of  extracts  of  meat  (concentrated  bouillon,  sauces),  and  the 
spicy  preparation  of  food  in  general,  above  all,  such  food  products  as  require 
prolonged  mastication.  A  rational  arrangement  of  the  meals  also  appears 
to  be  highly  important  in  hyperacidity.  It  is  directly  opposed  to  the  true 
conception  of  the  nature  of  hyperacidity  that  a  patient  with  this  affection 
should  take  frequent  but  small  meals.  The  essential  feature  of  hyperacidity 
consists  in  an  abnormal  irritability  of  the  secretory  apparatus  of  the  stom- 
ach, the  expression  of  which  is  not  manifest  during  the  period  when  the 
stomach  rests,  but  only  during  its  time  of  labor.  For  this  reason  I  main- 
tain, with  A.  Schmidt,  that  but  a  few  and — provided  there  are  no  definite 
factors  to  the  contrary — somewhat  larger  meals  are  indicated. 

In  regard  to  the  mixture  of  individual  food  products,  I  agree  with 
those  who  have  lately  recommended  a  vegetable  or  a  lacto-vegetable  regime 
in  the  treatment  of  all  those  cases  of  hyperacidity  in  which  this  appears 
to  be  the  consequence  of  a  functional  neurosis,  or  in  which  the  symptoms 
of  the  latter  at  least  dominate  the  clinical  picture.  According  to  my 
experience,  in  the  remaining  cases,  the  administration  of  a  mixed  diet 
is  best, — one  which,  in  a  normal  calory  amount,  contains  considerable  fat 
(from  150  to  180  grams) — especially  milk  fat,  such  as  cream,  butter, 
Jaworski's  "  kraftmilch,"  or  Gaertner's  fat  milk,  fat  cheese,  oil  (according 
to  Walko,  even  by  the  stomach-tube),  emulsions  of  almond  oil,  etc.,  but 
not  bacon  and  beef  fat — as  well  as  a  normal  quantity  of  albumin  (amount- 
ing to  about  120  grams)  only  a  small  part  of  which  should  consist  of  meat, 
preferably  broiled  meat,  or  of  fish.  Starches  had  best  be  administered  in 
the  form  of  thick  soups,  gruels  (mashed  potatoes,  flour,  rice,  etc.),  and 
tender,  well-cooked  vegetables  dressed  with  considerable  butter;  it  is  ad- 
visa])le  in  general  not  to  give  more  than  250  or  300  grams,  but  the  amount 
permissible  depends  very  much  upon  the  form  in  which  it  is  given.  As 
soups  rich  in  extracts  are  usually  unsuitable  for  patients  with  hyperacidity, 
car])ohydrates,  if  not  fluid  or  also  taken  in  other  ways,  may  be  given  in 
flour  soup,  milk  soup  or  fruit  soup.  Bread,  whenever  possible,  should  be 
ricli  in  albumin  (aleuron^t,  roborat  or  casein  breads)  or  fat  containing, 
as  bread  and  butter  or  Rademann's  nutritive  toast  (Niihrtoast),  etc.  Some- 
times foods  containing  oil  (sardines  in  oil)  may  be  permissible,  or  a  dose  of 


HYPERACIDITY  111 

emulsion  of  almond  oil  before  meals,  or  a  not  too  strong  fatty  cheese,  as, 
for  example,  the  creme  double  de  Normandie,  which  gourmands  even  eat 
with  sugar,  or  with  whipped  cream  and  sugar.  The  effect  of  the  latter, 
as  has  already  been  stated,  justifies  the  use  of  sweets,  such  as  fruit  jellies, 
creams,  sweet  stewed  fruits,  and  fruit  syrups,  such  as  raspberry  syrup, 
grape  juice,  etc. — also  in  the  form  of  Nectar  and  Pomril — as  well  as  malt 
extract,  malt  beer,  porter,  and  honey ;  in  this  respect  the  particular  idiosyn- 
crasy of  the  patient  suffering  from  hyperacidity  is  to  be  considered.  Among 
wines,  as  a  rule,  red  wine  is  preferable,  which  had  best  be  diluted  with 
an  alkaline  mineral  water.  Among  the  Ehine  wines,  the  acid  varieties 
must  be  avoided;  white  Bordeaux  wine  and  white  Burgundy  are  preferable 
to  Moselle  wine.  The  tolerance  of  beer  varies  greatly  in  the  individual 
case;  in  general,  those  rich  in  carbohydrates  are  preferable  to  those  defi- 
cient. Coffee  is  usually  badly  borne;  tea  and  cocoa  frequently  agree  well 
with  the  patient,  particularly  if  given  with  large  quantities  of  cream. 

Physical  Treatment. — The  curative  factors  of  physical  therapy  from 
a  symptomatic  standpoint  may  aid  us  greatly;  moist,  warm  compresses  as 
well  as  dry  heat  (thermophore,  Japanese  stove)  are  particularly  effective 
for  the  unpleasant  sensations  produced  by  hyperacidity.  Simon  maintains 
the  favorable  influence  of  sweating  upon  the  gastric  juice  secretion,  which 
coincides  with  the  researches  Edel  made  in  Riegel's  Clinic.  I  have  been 
unable  to  find  these  so  frequent  as  to  make  the  method  worthy  of  general 
acceptance.  However,  other  hydrotherapeutic  measures  are  not  rarely  in- 
dicated in  those  cases  going  hand  in  hand  with  neurasthenia  or  attributable 
to  this. 

Drug  Treatment. — Drug  treatment  is  employed  in  hyperacidity  for 
various  purposes.  For  the  hyperacidity  itself  subcutaneous  injections  of 
atropin  were  advised  by  Riegel  as  valuable  on  account  of  the  experiments 
which  he  made  in  dogs  with  fistula,  and  from  his  own  clinical  experience. 
Unfortunately,  however,  the  dose  required  decidedly  to  inhibit  secretion 
is  so  great  that  atropin  can  only  be  employed  for  relatively  brief  periods 
daily,  unless  we  wish  to  run  the  risk  of  poisoning  from  atropin.  For  this 
reason  atropin  in  doses  of  one  milligram  is  particularly  indicated  in  the 
treatment  of  acute  exacerbations  of  hyperacidity.  Whether  bismuth  and 
silver  nitrate  also  possess  the  power  to  inhibit  secretion  is  not  certain.  In 
systematic  investigations  of  the  gastric  juice  secretion  prior  to  and  after 
treatment  with  bismuth  and  silver  nitrate  lasting  for  several  weeks,  I  have 
personally  been  unable  to  determine  any  absolute  decrease  of  the  gastric 
juice  secretion.     Nevertheless,  these  drugs  at  least  deserve  mention. 

Alkalies  for  a  long  time  quite  properly  played  a  role  in  the  symptomatic 
drug  treatment.  It  is  wise  to  give  the  alkali  or  the  alkaline  mixture — 
usually  a  mixture  of  various  alkalies  is  given  to  which,  in  cases  compli- 
cated with  constipation,  a  laxative  salt  is,  as  a  rule,  added — to  the  patient 
only  on  special  indications,  i.  e.,  only  when  acidity  becomes  noticeable,  and 


112  SECRETORY   DISTURBANCES   OF  THE   STOMACH 

then  not  in  small,  divided  doses  but  at  once  in  a  decided  dose  (at  least  what 
will  cover  the  tip  of  a  knife,  and,  if  necessary,  from  one-half  to  one  tea- 
spoonful).  The  immediate  effect  of  the  alkaline  treatment  upon  the  symp- 
toms in  hyperacidity  proves  more  absolutely  than  any  theoretic  considera- 
tion that  a  causal  relation  must  exist  between  the  excess  of  acid  and  the 
manifestation  of  the  symptoms.  It  appears  that  by  the  administration  of 
alkalies  this  plus  of  hydrochloric  acid  which  has  a  disagreeable  effect  upon 
the  patient  is  neutralized.  The  prompt  action  of  alkalies  may  very  well 
be  explained  by  the  assumption  that  a  pyloric  spasm  and  its  consequences 
(painful  contraction,  retention  of  gases,  etc.)  are  arrested  by  neutralizing 
the  acid,  or  that  in  hyperesthesia  gastrica  the  acid  irritation  is  removed. 
That  the  alkaline  therapy  is  injurious  is  neither  maintained  by  those  who 
have  had  great  experience  in  this  treatment  of  hyperacidity,  nor  by  other 
observations  such  as  have  been  made,  for  example,  in  the  treatment  of 
acidosis  with  large  doses  of  an  alkali.  An  excess  of  alkali  is  removed  from 
the  body  with  relative  rapidity.  In  numerous  original  experiments,  on 
the  administration  of  10  grams  of  sodium  bicarbonate,  alkalinity  of  the 
urine  usually  occurred  in  from  ten  minutes  to  an  hour  and  a  half,  and 
rarely  lasted  longer  than  sixteen  hours.  The  administration  of  alkalies 
to  patients  with  hyperacidity  may,  under  certain  circumstances,  even  in- 
crease amylolysis,  which  in  practice  is  all  the  more  striking  since  in  the 
treatment  of  hyperacidity  the  resistance  of  saccharifying  ferments  accom- 
plishes but  little.  In  association  with  Stargard  I  determined  this  for  the 
remedy  last  advised,  takadiastase. 

The  treatment  of  hyperacidity  naturally  remains  incomplete  so  long 
as  only  the  irritative  condition  of  the  gastric  mucous  membrane  is  com- 
bated, and  not  the  cause  which  produces  the  condition.  Although  this 
is  not  the  place  in  which  to  consider  this  subject  minutely,  nevertheless 
it  must  be  here  emphasized,  above  all,  that  in  a  great  number  of  cases 
of  hyperacidity  the  simultaneous  constipation  largely  demands  our  thera- 
peutic interest,  for,  in  fact,  it  almost  gives  us  the  impression  that  hyper- 
acidity may  often  be  more  readily  cured  by  attacking  the  intestine  than 
the  stomach.  In  a  certain  sense  the  relations  are  here  inverted,  as  in  the 
diarrhea  of  apepsia  gastrica.  Therefore,  at  least  in  all  cases  of  hyper- 
acidity in  which  the  bowel  action  is  not  perfectly  normal,  a  systematic 
Carlsbad  cure — either  with  natural  Carlsbad  water  or  Carlsbad  salts — is 
indicated,  and  all  the  more  so  as  in  cases  of  hyperacidity  without  constipa- 
tion we  occasionally  observe  very  decided  improvement  under  the  influence 
of  Carlsbad  salt  or  Carlsbad  water.  In  every  individual  case  of  hjrper- 
acidity  we  should,  however,  as  therapeutists,  reflect  upon  the  limits  of  our 
differential  diagnosis,  which  in  this  affection  are  not  infrequently  revealed 
when  a  case  which  we  have  believed  to  be  "  only  "  hyperacidity  proves  to 
be  an  ulcer  of  the  stomach,  and  demands  of  us  special  consideration  in 
the  treatment. 


HYPERSECRETION  113 


HYPERSECRETION 

In  contrast  to  h3rperacidity,  hypersecretion  (parasecretion,  gastrosuc- 
chorrhea,  Reichmann's  disease,  etc. )  is  distinguished  by  a  continuous  "  flow 
of  gastric  juice,"  therefore  is  a  condition  in  which  the  stomach,  even  with- 
out the  stimulus  of  the  ingesta,  secretes  gastric  juice.  Although  hyper- 
secretion is  a  substantive  condition,  nevertheless  it  is  not  an  etiologic  unity, 
for  it  arises  under  varying  circumstances.  Its  recognition  depends  upon 
the  proof  of  greater  or  less  amounts  of  secretion  in  the  stomach  devoid 
of  food,  and  we  will  therefore  first  consider  the  question,  what  conditions, 
under  normal  circumstances,  promote  secretion  in  the  empty  stomach? 
As  investigations  of  this  point  by  various  authors — I  shall  mention  here 
Riegel,  Rosin,  Martins,  Schreiber,  Gintl  and  others — have  furnished  results 
in  part  contradictory,  in  answering  this  question  I  shall  primarily  relate 
my  own  observations.  Years  ago,  in  experiments  which  I  made  in  Ewald's 
wards  of  the  Augusta  Hospital  in  Berlin,  I  found  in  38  persons  that  note- 
worthy quantities  of  actual  gastric  juice  were  not  present  in  the  normal 
stomach,  but  I  noted  the  same  condition  in  several  hundred  observations 
which  I  had  an  opportunity  of  making  in  the  course  of  years  while  intro- 
ducing the  stomach-tube  into  the  stomach  empty  of  food — partly  for  diag- 
nostic, partly  for  therapeutic,  and  partly  for  clinico-experimental  purposes. 
Therefore,  I  agree  with  Riegel,  Ewald,  and  numerous  other  authors  even 
more  fully  to-day  than  formerly  in  believing  that  the  presence  of  appre- 
ciable quantities  of  fluid  which  presents  all  the  peculiarities  of  gastric  juice 
is  abnormal,  and  that  in  cases  in  which  this  fluid  reaches  a  certain  amount, 
say  exceeding  30  c.c,  we  have  a  pathologic  condition. 

What  are  the  properties  which  lend  to  a  fluid  the  characteristics  of  the 
gastric  juice'?  , 

The  fluid  which  usually  flows  in  a  stream  from  the  tube  is,  as  a  rule, 
clear  as  water  or  turbid,  of  a  light  grey  color,  or  may  also  show  a  greenish 
discoloration.  The  latter  change  is  readily  produced  in  the  fluid  from 
the  fact  that  during  the  act  of  expression  the  pylorus  occasionally  opens 
and  bile  regurgitates  from  the  small  intestine  into  the  stomach.  In  numer- 
ous observations  which  I  had  an  opportunity  of  making,  the  closure  of 
the  pylorus  during  the  act  of  expression  is  more  readily  overcome  when 
fluid  is  present  in  the  stomach  than  when  it  contains  a  thick,  pappy  mass. 
The  pure  secretion  of  the  empty  stomach,  compared  with  the  "  residue  " 
which  represents  remains  of  food  containing  chyme  without  a  distinctly 
recognizable  admixture  of  the  remains  of  food,  filters  rapidly  as  a  thin 
fluid,  either  clear  as  water,  or  occasionally  slightly  opalescent,  or  somewhat 
greenish  (in  the  latter  case  after  standing  a  few  days  the  green  color  is 
frequently  increased  on  admixture  with  air).  If  the  fluid  which  has  be- 
come turbid  from  admixture  with  leukocytes  and  remains  of  epithelia.  as 
well  as  from  shreds  of  mucus — occasionally  resembling  the  water  with  which 


IL 


114  SECRETORY   DISTURBANCES  OF  THE  STOMACH 

the  mouth  has  been  cleansed — is  allowed  to  stand,  a  sediment  forms  which 
in  more  than  fifty  examinations  of  this  kind  I  have  rarely  found  to  be 
higher  than  4  to  5  per  cent,  of  the  total  fluid.  This  sediment  consists 
almost  exclusively  of  mucus  flocculi  and  nuclei  of  leukocytes  whose  proto- 
plasmic ring  has  been  digested,  but  also  contains  esophageal  and  gastric 
epithelia  which  produce  the  turbidity.  Now  and  then  a  few  starch  granules 
are  noted,  their  amount  being  slight,  so  that  in  a  test-tube,  and  on  the 
addition  of  a  few  drops  of  Lugol's  solution,  the  sediment  in  pure  cases  does 
not  show  a  blue  color.  The  specific  gravity  of  the  filtrate  is,  as  a  rule, 
abnormally  low  (about  1.004  to  1.008).  The  addition  of  iodin  solution  to 
the  filtrate  produces  no  change  of  color.  Trommer's  test  is  also  negative, 
but  the  biuret  test  is,  as  a  rule,  positive.  Upon  polarization  a  rotation  to 
the  left  of  0.2-1.0  per  cent,  is  shown.  That  true  gastric  juice  must  con- 
tain hydrochloric  acid  is  self-evident;  the  values  for  total  acidity  and  for 
free  hydrochloric  acid,  however,  vary  greatly.  The  amount  of  combined 
hydrochloric  acid  is,  as  a  rule,  not  very  high,  and  the  amount  of  acid  phos- 
phates is  usually  less  than  in  a  trial  breakfast.  These  are  the  conditions, 
provided  there  is  simultaneously  no  obvious  motor  insufficiency.  When  this 
is  not  present  in  the  "  secretion  from  an  empty  stomach,"  we  find  no  sar- 
cinae  nor  sprouting  yeast,  and  in  the  incubation  oven  the  fermentation  test 
is  also  negative.  In  pure  cases  of  the  disease  we  find  these  conditions, 
immaterial  whether  the  stomach  has  been  thoroughly  washed  out  the  even- 
ing before  or  whether  we  have  limited  ourselves  to  prohibiting  the  patient 
from  taking  food  after  his  supper.  As  Riegel  emphasized,  and  as  I 
demonstrated  in  quite  a  number  of  cases  of  hypersecretion,  upon  introduc- 
ing the  stomach- tube  and  removing  the  contents  of  the  stomach  at  inter- 
vals of  an  hour  or  every  two  hours,  we  invariably  observe  a  decided  amount 
of  secretion  in  the  stomach  although  the  patient  in  question  has,  in  the 
meantime,  entirely  abstained  from  alimentary  stimulation. 


SYMPTOMS 

From  this  peculiarity  hypersecretion  is  accorded  a  special  clinical  posi- 
tion, as  is  its  due  also  in  a  clinico-symptomatologic  aspect,  because  the 
symptoms  which  bring  the  patient  to  the  physician  often  present  more  or 
less  uniformity.  The  patients  upon  prolonged  duration  of  the  disease  and 
in  spite  of  a  good  appetite  are  usually  emaciated  with  tissues  deficient  in 
fluid  (dry  skin!),  they  complain  of  gnawing  and  painful  sensations  in  the 
gastric  region  which  are  generally  persistent,  and — what  is  symptom atolog- 
ically  worthy  of  remark — these  are  present  both  night  and  morning,  and 
are  relieved  by  vomiting.  The  vomitus  itself  is  usually  a  thin  fluid,  of 
acid  taste,  and  often  without  admixture  of  food.  In  consequence  of  the 
loss  of  large  amounts  of  gastric  juice,  there  is,  as  a  rule,  thirst  and  con- 
stipation, and  the  urine  on  account  of  an  increas§  of  its  alkalinity  fre- 


HYPERSECRETION  115 

quently  shows  a  phosphate  sediment  (gastrogenous  phosphaturia) .  In 
typical  cases  the  test  breakfast  reveals  certain  peculiarities  which  are  con- 
spicuous to  the  expert.  There  is  a  large  amount  (400  c.c.  and  more)  of 
very  thin,  fluid,  stomach  contents  which  show  relatively  slight  sediment  (the 
layer  quotient  rarely  amounts  to  more  than  30  or  30  per  cent. ) .  The  sedi- 
ment has  an  extraordinarily  fine,  puree-like  appearance,  in  consequence  of 
the  excellent  amylorrhexis  due  to  prolonged  contact  of  the  gastric  contents 
and  gastric  juice.  The  trial  breakfast  generally  filters  very  rapidly,  and 
the  watery  filtrate  upon  addition  of  an  iodin  solution  (in  consequence  of 
disturbed  amylolysis)  usually  assumes  a  violet  or  more  or  less  bluish  color. 
The  values  for  total  acidity  and  for  free  hydrochloric  acid  vary.  Not  rarely 
— but  by  no  means  always — hyperacidity  is  present.  In  several  cases  of 
hypersecretion  with  simultaneous  disturbance  in  motility  I  have  noticed 
the  peculiar  circumstance  that  a  few  hours  after  the  ingestion  of  one-half 
to  one  liter  of  milk  into  a  stomach  which  was  previously  washed  clean,  an 
opalescent,  turbid  fluid  without  casein  flocculi  (which  are  otherwise  pres- 
ent but  here  are  digested  with  enormous  rapidity)  was  obtained  and  at  the 
upper  border  of  the  fluid  sometimes  a  thin,  at  other  times  a  thicker,  coat- 
ing of  cream  accumulated  so  that  a  well  developed  intermediary  layer  con- 
sisting of  fluid  and  fat  was  formed. 


DIAGNOSIS 

In  the  diagnosis  of  hypersecretion  the  introduction  of  the  stomach- 
tube  upon  an  empty  stomach  is  absolutely  necessary,  and  in  the  diagnostic 
judgment  of  the  contents  which  are  evacuated  from  the  empty  stomach  the 
constituents  of  the  secretion  which  have  here  been  described  are  important 
for  the  reason  that  the  "  residue "  of  the  empty  stomach  may  easily  be 
confounded  with  the  "  secretion  "  of  the  same.  The  finding  in  the  empty 
stomach  of  an  appreciable  "  residue "  which  constantly  shows  a  higher 
layer  quotient  than  that  of  the  "  secretion  "  from  the  empty  stomach,  is 
always  a  sign  of  motor  insufficiency.  In  those  cases  in  which  we  must 
decide  the  question  whether  pure  hypersecretion  or  hypersecretion  combined 
with  disturbance  of  motility  is  present,  I  advise  as  the  first  step  in  the 
differential  diagnosis  the  administration  of  a  teaspoonful  to  a  tablespoonful 
of  currants,  the  stomach  having  been  washed  out  the  evening  before,  also 
the  microscopic  examination  of  the  gastric  contents  for  micro-parasites, 
finally,  the  fermentation  test  conducted  in  an  incubation  oven.^     A  minute 

^  In  the  microscopic  examination  of  the  contents  of  the  stomach  in  cases  of 
hypersecretion  with  disturbance  of  motility,  at  a  time  when  it  should  have  been 
empty,  I  have  occasionally  found  a  remarkably  slight  amount  of  yeast  present,  and 
subsequently,  a  few  times,  chains  of  a  delicate,  thin,  elongated  variety  of  bacteria, 
as  well  as  once  distinct  fungi  mycelia  which  I  also  found  in  two  cases  of  subacidity, 
and  to  which  I  attach  no  particular  diagnostic  significance. 


116  SECRETORY   DISTURBANCES   OF  THE   STOMACH 

investigation  of  gastric  motility  by  the  objective  method  of  the  currant 
test,  and  microscopic  examination  and  fermentation  in  the  incubation  oven, 
appear  to  me  to  be  particularly  important  because  in  the  investigation  of 
cases  of  hypersecretion  the  proofs  whether  a  disturbance  in  motility  is 
present  or  absent  must  be  established.  This  differentiation  is  of  vital  im- 
portance for  the  clinical,  especially  for  the  theoretic,  conception  of  cases, 
much  more  so  than  the  otherwise  justifiable  classification  of  cases  of  hyper- 
secretion into  acute  or  chronic,  into  intermittent  or  relapsing,  forms. 


PATHOGENESIS 

Disputes  have  arisen  as  to  the  pathogenesis  of  hypersecretion.  The 
controversy  above  all  has  revolved  about  the  question  whether  every  case 
of  liypcrsGcretion  is  the  result  of  pyloric  stenosis  expressed  functionally 
or  whether  it  is  motor  insufficiency.  In  truth,  a  number  of  authors  look 
upon  hypersecretion  merely  as  a  retention  of  secretion  produced  by  motor 
insufficiency,  basing  their  views  upon  the  fact  that  the  finding  of  motor 
insufficiency  in  cases  of  hypersecretion  is  not  unusual,  but  even  very  fre- 
quent. Nevertheless,  various  authors  (Riegel,  Wilkens,  Martins,  Licht- 
lieim,  Gintl  and  others)  have  observed  undoubted  cases  of  chronic  hyper- 
secretion in  which  no  objective  symptoms  of  motor  insufficiency  could  be 
detected,  and  I  have  reported  two  cases  of  this  kind  which  led  me  to  look 
upon  hypersecretion  as  the  expression  of  a  chronic  irritative  condition  of 
tlie  secreting  parenchyma  in  the  etiology  of  which  various  factors  play 
a  part.  The  hypothesis  that  every  hypersecretion  is  a  simple  retention  of 
secretion,  therefore,  appears  to  me  to  be  insufficient,  because  other  authors 
as  well  as  I  have  observed  cases  of  motor  insufficiency  in  which,  after  the 
disturbance  in  motility  had  been  removed,  the  symptoms  of  hypersecretion 
persisted  for  days  and  weeks  before  they  disappeared,^  and  because  in  a 
series  of  researches  which  I  have  not  as  yet  published  I  demonstrated  (in 
contrast  to  Boas)  that  under  rectal  nutrition — therefore  when  local  stimu- 
lus from  the  stomach  contents  was  entirely  absent — ^the  amount  of  secre- 
tion obtained  from  the  empty  stomach  was  just  as  profuse  as  during  the 
time  wlien  food  was  introduced  by  mouth.  For  this  reason  I  consider  the 
nature  of  continuous  hypersecretion  to  be  a  persistent  irritability  of  the 
secreting  parenchyma  which  itself  may  be  due  to  a  number  of  causes,  among 
otliers  the  irritation  of  stagnant  masses  of  food.  However,  as  Riegel  has 
emphasized  there  is  in  the  latter  a  disproportion  between  the  amount  of 
irritation  and  the  amount  of  secretion,  therefore  a  special  irritability  of 

^  Tliat  such  an  irritation  of  the  parenchyma  may  exist  for  some  weeks  after  a 
successful  gastroenterostomy  I  recently  saw  proven  by  the  cure  of  a  case  of  motor 
insufficiency  due  to  perigastritis,  which  should  be  of  deep  interest  because  the  peri- 
gastritis was  the  consequence  of  a  laparotomy  performed  to  recover  a  stomach-tube 
which  liad  been  swallowed  by  the  patient   (not  while  in  the  hospital). 


HYPERSECRETION  117 

the  secreting  parenchyma  must  be  presupposed  if  the  symptoms  of  hyper- 
secretion become  prominent.  In  regard  to  the  etiologic  importance  of 
spasm  of  the  pylorus  which  is  occasionally  observed  in  ulcer  of  the  stomach 
— not  rare  in  chronic  hypersecretion — I  limit  myself  to  the  remark  that 
such  spasms  of  the  pylorus,  under  some  conditions,  may  certainly  lead 
to  a  retention  of  secretion  in  the  stomach  free  from  food,  namely,  if  they 
have  begun  during  a  time  in  which  the  stomach  contained  no  food.  With 
the  exception  of  ulcer  of  the  stomach,  which  is  frequent  in  hypersecretion, 
the  pathologic  anatomy  of  cases  of  hypersecretion  has  as  yet  taught  us 
little  regarding  the  pathogenesis  of  this  morbid  condition;  for,  in  so  far 
as  exact  investigation  of  the  various  areas  of  the  stomach  is  concerned,  the 
number  of  cases  studied  is  quite  scant.  In  a  case  reported  by  Myer  and 
myself  a  few  years  ago  there  was  but  slight  tortuosity  and  dissemination 
of  the  glands,  also  but  slight  change  in  the  interstitial  tissue.  These  find- 
ings were  absent  in  a  second  case  which  I  clinically  observed.  The  litera- 
ture, too,  of  the  anatomical  findings  in  cases  of  hypersecretion,  which  I 
cannot  here  describe,  is  contradictory.  Nevertheless,  in  discussing  the 
anatomy,  I  cannot  refrain  from  stating  that  in  cases  of  hypersecretion  I 
have  repeatedly  observed  gastroptosis,  which,  however,  was  usually  the 
mechanical  consequence  of  habitual  overloading  of  the  stomach  with  secre- 
tion, and  also  that,  in  those  cases  of  hypersecretion  in  which  an  ulcer  of 
the  stomach  existed,  a  permanent  secretory  irritation  was  perhaps  due  to 
the  fact  that  exposed  nerves  upon  the  floor  of  the  ulcer  were  irritated  by 
the  gastric  contents  or  the  gastric  juice,  and  this,  perhaps,  produced  inflam- 
matory changes.  Of  the  neurogenous  type  of  hypersecretion  those  cases 
observed  during  gastric  crises  are  the  best  examples.  To-day,  when  we 
have  learned  from  Pawlow's  classical  investigations  to  appreciate  the  rela- 
tion of  the  nervous  system  to  the  secretion  of  the  gastric  juice,  it  hardly 
appears  remarkable  that  hypersecretion  may  be  of  neurogenic  origin.  It 
is  interesting,  too,  to  note  that  hypersecretion  is  chiefly  a  disease  of  middle 
life,  that  it  occurs  more  often  in  men  than  in  women,  and  that  it  is  more 
frequent  in  countries  in  which  ulcer  and  hyperacidity  are  common  than  in 
other  regions. 

TREATMENT 

The  treatment  of  hypersecretion,  primarily,  is  identical  with  the  treat- 
ment of  the  underlying  cause.  Where  there  is  a  disturbance  in  motility, 
this  must  be  combated  with  all  the  measures  at  our  command.  In  those 
cases  in  which  no  disturbance  of  motility  exists — which  are  decidedly  the 
rarer — all  the  points  come  into  question  which  have  already  been  described 
under  the  treatment  of  hyperacidity,  and  here  the  plentiful  administration 
of  fat  appears  to  be  in  order,  since  other  authors,  as  well  as  I,  have  seen 
improvement  and  even  cure  follow  its  use  in  cases  of  hypersecretion.  Con- 
centrated solutions  of  sugar  must  be  avoided,  because  the  stomach  in  hj^er- 


118  SECRETORY   DISTURBANCES   OF  THE   STOMACH 

secretion,  in  consequence  of  habitual  overloading  with  secretion,  already 
has  a  tendency  to  myoparesis.  The  latter  factor,  in  combination  with  our 
purpose  of  frequently  introducing  acid-combining  material  into  the  stom- 
ach, shows  the  wisdom  of  administering  small  and  frequent  meals.  For 
several  reasons,  those  substances  which  increase  the  secretion  of  the  gastric 
juice  should  not  be  employed  as  food.  Alkalies  are  advisable  when  a  hyper- 
acid secretion  causes  spasm  of  the  pylorus,  as  in  the  case  of  hyperacidity. 
Frequently,  however,  the  pains  are  mitigated  by  the  administration  of  other 
acid-combining  substances,  for  example,  eggs  or  milk.  In  the  general  diet, 
the  amount  of  albuminous  food,  on  account  of  the  acid-combining  proper- 
ties of  the  albumin,  should  not  be  too  small.  If  the  palliative  measures 
Just  mentioned  are  not  sufficient,  amelioration  may  often  be  produced  by 
the  subcutaneous  administration  of  atropin,  and  Reichmann  advises  also 
the  internal  administration  of  not  too  minute  doses  of  silver  nitrate.  In 
well  developed  cases  of  long  duration  we  cannot  get  along  without  the 
introduction  of  the  stomach-tube,  which  serves  a  particularly  useful  pur- 
pose in  evacuating  the  surplus  amount  of  secretion  present  at  an  improper 
time.  Lavage  of  the  stomach  with  water  is  only  necessary  when  there  is 
simultaneous  disturbance  of  motility.  When  this  becomes  expedient,  Rie- 
gel  advises  the  use  of  an  alkaline  water,  and  Rosenheim,  as  well  as  Rost, 
praises  irrigations  with  a  1-1000  solution  of  silver  nitrate.  Only  when 
the  measures  that  have  been  described  prove  inadequate,  and  absolute  rest 
of  the  stomach  for  some  time  by  rectal  alimentation  is  ineffectual,  does 
gastroenterostomy  come  into  question.  In  those  cases  in  which  there  is 
no  disturbance  in  motility  this  operation  has  a  curative  effect  by  promoting 
the  discharge  from  the  stomach  of  irritating  and  burdensome  secretions 
which  prevent  the  healing  of  wounds  that  may  be  present,  and  by  prevent- 
ing the  vomiting  of  food  and  gastric  juice  protects  the  patient  from  under- 
nutrition and  losses  of  chlorin.  In  some  cases  the  treatment  must  also 
take  into  consideration  the  consequences  of  hypersecretion,  for  example, 
the  gastroptosis,  as  well  as  the  general  loss  or  general  dryness  of  tissue, 
but  this  is  not  the  place  in  which  to  outline  the  treatment  of  these  special 
pathologic  conditions. 

In  reviewing  what  is  here  stated  of  the  diagnosis  and  treatment  of 
secretory  disturbances  of  the  stomach,  the  conclusion  will  be  reached  that 
the  last  quarter  of  the  preceding  century,  in  particular,  has  very  materially 
added  to  our  knowledge  of  these  affections  and  broadened  our  sphere  of 
action.  Our  present  methods  have  been  built  upon  a  firm  foundation, 
which  may  be  more  readily  reviewed  than  was  formerly  the  case.  This 
development  of  an  important  diagnostic  and  therapeutic  branch  of  gastric 
])athology  is  due  not  only  to  a  generally  recognized  impetus  given  to  medi- 
cine in  the  second  half  of  the  preceding  century,  to  the  methods  of  research 
and  the  exact  results  of  scientific  investigations,  but,  above  all,  to  the 


SUPPLEMENT  119 

acumen  and  well-directed,  energetic  labors  of  those  men  who  have  made 
the  stomach-tube  the  common  property  of  the  clinic  and  the  practising 
physician  (Kussmaul,  v.  Leube  and  others).  The  introduction  of  the 
stomach-tube,  and  particularly  the  introduction  of  the  soft  stomach-tube 
into  medical  practice — due  to  Ewald — was  an  event  of  almost  historic 
importance,  as  is  pointed  out  in  another  article  in  this  volume.  To  ac- 
knowledge this,  and  to  express  it,  can  nowhere  be  more  fitting  than  in  con- 
cluding a  description  of  a  branch  of  medicine  in  which  accurate  knowledge 
and  full  comprehension  have  been  made  possible  only  by  the  use  of  the 
stomach-tube. 

SUPPLEMENT 

In  this  article  on  the  analysis  of  clinical  symptoms  of  individual  secre- 
tory disturbances,  it  has  been  repeatedly  intimated  that  an  actual  relation 
between  definite,  clinical  symptom-complexes  and  definite  disturbances  of 
secretion  cannot  always  be  demonstrated.  Therefore,  it  is  still  a  mooted 
question  in  which  cases  the  practitioner  is  justified  in  making  an  exact 
investigation  of  the  gastric  juice  secretion  by  evacuating  the  gastric  con- 
tents. This  question  can  only  be  answered  in  a  general  way  by  the  state- 
ment that  a  test  of  the  gastric  contents  appears  to  be  indicated  in  all  those 
cases  in  which,  without  such  examination,  the  diagnosis  remains  uncertain, 
and  in  which  there  are  contraindications  (in  regard  to  this  point  see  the 
article  by  Fleiner,  pages  48  and  49)  to  the  introduction  of  the  gastric 
tube.  As  nothing  of  importance  in  the  macroscopic  investigation  of  the 
contents  removed  from  the  stomach  can  here  be  added  to  what  was  men- 
tioned in  the  preceding  articles,  the  method  of  chemical  examination  shall 
be  briefly  described :  In  each  individual  case  we  begin  with  dipping  a  piece 
of  Congo  paper  in  the  filtered  (and  also  in  the  non-filtered)  gastric  con- 
tents. The  result  of  this  examination  indicates  what  further  steps  are 
to  be  taken  in  the  investigation,  since,  according  to  what  was  said  in  the 
preceding  article,  if  free  hydrochloric  acid  is  absent  we  ascertain  by  test- 
ing with  litmus  paper  whether  the  gastric  contents  have  an  acid  reaction, 
and,  if  this  be  the  case,  we  examine  for  lactic  acid.  For  the  latter  pur- 
pose I  advise  my  modification  of  Uffelmann's  process,  since  only  pathologic 
amounts  of  lactic  acid  can  be  demonstrated  after  a  test  breakfast.  This 
is  carried  out  by  using  a  graduated  test-tube  specially  constructed  for  this 
purpose,  which  may  be  shaken,  so  that  5  c.c.  of  filtered  gastric  contents 
are  shaken  up  with  20  c.c.  of  ether;  the  gastric  juice  and  15  c.c.  of 
ethereal  extract  are  allowed  to  flow  off,  and  the  remaining  5  c.c.  of  ethereal 
extract  with  20  c.c.  of  water  are  shaken  up  with  2  drops, of  a  1  per  cent, 
iron  chlorid  solution  (liquor  ferri  sesquichlorati,  1-10).  If  lactic  acid  is 
present  in  a  proportion  of  5  to  1000  or  more,  the  water  turns  decidedly 
green.  If  any  doubt  exists  in  regard  to  the  lactic  acid  test,  it  is  always 
advisable  to  investigate  the  gastric  contents  microscopically  for  an  increase 


120  SECRETORY   DISTURBANCES   OF  THE   STOMACH 

of  bacteria,  especially  the  long  bacteria  commonly  found  therein.  In  those 
cases  in  which  we  are  unable  to  obtain  much  material  with  the  stomach- 
tube,  the  latter  process  should  never  be  omitted,  because  the  microscopic 
finding  of  numerous  long  bacteria  in  the  gastric  contents,  as  well  as  the 
presence  or  absence  of  the  protoplasmic  ring  of  leukocytes  in  those  cases 
in  which  a  chemical  examination  of  the  gastric  contents  cannot  be  made 
for  want  of  sufficient  material,  may  give  us  valuable  information  concern- 
ing tlic  gastric  juice  secretions. 

The  total  acidity  is  ascertained  by  the  method  Prof.  Leo  described  in 
his  article  (which  see),  and  phenolphthalein  is  generally  used.  When  we 
suspect  apepsia  this  may  be  advantageously  supplemented  by  a  compara- 
tive titration  with  tincture  of  cochineal  (or  with  tincture  of  litmus).  In 
tlie  few  cases  in  which  we  desire  to  determine  the  combined  HCl,  Leo's 
method  is  advisable.  If,  for  any  reason,  we  wish  to  ascertain  the  quantita- 
tive amount  of  free  hydrochloric  acid,  a  few  drops  of  a  one-half  per  cent. 
alcoliolic  solution  of  dimethylamidoazobenzol  is  added  to  a  measured  quan- 
tity (10  c.c.)  of  filtered  gastric  contents  and  titrated  with  a  decinormal 
solution  of  soda  until  the  red  color  disappears;  or  we  may  use  the  dipping 
method  with  Congo  paper.  When  employing  the  latter  the  platinum  loop 
is  advised  for  withdrawing  small  amounts  (Ewald),  and  the  best  way  of 
proceeding  is  to  compare  the  drop  taken  from  the  gastric  contents  with  a 
drop  of  water  of  the  same  size  placed  upon  Congo  paper.  In  case  Linos- 
siers  reagent  is  not  used  from  the  onset  (dimethylamidoazobenzol  0.25, 
phenolphthalein  2.0,  alcohol  100.0),  after  the  amount  of  free  hydrochloric 
acid  has  been  obtained  a  few  drops  of  an  alcoholic  solution  of  phenol- 
phtlialein  is  added,  and  the  total  acidity  is  determined  by  the  same  test. 

Mett's  process  for  the  quantitative  estimation  of  pepsin,  which  may 
under  some  circumstances  be  of  practical  use  in  the  diagnosis  of  apepsia 
gastrica  or  for  the  topical  diagnosis  of  gastric  carcinoma,  is  best  carried 
out  in  daily  practice  in  the  following  way:  10  c.c.  of  the  filtered  anacid  or 
subacid  gastric  contents,  to  which  one  c.c.  of  a  2  per  cent,  solution  of  hydro- 
cliloric  acid  which  is  kept  on  hand  should  be  added,  are  placed  in  a  small 
ghiss  l)ottIe  with  a  beveled  cover,  or  in  some  other  low  and  proportionately 
wide  ghiss  vessel  closed  with  a  glass  stopper.  With  an  albumin  tube, 
]irej)are(l  according  to  the  method  described  upon  page  92,  well  washed 
for  iM  hours  before  use,  and  with  the  aid  of  a  magnifying  glass,  we  deter- 
mine the  total  amount  of  albumin  digested  during  this  time.  According 
to  my  experience  (and  when  the  test  is  made  in  the  manner  described),  in 
the  normal  person  this  rarely  amounts  to  less  than  5  mm.,  sometimes,  how- 
ever, to  decidedly  more  (occasionally  to  double  this  amount).  Schorlem- 
mer  (Arrhiv  fur  Verdauungsl-rankheiien,  Bd.  VIII,  Heft  3  und  4)  has  re- 
c(>ntly  advised  an  ingenious  modification  of  Mett's  method  of  examination, 
hut  it  would  be  Avell  first  to  decide  by  comparative  investigations  whether 
the  additions  to  improve  the  process  are  absolutely  necessary  in  daily  prac- 


SUPPLEMENT  121 

tice.  The  dilution  recently  proposed  by  Nirenstein  and  Schiff  (Archiv 
fur  Verdauungskrankheiten,  Bd.  VIII,  Heft  6)  with  a  l-20th  normal 
hydrochloric  acid  solution  in  the  proportion  of  1  to  16  for  those  cases  in 
which  we  have  pronounced  the  estimations  of  pepsin  as  valuable — cases  of 
extreme  subacidity — is  unnecessary,  as  in  these  cases,  particularly,  the 
results  of  the  diluted  and  non-diluted  test  appear  to  be  almost  exactly  alike. 

The  estimation  of  lab-zymogen  in  accordance  with  the  method  proposed 
by  Boas  is  best  made  in  the  following  manner:  2  c.c.  of  gastric  juice  (with 
high-graded  secretory  insufficiency  a  neutralization  of  the  acid  by  alkalies 
is  only  necessary  when  lactic  acid  is  present  and — to  prevent  a  greater  dilu- 
tion— this  is  best  done  with  a  normal,  not  a  decinormal,  soda  solution)  are 
placed  in  a  small  measuring  glass  and  diluted  with  8  c.c.  of  water  and 
5  c.c.  of  milk  (this  must  not  be  of  acid  reaction)  mixed  in  a  test-tube 
(dilution  of  1  to  10).  The  remaining  5  c.c.  are  mixed  with  5  c.c.  of  water 
so  as  to  produce  10  c.c,  and  5  c.c.  of  this  mixture  are  added  to  5  c.c.  of 
milk  (dilution  of  1  to  30).  The  5  c.c.  remaining  from  this  test  are  added 
as  before  to  5  c.c.  of  water,  and  one-half  of  this  is  poured  ofiE  and  mixed 
with  5  c.c.  of  milk  (dilution  of  1  to  40).  By  repeating  this  process  we 
produce  dilutions  of  1  to  80,  1  to  160,  and  1  to  320.  After  the  addition 
to  each  of  one  c.c.  of  a  one  per  cent,  calcium  chlorid  solution,  the  entire 
series  is  placed  in  the  incubation  oven,  heated  to  37°  C,  and  allowed  to 
remain  for  half  an  hour.  Under  these  conditions  the  filtrate  from  a  stom- 
ach which  functions  normally  will  coagulate  milk  in  a  dilution  of  1  to  80 
or  even  1  to  160.  Glassner  (Berliner  klin.  Wochenschr.,  1902,  Nr.  29), 
reports  that  the  normal  amount  of  lab-ferment  in  the  gastric  juice  obtained 
by  a  test  breakfast  is  1  to  100,  i.  e.,  0.1  c.c.  of  neutralized  gastric  juice 
will,  within  half  an  hour,  caseate  10  c.c.  of  milk  at  a  temperature  of 
30°  to  40°  C. 

For  further  details  of  the  methods  of  examination,  the  reader  is  referred 
to  recent  text-books  upon  the  diagnosis  and  therapy  of  gastric  diseases, 
especially  to  those  of  Boas,  Ewald,  Fleiner,  Eiegel,  and  Rosenheim,  as  well 
as  to  the  text-books  upon  microscopico-chemical  diagnosis  by  v.  Jaksch, 
Lenhartz  and  others.  A  critical  compilation  of  the  literature  up  to  the 
year  1892  concerning  the  various  methods  of  examination  of  the  gastric 
juice  is  found  in  the  monograph  by  Martius-Liittke :  "  Die  Magensaure  des 
Menschen,"  Stuttgart,  F.  Enke,  1892. 


\ 


DIAGNOSIS    AND    TREATMENT    OF    GASTRIC 

DILATATION 

By  F.  RIEGEL,  Giessen 

CLINICAL    FORMS 

When  a  patient  presents  himself  to  us  and  states  that  he  suffers  from 
frequent  vomiting  of  large  residua  of  food,  and  that  he  repeatedly  finds 
remains  of  food  that  he  had  consumed  several  days  before,  when,  upon 
examination  of  the  patient,  the  lower  boundary  of  the  stomach  is  found 
below  the  umbilicus  with  an  approximate  normal  position  of  the  upper, 
and  when,  throughout  this  entire  region,  a  loud  succussion  sound  can  be 
produced,  the  suspicion  of  dilatation  of  the  stomach  is  obvious.  If,  in 
such  a  case,  seven  hours  after  a  test-meal,  profuse  quantities,  a  liter  or 
more,  are  evacuated  from  the  organ,  and  if  an  ev^uation  in  the  morning 
upon  a  presumably  empty  stomach  shows  profuse  remains,  we  speak  of 
gastric  dilatation,  or  gastrectasis. 

Two  factors  are  necessary  for  the  diagnosis  of  gastric  dilatation — a 
decided  increase  in  the  size  of  the  organ  and  an  insufficient  motor  activity, 
a  so-called  motor  insufficiency. 

I  do  not  agree  with  those  modern  investigators  who  recently  have  re- 
peatedly declared  that  the  terms  "  ectasis  "  and  "  dilatation  of  the  stomach  " 
are  no  longer  expressive  of  present  scientific  views,  if  they  intend  to  elim- 
inate the  term  "  gastric  dilatation  "  from  pathology,  and  to  put  in  its 
place  "  mechanical  insufficiency,  myasthenia  gastrica,  ichochymia,  motor 
gastric  debility "  or  the  like,  which  denote  exclusively  insufficient  motor 
activity.  These  authors  are  certainly  correct  when  they  declare  that  the 
size  of  the  stomach  is  no  measure  of  its  motor  activity.  A  stomach  may 
l)C  larger  than  normal,  yet,  notwithstanding,  have  sufficient  motor  power, 
niul  aiiotbcr  stomach  may  be  well  within  the  usual  physiologic  limits,  and, 
Tiovertheless,  show  motor  insufficiency.  Boas  is,  therefore,  certainly  right 
when  lie  says  that  we  drift  from  a  positive  foundation  in  diagnosis  when  we 
make  the  limits  and  size  of  the  stomach  a  criterion  in  deciding  upon  an 
existing  gastric  dilatation.  But  no  conscientious  physician  will  to-day 
diagnosticate  gastric  dilatation  upon  the  basis  alone  of  a  large  extension  of 
the  gastric  limits. 

The  stomach  may  have  suffered  in  its  elasticity,  may  be  more  distensi- 
ble, yet,  nevertheless,  still  be  capable  of  propelling  its  contents  at  the  proper 
122 


CLINICAL  FORMS  123 

time.  If  such  a  stomach  be  inflated  with  air  or  carbonic  acid,  it  reaches 
far  beyond  the  normal  limits ;  such  a  stomach  is  abnormally  elastic ;  never- 
theless, it  may  be  able  to  propel  the  ingesta  at  the  right  time  like  a  normal 
stomach.     This  condition  is  designated  megalogastria. 

Such  cases  are  discovered  purely  by  accident;  for  megalogastria,  as 
such,  does  not  give  rise  to  symptoms.  The  conception  of  ectasis  demands 
more  than  an  increase  of  size,  more  than  abnormal  elasticity;  above  all, 
it  is  necessary  that  the  stomach  should  be  unable  to  propel  its  contents  at 
the  proper  time,  that  during  the  long  period  in  which  a  normal  stomach 
receives  no  food,  more  or  less  profuse  contents  are  still  within  its  walls. 

We  are  forced  to  admit  that  the  designation  "gastric  dilatation"  pri- 
marily implies  only  a  larger  extent  of  space.  Nevertheless,  this  same  term 
"  dilatation,"  in  a  certain  sense,  also  indicates  a  condition  of  motor  insuSi- 
ciency,  for,  from  what  other  cause  has  the  patient  with  gastrectasis  a  dilated 
stomach,  wherein  is  the  root  of  his  difficulties  except  in  this,  that  the 
stomach  is  incapable  of  propelling  its  contents,  and  is,  therefore,  constantly 
overfilled !  Even  the  older  physicians  in  their  conception  of  gastric  dilata- 
tion not  only  held  the  view  of  an  abnormally  large  extension,  but  also  that 
the  stomach  lacked  the  power  of  timely  propulsion  of  its  contents.  That 
stomach  alone  is  permanently  dilated  which  cannot  empty  itself  at  normal 
periods. 

If  this  view  of  gastric  dilatation  be  accepted — and  formerly  it  was  uni- 
versal— there  is  absolutely  no  reason  for  discarding  the  old,  established 
designation  "  gastric  dilatation."  It  is  true  that  the  determination  of  the 
size  of  the  stomach  alone  is  not  sufficient,  it  is  also  necessary  to  ascertain 
the  motor  activity  of  the  dilated  organ.  At  the  bedside  it  is  never  satis- 
factory to  determine  the  physical  changes  only  of  the  diseased  organ;  we 
must  also  picture  to  ourselves  the  disturbed  function. 

Similarly,  we  speak  of  a  dilatation  of  the  heart ;  but  as,  in  the  heart, 
the  determination  merely  of  an  increase  in  size  is  not  sufficient,  so,  in  every 
case,  we  study  the  effect  of  this  dilatation  upon  the  circulation,  both  in 
the  arterial  and  venous  system,  since  increase  in  size  is  by  no  means 
always  of  like  importance;  this  is  also  true  of  the  stomach.  In  the  con- 
ception of  dilatation,  a  decrease  in  the  motor  power  is  included  as  well  as 
increase  of  size.  At  the  onset,  however,  it  is  clear  that  it  makes  a  decided 
difference  whether  a  stomach  shows  only  decreased  motor  power,  or  whether 
it  simultaneously  shows  a  decided  and  permanent  increase  in  size. 

It  must  be  admitted  that  formerly  the  error  was  frequently  made  of 
diagnosticating  gastric  dilatation  solely  because  of  an  increase  in  size. 
But  to-day  no  conscientious  physician,  upon  suspicion  of  gastric  dilata- 
tion, will  limit  himself  only  to  determining  the  boundaries  of  the  stomach. 
This  would  be  Just  as  one-sided  and  wrong  as  to  make  a  diagnosis  of  gas- 
tric disease  from  the  determination  of  the  acidity  alone,  or  to  diagnosticate 
carcinoma  from  the  absence  of  free  hydrochloric  acid  alone.     The  increase 


124         DIAGNOSIS   AND  TREATMENT   OF   GASTRIC   DILATATION 

in  size  primarily  awakens  the  suspicion  of  dilatation,  but  this  is  insuffi- 
cient warrant  for  a  diagnosis. 

When  there  is  a  decided  distention  of  the  stomach  combined  with  sub- 
jective symptoms,  the  physician  should  not  neglect  to  introduce  the  stomach- 
tube,  to  determine  the  functions  of  the  stomach  in  regard  to  motion  and 
secretion. 

The  name  "  motor  insufficiency  "  indicates  only  a  disturbance  in  func- 
tion which  may  occur  in  the  most  varied  diseases,  and  is  manifest  when 
the  gastric  contents  are  not  expelled  at  the  proper  time.  This  may  occur 
in  a  dilated  stomach,  in  a  normal  one,  and  even  in  a  stomach  decreased  in 
size.  The  designation  "  motor  insufficiency  "  in  place  of  "  dilatation  "  can- 
not be  regarded  as  correct,  for  the  reason  that  motor  insufficiency  is  possi- 
ble without  any  enlargement  of  the  stomach.  It  is,  however,  a  matter  of 
consequence,  whether,  in  the  given  case,  the  motor  insufficiency  has  led 
to  a  permanent  abnormal  distention  of  the  stomach  or  not,  but  only  in  the 
latter  case  do  we  speak  of  dilatation. 

Atony  is  a  special  form  of  motor  insufficiency.  By  this  we  mean  a 
condition  in  which  the  tonus  of  the  gastric  musculature  is  diminished,  in 
consequence  of  which  there  is  delay  in  propelling  its  contents,  without  the 
boundaries  of  the  stomach  having  exceeded  their  normal  limits.  Atony 
may  lead  to  dilatation,  but  need  not  necessarily.  When  the  latter  is  the 
case,  we  speak  of  atonic  dilatation.  The  atonic  stomach  propels  the  gastric 
contents  more  slowly  than  is  normal,  but  does  finally  propel  them. 

We  must,  therefore,  differentiate  between  motor  insufficiency,  atony  (a 
special  variety  of  motor  insufficiency),  and  dilatation.  Megalogastria  does 
not  here  come  into  question. 

Before  proceeding  to  the  clinical  picture  of  dilatation — and  I  purposely 
speak  of  the  clinical  picture  of  dilatation,  and  not  of  the  disease  "  eotasis," 
for  it  is  not  a  disease,  sui  generis — I  thought  it  necessary  to  explain  the 
conception  of  the  term.  On  this  point,  as  a  glance  at  the  literature  of 
recent  years  will  show,  there  is  a  great  difference  of  opinion.^ 

An  attempt  has  been  made  to  substitute  a  different  designation  for  the 
term  in  general  use,  "  dilatation."  If  the  conception  "  gastric  dilatation  " 
is  considered  in  the  above  mentioned  sense,  there  is  no  reason  for  the 
introduction  of  new  terms,  as  they  have  no  advantage  over  the  old.  Natur- 
ally, in  determining  a  dilatation  we  must  not  limit  ourselves  to  the  mere 
estimation  of  the  size,  but  we  must  endeavor  to  investigate  the  intensity 
of  the  disturbance  in  function  in  connection  therewith. 

There  are  varying  degrees  in  the  nature  of  the  clinical  picture  which 
we  designate  by  the  term  "  ectasis,"  but  no  well-defined  limit  from  which 
we  may  speak  of  dilatation  and  from  which  we  should  speak  of  motor 

'  1  refer  particularly  to  Hesse,  "  The  Conception  of,  and  the  Term,  '  Gastric  Dilata- 
tion.' in  German  Literature  since  1875."  Berliner  klin.  Wochenschr.  1900,  Nos.  23 
,uid  2-4. 


CLINICAL   FORMS  125 

insufficiency  and  atony.  The  diagnosis  of  gastric  dilatation  is  easy  when 
the  stomach  permanently  contains  decided  residue  of  food,  and  when  its 
boundaries,  therefore,  far  exceed  the  normal  limits.  In  milder  cases  the 
condition  is  different. 

No  stomach,  not  even  a  normal  one,  constantly  shows  the  same  dis- 
tention ;  its  boundaries  vary,  we  may  almost  say  hourly.  The  same  is  true 
of  the  dilated  stomach,  and  also  of  the  stomach  with  motor  insufficiency, 
which,  although  it  finally  expels  the  ingesta,  does  this  decidedly  more 
slowly  than  the  normal  organ.  The  stomach  with  motor  insufficiency  is 
relatively  dilated  in  so  far  that  it  still  retains  ingesta  at  a  time  when  a 
normal  stomach  has  already  expelled  it. 

In  this  sense  we  speak  of  relative  dilatation  if  a  stomach,  seven  hours 
after  a  test-meal,  still  contains  considerable  remains  of  food,  while  its  limits 
do  not  exceed  the  normal  boundaries.  For,  at  this  time,  the  stomach  should 
be  empty  and  markedly  contracted.  In  such  cases  we  do  not  make  a  diag- 
nosis of  gastric  dilatation,  but  only  when  the  lower  and  lateral  borders  of 
the  stomach  permanently  exceed  the  normal  boundaries,  and  when  the 
stomach  permanently  retains  ingesta.  In  spite  of  this,  in  the  first  men- 
tioned case,  there  is  a  relative  and  temporary  increase  in  size,  and  there 
can  be  no  doubt  that,  upon  prolonged  duration  and  long-continued  action 
of  these  deleterious  causes  in  such  a  dilated  stomach,  true  dilatation  may 
gradually  develop. 

It  is,  therefore,  evident  that  there  is  no  sharp  dividing  line  between 
dilatation  and  motor  insufficiency.  Dilatation  naturally  includes  motor 
insufficiency,  for  the  stomach  can  only  be  dilated  when  its  contents  are  not 
entirely  expelled  at  the  right  time.  Every  true  dilatation,  therefore,  must 
be  accompanied  by  motor  insufficiency ;  but  not  every  insufficiency  need  lead 
to  true  ectasis.  It  is  obvious,  therefore,  that  in  discussing  dilatation  we 
also  consider  motor  insufficiency  and  atony.  • 

As  to  the  causes  of  dilatation,  it  must  be  remembered  that  this  can  only 
develop  upon  a  basis  of  motor  insufficiency.  If  the  stomach  cannot  dis- 
charge its  contents  fully  and  at  the  proper  time,  it  must  be  distended  longer 
than  is  normal,  it  n^ust  remain  abnormally  weighted.  Gradually,  decided 
distention  occurs,  and,  finally,  true  ectasis. 

Motor  insufficiency  can  only  arise  where  there  is  a  disproportion  be- 
tween requisite  labor  and  the  capacity  for  labor,  where  requisite  labor  and 
power  of  labor  no  longer,  as  in  the  norm,  maintain  an  equilibrium.  When 
the  motor  power  of  the  stomach  is  no  longer  commensurate  with  the  de- 
mands made  upon  it,  the  work  is  only  imperfectly  done  or  after  a  long 
period ;  i.  e.,  the  stomach  will  expel  the  ingesta  only  partially  or  after  a  pro- 
longed period  of  time.  The  causes  of  this  diminished  motor  activity  are 
various,  and  may  be  expressed  as  follows :  1.  The  amount  to  be  propelled  is 
abnormally  large,  as,  for  example,  in  acute,  or  prolonged,  or  frequently  re- 
peated over-distention  of  the  stomach;  2.  The  expelling  power,  the  muscular 


126         DIAGNOSIS   AND  TREATMENT   OF   GASTRIC   DILATATION 

power  of  the  stomach,  is  deficient ;  3.  There  is  an  abnormal  resistance  to  the 
expulsion  of  the  ingesta  from  the  stomach. 

While,  in  the  group  first  mentioned,  we  are  dealing  with  a  direct  dam- 
age or  diminution  of  the  motor  power,  in  the  third  group,  that  of  mechan- 
ical hindrance  to  the  expulsion  of  the  ingesta,  we  often  find  the  muscular 
power  increased,  the  muscularis  even  hypertrophic  the  same  as  in  stenosis 
of  a  valve  of  the  heart,  that  portion  of  the  heart  anterior  to  the  stenosis 
is  not  only  dilated  but,  at  the  same  time,  it  becomes  hypertrophic.  Never- 
theless, it  is  incapable  of  increased  labor.  This  group  represents  by  far 
the  greatest  number  of  dilatations,  and  includes  the  stenoses  of  the  pylorus 
and  its  surroundings. 

Much  rarer  is  insufficiency,  the  atony  and  atonic  dilatation  which  go 
hand  in  hand  with  flaccidity  of  the  muscularis.  Moderate  degrees  of  atony 
are  not  rare.  Such  an  atony  may  arise  when  the  stomach  either  temporarily 
or  for  a  long  time  has  an  unusual  amount  of  work  to  perform.  Thus,  we 
see  atony  as  an  accompanying  symptom  of  various  affections  of  the  stomach. 
We  observe  it  particularly  after  acute  distention  of  the  stomach  with  food 
difficult  to  digest,  we  see  it  in  persons  who  eat  hurriedly  and  abundantly, 
and  chew  their  food  insufficiently.  True  dilatation  may  arise  in  conse- 
quence of  such  over-distention ;  in  children,  particularly,  acute  dilatation 
not  rarely  occurs  in  this  manner.  Occasionally  it  increases  to  an  extreme, 
and  not  seldom  such  acute  dilatations  have  a  lethal  outcome.  In  the  latter 
case,  other  factors  besides  an  acute  distention  of  the  stomach  may  play  a 
role.  Thus  Kussmaul  ^  many  years  ago  called  attention  to  the  fact  that 
in  gastric  dilatation  all  the  symptoms  of  complete  closure  may  occasionally 
appear  and  continue  until  large  amounts  of  the  stomach  contents  are  ex- 
pelled by  vomiting  or  by  lavage. 

As  Kussmaul  pointed  out,  such  cases  cannot  be  due  to  a  paralysis  of 
the  muscular  wall*  by  immoderate  distention,  for  peristalsis  of  the  stomach 
is  seen  to  be  markedly  active  when  the  stomach  contents  can  no  longer  be 
propelled.  Kussmaul  believes  that  in  cases  of  this  kind  a  narrowing  from 
tug  and  tension  occurs  at  the  point  where  the  horizontal  portion  of  the 
duodenum  leads  into  the  vertically  fixed  part  at  the  vertebral  column. 

This  conception  of  the  combined  action  of  a  mechanical  hindrance  has 
gained  decided  support  by  the  recent  investigations  of  Albrecht  ^  regard- 
ing "  Arterio-Mesenteric  Intestinal  Occlusion  at  the  Duodenal  Jejunal 
Boundary  and  its  Causal  Eelation  to  Gastrectasis."  Albrecht  has  proven 
that  the  cases  of  acute  gastric  dilatation,  above  all  with  symptoms  of  ileus 
(intestinal  obstruction),  often  have  their  origin  in  an  arterio-mesenteric 
invagination  of  the  inferior  transverse  portion  of  the  duodenum,  in  that  the 
stomach,  as  it  dilates  more  and  more,  forces  the  transverse  colon  and  the 

' "  Peristaltic  Unrest  of  the  Stomach."     Yolkmann's  Sdmml.  klin.  Vortr.  Nr.  181. 
2  Virchow's  Archiv,  CLVI. 


CLINICAL   FORMS  127 

loops  of  the  small  intestine  downward  toward  the  pelvis,  the  mesentery,  and 
particularly  the'  arched  fold  under  which  the  duodenum  enters  into  the 
jejunum,  becomes  tense,  and  thus  a  constriction  is  caused  in  the  mesenteric 
artery  at  the  duodeno- jejunal  boundary.  Albrecht  quite  properly  states  that 
the  vicious  circle  which  is  formed  by  the  downward  sinking  of  the  folds  of 
the  small  intestine  causes  tension  in  the  mesentery  which  completes  the 
compression  of  the  duodenum.  Thus  the  contents  of  the  duodenum  be- 
come more  and  more  engorged,  and  the  stomach  constantly  more  full  and 
dilated.  The  horizontal  portion  of  the  duodenum  becomes  still  more  over- 
loaded, and  the  downward  displacement  of  the  colon  and  the  small  intes- 
tine still  further  increased. 

That  an  acute  atony  of  the  stomach,  an  acute  gastric  dilatation,  may 
favor  the  development  to  a  high  degree  of  an  arterio-mesenteric  duodenal 
incarceration  is  clear.  In  other  cases,  the  compression  of  the  duodenum 
by  the  mesentery  of  the  small  intestine  may  have  been  the  beginning  of 
the  disastrous  chain.  In  incomplete  closure,  and  with  an  incomplete  dis- 
location of  the  duodenum,  there  may  be  chronic  dilatation  with  vomiting 
of  bilious  masses. 

In  cases  of  this  kind  recently  reported,  the  symptom-complex  was  ob- 
served after  chloroform  narcosis  preceding  various  operations,  among  them 
some  upon  the  biliary  passages.  Baumler,^  in  reports  of  two  cases  belong- 
ing to  this  category,  has  recently  stated  that  numerous  factors  favor  this 
form  of  intestinal  immobility,  and  he  groups  these  as  follows:  1.  Greater 
length  of  the  mesentery  of  the  small  intestine;  2.  Gastroptosis ;  3.  En- 
teroptosis  in  its  influence  upon  the  position  of  the  duodenum  and  upon 
the  root  of  the  mesentery ;  4.  The  position  of  the  duodeno-jejunal  boundary 
in  relation  to  the  vertebral  column;  5.  Marked  lumbar  lordosis;  6.  High- 
graded  emaciation  and  debility  from  preceding  disease;  7.  Chronic  gastric 
dilatation  in  consequence  of  congenital  or  acquired  stenosis  of  the  pylorus; 
8.  Prolonged  dorsal  decubitus  after  operations ;  9.  Very  complete  emptying 
of  the  intestine  prior  to  an  operation. 

Further  predisposing  factors  for  the  development  of  atony  in  general 
are  preceding  severe  infectious  diseases,  general  constitutional  affections, 
anemia,  chlorosis,  and  the  like. 

Those  who  are  poorly  nourished,  or  debilitated  by  sexual  excess  or  other 
causes,  are  highly  susceptible  to  atony.  Abnormal  position  of  the  stomach, 
gastroptosis,  enteroptosis,  extreme  flaccidity  of  the  abdominal  walls  may 
be  designated  as  predisposing  factors,  even  although  they  do  not  in  them- 
selves cause  atony. 

In  some  cases,  the  so-called  weak,  atonic  stomach  is  hereditary.  Fre- 
quently, the  nutrition  habitual  from  childhood  may  here  play  a  role.  Like 
every  muscular  organ,  the  stomach,  from  childhood,  should  be  accustomed 

*  Munchener  med.  Wochenschr.     1901,  Nr.  17. 
10 


128         DIAGNOSIS  AND  TREATMENT   OF   GASTRIC   DILATATION 

to  proper  food,  as  this  develops  its  muscular  activity.  Monotonous  diet 
which  is  deficient  in  residue  may  so  weaken  the  stomach  that  when,  under 
unusual  circumstances,  demands  are  made  upon  it  which  can  hardly  be 
designated  as  harmful,  its  muscular  tonus  suffers  and  reacts  by  becoming 
flaccid. 

At  the  onset,  we  might  suppose  that  disturbances  in  the  secretion  of 
the  gastric  juice  would  decidedly  influence  the  propulsion  of  the  gastric 
contents,  and  thus  indirectly  cause  disturbances  of  motor  activity.  Clinical 
observation  shows  that  this  is  not  the  case  to  the  extent,  and  in  the  manner, 
that  we  might  be  inclined  to  assume.  Such  a  reaction  we  should  most  look 
for  in  pure  achylia  in  which  the  secretion  of  gastric  juice  is  entirely  absent. 
But  here,  particularly,  such  a  disturbance  does  not  appear;  on  the  con- 
trary, the  motor  power  is  good  throughout,  and  even  increased.  This  is 
best  explained  by  studying  the  remarkable  results  of  the  experiments  of 
Pawlow  '  in  which  he  proved  that  the  duodenal  mucous  membrane  regulates 
the  propulsion  of  the  gastric  contents  into  the  intestine,  regardless  of  the 
condition  of  fulness  in  the  latter,  from  the  fact  that  it  depends  upon  the 
reaction  of  the  gastric  contents  and  their  acidity.  Alkaline  contents  usu- 
ally pass  from  the  stomach  very  soon.  On  the  other  hand,  after  the  intes- 
tine has  received  a  portion  of  the  acid  gastric  contents,  it  causes  by  reflex 
action  a  temporary  closure  of  the  pylorus.  The  acid  food  mass,  which  the 
pylorus  has  permitted  to  pass  through,  causes  an  increased  secretion  of 
pancreatic  juice,  and  by  and  by  becomes  neutralized.  Only  after  this  has 
occurred  is  the  expulsion  of  further  acid  masses  from  the  stomach  per- 
mitted, and,  accordingly,  the  quickened  motor  activity  of  the  stomach  in 
achylia  is  readily  understood. 

On  the  other  hand,  in  cases  of  increased  gastric  juice  secretion,  par- 
ticularly in  hypersecretion,  we  not  infrequently  see  disturbances  of  the 
motor  activity  in  the  form  of  delayed  expulsion  of  the  ingesta,  and  not 
rarely  also  of  ectasis.  The  connection  between  these  is  a  varying  one, 
Many  authors  regard  hypersecretion  in  all  cases  as  secondary,  as  the  conse- 
fiuence,  not  the  cause,  of  ectasis.  That  hypersecretion  and  ectasis  are  fre- 
(luently  observed  in  combination  is  certain;  which  is  primary,  and  which 
secondary,  cannot  be  so  readily  decided.  Even  where  an  organic  pyloric 
stenosis  can  be  determined,  this  does  not  prove  that  the  mechanical  obstruc- 
tion is  the  cause  of  the  hypersecretion.  Pyloric  stenosis  in  which  there  is 
a  sufficient  secretion  of  gastric  juice  by  no  means  always  leads  to  hyper- 
secretion. That  hypersecretion  often  rapidly  disappears  after  gastro- 
enterostomy, which  so  greatly  facilitates  the  flow  of  the  secretion,  cannot 
be  regarded  as  a  proof  that  the  latter  is  a  consequence  of  the  stasis.  Pro- 
longed stasis  may  keep  up  the  irritative  condition,  its  disappearance  may 

'  "  Das  pxporiment  als  zeitgemasse  und  einheitliche  Methode  medicinischer  For- 
schung."     Wiesbaden,  1900. 


CLINICAL  FORMS  129 

remove  it,  and  facilitate  the  outpouring  of  the  secretion;  but  stenosis  in 
itself  does  not  explain  the  prolonged  secretion  of  gastric  juice. 

The  secretion  of  gastric  juice  normally  is  not  continuous,  but  periodic. 
As  Pawlow  ^  first  showed  by  conclusive  experiments,  the  normal  stomach, 
empty  of  food,  does  not  secrete  gastric  juice.  It  only  secretes  it  upon 
digestive,  not  upon  mechanical,  stimulation.  For  this  reason,  therefore,  it 
is  not  to  be  expected  that  stenosis  in  itself  will  cause  a  continuous  secretion 
of  gastric  juice.  If  the  stomach  of  a  patient  suffering  from  hypersecretion 
is  washed  perfectly  clean,  and  is  evacuated  after  a  few  hours,  during  which 
time  the  patient  has  taken  no  food,  a  greater  or  less  amount  of  secretion  is 
nevertheless  found.  The  stomach  therefore,  despite  the  absence  of  any 
digestive  stimulation,  has  spontaneously  secreted  gastric  juice.  This  cer- 
tainly favors  abnormal  stimulation.  On  the  other  hand,  we  also  see, 
although  not  so  frequently,  cases  of  hypersecretion  without  pyloric  stenosis 
and  without  actual  dilatation.  It  is  true  these  cases  are  readily  overlooked. 
Hence  it  follows  that  pyloric  stenosis  in  itself  is  not  the  primal,  and  not 
the  only,  cause  of  hypersecretion.  Inversely,  however,  it  is  doubtless  true 
that  hypersecretion  alone  may  lead  to  dilatation  by  limiting  the  transforma- 
tion of  the  amylacea  to  such  a  degree  that  upon  prolonged  retention  ffer- 
mentation  of  gas  is  produced,  and,  finally,  if  this  continue  for  some  time 
causes  dilatation.  According  to  Pawlow's  investigations,  the  abnormally 
acid  contents  and  the  profuse  amount  of  acid-secretion  remain  in  the  stom- 
ach a  much  longer  time  than  the  gastric  contents  which  are  normally  acid. 
The  transformation  of  the  acid  gastric  digestion  to  the  alkaline  intestinal 
digestion  by  the  pancreatic  juice  must  be  slow  and  difficult  in  those  cases 
in  which  a  much  higher  degree  of  acidity  and  a  much  larger  amount  of 
acid  gastric  juice  is  present  than  in  the  normal,  as  is  the  case  in  hyper- 
secretion. 

Particularly  in  the  case  of  hypersecretion,  spastic  processes  at  the  pylorus 
are  observed  which  inhibit  the  exit  of  the  acid  ingesta;  this,  accordingly, 
can  only  be  regarded  as  a  proper  preventive,  as  a  protection  against  a  dis- 
turbance of  digestion  of  the  small  intestine.  These  factors  are  calculated 
to  produce  a  long  stagnation  of  the  ingesta  even  without  the  existence  of 
a  stenosis.  Hypersecretion  in  itself  must  cause  stasis,  and  may,  therefore, 
in  itself  finally  produce  dilatation.  Hence  it  cannot  appear  strange  that, 
particularly  in  the  case  of  hypersecretion,  a  change  in  the  symptoms  is 
observed,  sometimes  improvement,  sometimes  aggravation,  sometimes  an 
increase  of  the  motor  insufficiency. 

It  has  been  maintained  that  marked  psychical  influences  give  rise  to 
such  atonies.  That  psychical  influences  may  affect  the  secretion  of  the 
gastric  juice  and  also  the  motility  of  the  stomach  is  no  doubt  true.  But 
these  are  only  transitory  disturbances.  It  has  not  yet  been  proven  that 
chronic  ectasis  may  develop  upon  a  purely  nervous  basis. 

^ "  Die  Arbeit  der  Verdauungsdriisen,"  1898. 


130         DIAGNOSIS  AND  TREATMENT   OF  GASTRIC   DILATATION 

Whether,  and  in  how  far,  diseases  of  the  central  nervotis  system  lead 
to  atony  and  dilatation  has  not  yet  been  determined  with  certainty.  Iso- 
lated, recent  observations  appear  to  favor  the  possibility  of  the  develop- 
ment of  gastric  dilatation  from  central  influences. 

The  cases  are  not  rare  in  which  patients  with  gastrectasis  refer  the 
beginning  of  their  disturbances  to  a  single  trauma  in  the  gastric  region. 
As  is  shown  by  careful  analysis  of  these  cases,  many  of  the  ectases  are 
caused  by  a  stenosis  of  the  pylorus  or  in  its  vicinity.  This  stenosis  in  a 
number  of  cases  originates  in  a  cicatricial  narrowing  brought  about  by 
necrosis  and  ulceration  due  to  trauma;  in  other  cases  the  trauma  first 
causes  a  perigastritis,  and,  in  consequence  of  this,  adhesions  to  the  neighbor- 
ing organs;  when  these  adhesions  in  their  further  course  affect  the  region 
of  the  pylorus,  they  also  lead  to  stenosis.  These  traumatic  stenoses  have 
the  peculiarity  that  the  stenotic  symptoms  never  develop  at  once,  but 
often  only  a  long  time  after  the  trauma. 

Simple  atony  may  also  develop  after  trauma;  it  has  been  noted  after 
operations  upon  the  abdomen.  In  contrast  with  the  form  just  mentioned, 
atonies  after  traumata  mostly  develop  suddenly  and  soon  after  the  injury; 
they  may  even  themselves  prove  fatal,  as  in  a  case  recently  reported  by 
Grundzach,^ 

Not  only  a  single  trauma,  but  also  frequently  repeated  ones  which  affect 
the  gastric  region  play  a  role  in  the  etiology  of  ectasis. 

Many  occupations  necessitate  that  the  labor  be  performed  in  a  position 
which  causes  the  body  to  be  bent  forward,  that  the  epigastrium  be  exposed 
to  the  pressure  of  tools  which  are  stemmed  against  it,  and  thus  subject 
it  to  long-continued  pressure.  This  may  cause  circulatory  disturbance,  a 
pressure  ulcer,  but  also  cicatricial  stenoses  or  perigastritis,  and  thus  lead 
to  gastrectasis.  But  we  cannot  assume  a  cicatricial  stenosis  in  every  case 
of  gastrectasis;  even  active  peristalsis  of  the  stomach  is  no  positive  proof. 
At  all  events,  in  a  number  of  dilatations  developed  in  this  manner,  we 
note  decided  variation  in  the  symptoms,  and,  under  some  circumstances, 
even  complete  retardation,  so  that  the  assumption  that  spasms  of  the 
pylorus  are  chiefly  the  cause  does  not  appear  unjustifiable. 

It  has  l:)een  maintained  that  some  narcotics,  such  as  alcohol  and  tobacco, 
haxG  a  relaxing  and  paralyzing  effect  upon  the  muscularis  of  the  stomach. 
No  cases  developing  in  this  manner  have  as  yet  been  determined  with 
certainty. 

Although  it  cannot  be  denied  that  gastrectasis  may  develop  upon  the 
basis  of  atony,  nevertheless,  at  the  onset,  in  every  dilatation  of  extreme 
degree  the  suspicion  is  justified  that  a  mechanical  hindrance,  or  an  organic 
stenosis  either  at  the  pylorus  or  in  its  vicinity,  is  the  cause  of  the  dilata- 
tion.    Mechanical  hindrances  are  hy  far  the  most  frequent  causes  of  ectasis, 

*  Revue  de  MMedne,  Mars,  1899. 


PATHOLOGY        .  131 

and  the  most  important  of  these  are  cicatrices  from  ulcers,  carcinoma,  and 
cicatrices  from  caustics. 

The  consequences  of  dilatation  will  naturally  also  appear  when  the 
obstruction  which  causes  stenosis  is  situated  somewhat  lower  down,  below 
the  pylorus  and  in  the  beginning  of  the  duodenum.  Foreign  bodies  which 
find  their  way  into  the  pylorus,  cherry  stones,  medlar  stones,  invaginated 
gall-stones,  have  caused  dilatation  there  or  in  the  duodenum.  Quite  ex- 
ceptionally, cases  of  tuberculous  stenosis  of  the  pylorus  have  been  observed. 
Jacobi  ^  has  recently  reported  such  a  case.  Very  rare  causes  of  pyloric 
stenosis  are  benign  tumors,  pediculated  polypi,  connective  tissue  hyper- 
trophy of  the  pylorus,  external  tumors  pressing  upon  the  pylorus  (large 
gall-stones  in  the  gall-bladder,  Minkowski). 

Pyloric  stenosis  is  rarely  congenital;  nevertheless,  quite  a  series  of 
reports  are  at  hand  in  which  a  decided  hypertrophy  of  the  pylorus  caused 
marked  symptoms  of  stenosis  in  nurslings.  It  is  true  a  number  of  cases 
of  supposed  congenital  pyloric  stenosis  admit  of  a  different  explanation. 
Pfaundler,^  particularly,  has  called  attention  to  the  fact  that  recently  in 
examining  cadavers  of  nurslings,  in  about  every  third  case  the  stomach 
was  found  in  a  peculiar  state  of  persistent,  muscular  rigidity.  The  pylorus 
itself,  in  consequence  of  the  permanent  contraction,  was  very  narrow,  and 
frequently  did  not  permit  the  passage  of  a  medium  thick  sound.  Pfaundler 
believes  that  many  cases  reported  as  congenital  pyloric  stenosis  correspond 
minutely  with  the  findings  in  systolic  stomachs  of  this  kind.  However, 
he  does  not  deny  that  there  are  actual  clinical  pictures  among  nurslings 
which  point  to  an  existing  pyloric  stenosis. 

These  are  the  most  important  causes  of  dilatation  and  motor  insuffi- 
ciency. The  degree  is  a  varying  one.  High-graded  ectasis  is  observed  in 
organic  stenosis,  among  which  by  far  the  most  frequent  causes  are  car- 
cinoma and  cicatrices  from  ulcers. 


PATHOLOGY 

Anatomically,  the  picture  presented  by  ectasis  is  in  proportion  to  the 
cause  and  duration  of  the  dilatation,  the  degree  and  nature  of  the  stenosis. 
Motor  insufficiency,  as  such,  so  long  as  it  does  not  give  rise  to  dilatation, 
is  not  susceptible  to  anatomical  diagnosis,  or,  at  most,  only  in  the  rare  cases 
with  cirrhotic  change  or  diffuse  malignant  degeneration  of  the  stomach. 

The  degree  of  dilatation  varies;  primarily,  and  chiefly,  the  fundus  and 
the  greater  curvature  which  bear  the  brunt  of  the  affection  are  involved 
in  the  dilatation.  But,  in  severe  grades,  the  dilatation  is  more  general, 
chiefly  lateral,  as  may  often  be  determined  intra  vitam. 


*  Wiener  klinische  Wochenschrift,  1900,  Nr.  48. 
'  Ibid.,  1898,  Nr.  52. 


132         DIAGNOSIS   AND  TREATMENT   OF   GASTRIC   DILATATION 

In  isolated  cases  of  ectasis  the  walls  of  the  stomach  are  very  differently 
affected;  sometimes  they  are  thinned,  in  other  cases  they  show  decided 
thickening.  This  variation  depends  primarily  upon  the  cause  of  the  dila- 
tation, and,  secondly,  upon  the  duration  of  the  affection. 

Decided  hypertrophy,  particularly  of  the  pylorus,  is  seen  chiefly  in 
stenoses  of  the  pylorus  and  of  its  surrounding  areas.  The  muscularis  is 
often  three  or  four  times  thicker  than  the  norm.  In  other  cases  there  is 
no  hypertrophy  of  this  kind;  on  the  contrary,  the  muscularis  appears  thin 
and  atrophic  as  in  the  case  of  atonic  dilatation;  not  infrequently  atrophy, 
and  fatty  and  other  forms  of  degeneration  of  the  muscularis  are  noted 
in  the  later  stages  of  long-existing  ectasis. 

The  relation  of  the  sub-mucosa  and  mucosa  depends  much  less  upon  the 
dilatation  itself  than  upon  the  underlying  causes  of  the  ectases.  But  in 
regard  to  these  points  we  must  refer  the  reader  to  the  individual  forms 
of  disease  which  produce  dilatation. 

SYMPTOMATOLOGY 

In  the  description  of  the  clinical  picture,  "  ectasis,"  I  shall  limit  myself 
entirely  to  the  symtomatology  of  dilatation.  It  would  be  too  great  a 
digression  if  I  were  to  consider  all  varieties  which  might  secondarily  cause 
dilatation,  such  as  carcinoma,  cicatrices  from  ulcers,  perigastric  adhesions, 
chronic  gastritis,  hypersecretion  and  the  like.  Here  we  will  consider  only 
the  clinical  picture  of  dilatation  as  we  meet  it  in  daily  practice.  It  is  true 
the  diagnosis,  "  ectasis,"  is  an  imperfect  one ;  it  tells  us  only  that  the 
stomach  is  dilated,  and  that  motor  insufficiency  is  present ;  our  object  must 
be  to  determine  the  cause,  and,  as  a  rule,  this  offers  no  insurmountable 
difficulty. 

The  cases  are  comparatively  rare  in  which  the  special  diagnosis  of  the 
cause  of  the  dilatation  is  difficult.  Often  the  examination  of  the  patient 
not  only  suffices  for  this  but  enables  us  to  determine  the  underlying  affec- 
tion which  produced  it.  Naturally,  there  are  cases  in  which  prolonged 
observation  and  the  most  minute  investigation  of  the  course  of  the  disease 
and  of  the  results  of  treatment  are  necessary;  but  at  the  bedside  we  should 
first  determine  the  dilatation;  and  then  seek  for  its  cause. 

The  symptomatology  naturally  varies  with  the  degree  of  the  dilatation. 
Mild  grades  of  ectasis  produce  less  prominent  symptoms  than  higher  grades. 
As  I  have  already  stated,  there  is  no  sharp  division  between  motor  insuffi- 
ciency and  dilatation,  in  spite  of  many  attempts  to  define  it.  It  is  impossi- 
l)lo  to  draw  a  line,  from  which  point  the  stomach  may  be  regarded  as 
dilatod.  This  might  be  feasible  in  an  organ  always  of  absolutely  the  same 
sixo,  l)ut  not  in  an  organ  which,  like  the  stomach,  shows  a  varying  exten- 
sion nt  different  periods.  Naturally  there  are  extreme  degrees  of  dilatation 
whicli  enable  us  to  say,  without  more  ado,  that  the  stomach  is  decidedly 


SYMPTOMATOLOGY  133 

dilated.  Slighter  degrees  are  designated  by  one  author  only  as  motor  in- 
sufficiency, by  another,  as  dilatation.  In  estimating  the  size  of  the 
stomach,  we  must  consider  the  period  as  well  as  the  absolute  degree  of 
distention. 

In  no  group  of  diseases  is  the  time  of  the  physical  examination  so 
important  as  in  gastric  affections.  It  is  by  no  means  immaterial  at  what 
time  of  the  day  we  examine  a  patient  suffering  from  gastric  disease.  If, 
early  in  the  morning  before  food  is  taken,  we  can  elicit  a  distinct  splash- 
ing sound,  and  so  prove  that  large  quantities  of  fluid  and  air  are  still 
in  the  stomach  when  it  should  be  empty,  we  decide  at  once  that  motor 
insufficiency  is  present.  In  a  certain  sense  we  may  also  consider  this 
stomach  to  be  dilated  although  its  lower  boundary  does  not  extend  below 
the  umbilicus.  For  it  is  at  least  temporarily  dilated ;  i.  e.,  more  than  nor- 
mally distended;  early  in  the  morning  it  should  be  empty  and  contracted. 
We  may,  therefore,  speak  of  relative  dilatation  in  contrast  to  absolute  and 
extreme  dilatation.  In  practice,  however,  it  is  necessary  not  only  to  deter- 
mine the  extreme  grades,  but  also  the  slighter  forms  of  dilatation  and 
motor  insufficiency. 

The  earlier  the  stage  in  which  the  diagnosis  is  made  the  greater  the 
chances  of  controlling  the  malady.  But,  as  I  should  like  to  emphasize 
at  this  point,  to  obtain  a  clear  insight  we  must  employ  all  methods  in 
the  examination.  A  well-trained  practitioner  will  sometimes,  on  first 
observing  the  abdomen,  be  able  to  diagnosticate  gastric  dilatation  just 
as  we  diagnosticate  tabes  dorsalis  from  the  gait,  and  aortic  insufficiency 
from  the  pulse.  But  no  conscientious  physician  would  be  content  with 
this.  For  the  name,  alone,  of  the  disease,  does  not  suffice,  but,  at  the  bed- 
side, we  must  fully  comprehend  the  nature  and  intensity  of  the  physiologic 
disturbance  of  function,  and  for  this  purpose  we  require  numerous  methods 
of  investigation. 

If  this  had  always  been  borne  in  mind  in  making  the  diagnosis  of 
ectasis,  we  should  not  have  erred  by  regarding  the  size  of  the  stomach  as 
of  most  importance,  and  of  considering  this  alone  the  decisive  factor.  But 
it  is  just  as  partial  and  extreme  to  determine  the  degree  of  ectasis  from 
the  amount  of  material  evacuated  or  from  the  amount  of  residue,  and 
to  consider  the  size  of  the  organ  as  entirely  secondary.  They  are  related  to 
each  other,  and  still  further  methods  of  investigation  must  be  resorted 
to  if  certainty  in  diagnosis  is  to  be  assured,  as  well  as  a  full  understanding 
of  the  nature  and  intensity  of  the  disturbances  in  a  given  case. 

To  begin  with  the  subjective  symptoms,  it  must  be  remarked  that 
these  vary  not  alone  according  to  the  degree  of  the  dilatation,  but  also  ac- 
cording to  the  cause  and  the  manner  of  its  development.  As  a  rule  the  first 
symptom  of  which  the  patients  complain  is  a  feeling  of  tension,  fulness, 
and  pressure  after  meals.  Some  experience  abnormal  sensations  of  this 
kind  even  after  light  meals ;  some  report  that  they  feel  better  in  the  recum- 


134        DIAGNOSIS   AND  TREATMENT   OF   GASTRIC   DILATATION 

bent  posture  than  when  standing,  particularly  after  a  somewhat  heavier 
meal. 

Others  complain  of  eructations  and  pyrosis,  others  again  of  a  sensation 
of  active  unrest  in  the  stomach  which  sometimes  increases  to  actual 
spasmodic  pain.  Occasionally  these  disturbances  are  relieved  by  vomiting. 
This  is  observed  chiefly  in  pyloric  stenosis  with  sufficient  or  increased  secre- 
tion of  gastric  juice;  but  spastic  conditions  of  the  pyloric  ring  may  also 
of  themselves  produce  painful  spasmodic  attacks. 

The  appetite  is  capricious;  as  a  rule  it  is  decreased;  only  rarely,  in 
mild  cases  is  it  normal  or  increased.  Often  the  patients  have  a  feeling  of 
satiety  after  partaking  of  small  amounts  of  food;  bulimia  occurring  par- 
oxysmally  is  rarely  complained  of. 

The  thirst  is  more  important  than  the  state  of  the  appetite.  In  almost 
all  well  marked  cases  there  is  complaint  of  thirst.  The  more  extreme  the 
degree  of  dilatation  and  motor  insufficiency,  the  more  markedly  is  thirst 
increased.  The  stomach  itself  does  not  absorb  water,  but,  on  the  contrary, 
a  more  or  less  active  excretion  of  water  occurs  in  the  stomach  with  the 
absorption  of  many  substances,  such  as  sugar,  dextrin,  alcohol,  peptone, 
etc. ;  with  well  marked  dilatation  of  the  stomach  the  propulsion  of  fluid  be- 
comes exceedingly  difficult.  This  remarkable  increase  in  thirst  is  readily 
explained;  and  the  fact  that  in  dilatation  more  fluid  is  frequently  found 
in  the  stomach  than  is  consumed  is  comprehensible.  The  decreased  absorp- 
tion of  water  corresponds  with  the  decreased  excretion  of  urine,  to  which 
we  shall  recur  in  describing  the  objective  symptoms. 

The  state  of  the  tongue  is  not  characteristic ;  in  the  more  marked  cases 
there  is  a  noteworthy  tendency  to  dryness.  In  general,  the  appearance 
of  the  tongue  varies;  but  it  is  by  no  means,  as  was  formerly  supposed,  a 
reflection  of  the  stomach. 

An  important  and,  probably,  the  most  important  symptom  of  dilatation 
is  vomiting.  In  the  milder  grades  of  motor  insufficiency  it  may  be  en- 
tirely absent;  in  well  marked  ectasis  it  is  almost  always  present,  naturally, 
in  varying  frequency.  In  some  cases  its  peculiarities  at  once  suggest  dila- 
tation. Thus,  if  the  quantity  of  the  vomited  material  exceed  the  quantity 
of  the  last  meal,  if  remains  of  food  which  had  been  taken  previously,  often 
some  days  before,  be  detected  in  the  vomitus,  motor  insufficiency  is  in- 
dicated. 

The  patients  are  usually  decidedly  relieved  by  vomiting.  For  this 
reason  they  often  attempt  to  produce  it  voluntarily.  Vomiting  may  be 
repeated  daily;  frequently  it  occurs  at  very  irregular  intervals. 

The  appearance  of  the  vomited  material  varies  greatly;  the  differences 
depend  chiefly  upon  the  underlying  affection  which  causes  the  dilatation 
and  upon  the  secretion  of  gastric  juice.  The  vomitus  in  dilatation  with 
hypersecretion  has  a  different  appearance  from  that  due  to  carcinoma  of 
the  pylorus.     In  the  former  case  we  observe  the  well  known  three  layers; 


SYMPTOMATOLOGY  135 

the  lower  layer  consisting  of  fine  remains  of  starch,  the  next  of  a  decidedly 
acid  fluid,  and  the  upper  layer  being  frothy  as  the  expression  of  gas  fer- 
mentation; in  the  latter  case  coarse  remains  of  food  are  seen,  particularly 
remains  of  meat,  with  an  absence  of  free  hydrochloric  acid,  and  a  decided 
reaction  for  lactic  acid.  I  cannot  here  describe  the  special  peculiarities 
of  the  vomited  material,  which  differ  according  to  the  underlying  affection 
that  causes  the  dilatation.  I  must  refer  the  reader  to  the  individual  dis- 
eases themselves. 

An  admixture  of  blood  in  the  vomitus  is  not  rare;  this  is  most  fre- 
quently seen  in  carcinoma,  but  it  also  occurs  in  other  processes.  Naturally 
this  finding  has  nothing  to  do  with  the  dilatation  as  such.  Moderate 
degrees  of  motor  insufficiency  often  exist  for  a  long  time  without  impair- 
ing the  general  condition.  Patients  with  high-graded  ectasis,  however,  as 
a  rule,  are  feeble,  weak,  and  incapable  of  exertion.  We  commonly  meet 
with  complaints  of  numbness  in  the  head,  of  headache  and  of  vertigo. 

The  bowels,  as  a  rule,  are  constipated,  occasionally  not.  Very  rarely 
do  the  patients  complain  of  diarrhea;  this  is  most  frequently  observed  in 
stenoses  with  marked  gaseous  fermentation. 

These  most  important  symptoms  of  the  patients,  as  will  be  noted,  show 
but  slight  peculiarities.  The  objective  symptoms  are  much  more  impor- 
tant, and  are  alone  decisive  in  diagnosis.  Xaturally  they  also  differ  accord- 
ing to  the  degree  of  the  dilatation.  Slight  grades  of  atoay  and  motor 
insufficiency  at  first,  that  is,  if  the  duration  has  not  been  too  prolonged, 
do  not  materially  affect  the  general  condition  and  nutrition.  It  is  different 
in  high-graded,  long-continued  dilatation.  Here  the  nutrition  suffers  de- 
cidedly. The  patients  are  more  or  less  emaciated;  the  fatty  layer  has  dis- 
appeared, the  skin  is  dry  and  withered,  it  may  be  raised  in  large  folds 
and  desquamates;  the  muscles  are  thin  and  atrophic.  This  picture  is  met 
with  not  only  in  cases  of  dilatation  due  to  carcinoma,  but  is  also  observed 
in  dilatation  occurring  in  benign  affections,  and,  naturally,  it  depends  upon 
the  duration  of  the  disease.  Carcinomatous  dilatation  leads  more  rapidly 
to  loss  of  strength  than  the  benign  forms.  But,  in  any  given  case,  the 
appearance,  the  degree  of  emaciation,  cannot  be  taken  as  positive  indica- 
tions of  the  nature  of  the  stenosis.  Any  one  who  has  seen  many  patients 
of  this  kind  will  admit  that  the  external  habitus  is  not  decisive.  The 
nature  of  the  stenosis  can  only  be  determined  by  a  study  of  the  entire 
condition. 

The  examination  of  the  diseased  organ  must  be  made  systematically, 
and,  in  every  case  of  gastric  disease,  should  begin  with  inspection.  I 
expressly  emphasize  this  method  of  examination  because  in  practice  it  is 
often  neglected.  As,  in  the  examination  of  the  heart,  the  sequence  of  the 
investigation  is  essential,  so  is  it  in  the  stomach.  Inspection  often  gives 
us  important  knowledge ;  naturally,  not  in  very  fat  persons.  On  the  other 
hand,  in  slender  persons,  poor  in  fat,  with  thin  flaccid  abdominal  walls. 


136         DIAGNOSIS   AND  TREATMENT   OF   GASTRIC   DILATATION 

wo  often  see  the  contours  of  the  protruding  and  dilated  stomach  without 
other  aid.  This,  of  course,  depends  upon  the  time  of  the  examination.  If 
we  examine  immediately  after  the  stomach  has  rid  itself  of  the  greater 
part  of  its  contents  by  vomiting  or  by  lavage,  inspection  usually  reveals 
nothing.  If  the  stomach,  however,  is  still  quite  full,  we  can  frequently 
trace  its  boundaries;  the  upper  portion  of  the  epigastrium,  perhaps  still 
somewhat  sunken,  is  seen  lower  down  extending  far  below  the  navel,  where 
a  protuberance  is  noted,  inside  of  which  there  is  often  active  peristaltic 
movement  from  left  to  right.  Upon  superficial  investigation  these  peristal- 
tic movements  may  perhaps  convey  the  impression  of  being  irregular;  on 
closer  examination,  however,  a  certain  regularity  is  observed,  and  eleva- 
tions and  depressions  may  be  recognized.  The  boundaries  of  the  stomach 
are  not  only  sharply  defined,  but  at  the  same  time  we  conclude  that  we 
are  not  dealing  with  a  simple  flaccidity.  In  atony  such  active  peristaltic 
movements  are  never  observed.  By  inspection  alone,  we  can,  under  some 
circumstances,  determine  the  presence  of  an  ectasis,  but  also  simultaneously 
tliat  the  stomach  labors  with  increased  force.  The  latter  circumstance 
favors  stenosis;  of  course,  this  need  not  be  an  organic  obstruction,  for  even 
a  functional  disturbance,  a  spasmodic  contraction  of  the  pylorus,  may  tem- 
porarily make  the  outfiow  difficult,  and  produce  an  increase  of  peristalsis. 

For  a  positive  diagnosis  of  dilatation  it  is  absolutely  necessary  to 
observe  accurately  not  only  the  lower  but  also  the  upper  boundary.  As  is 
well  known,  marked  dilatations  frequently,  even  as  a  rule,  accompany 
gastroptosis,  i.  e.,  the  whole  stomach  is  displaced  downward.  The  disloca- 
tion of  the  lower  border  alone  to  a  point  more  or  less  below  the  navel  does 
not  prove  dilatation,  for  this  also  happens  in  gastroptosis;  therefore,  the 
upper  boundary  must  be  accurately  located.  Normally  this  is  invisible; 
if  it  be  displaced  downward,  we  note  in  the  epigastrium  a  slight  flatten- 
ing, and  below  this  a  prominence  gradually  increasing  as  it  descends,  and 
with  its  convexity  directed  downward. 

I  shall  not  here  discuss  the  results  of  electric  illumination.  Apart 
from  the  fact  that  this  method  can  only  be  utilized  in  isolated  instances, 
it  gives  no  results  which  may  not  be  obtained  in  other  and  simpler  ways. 

Inspection  is  to  be  followed  by  palpation.  By  this  means  we  confirm 
the  results  of  inspection  and  also  gain  other  valuable  knowledge.  In  thin 
patients,  provided  the  stomach  is  not  empty,  we  may  often  distinctly  pal- 
pate the  organ  under  the  flaccid  abdominal  walls,  particularly  if  the  hand 
is  laid  flat  with  the  ulnar  surface  next  the  abdomen,  and,  lightly  stroking. 
<:lidcs  downward.  The  practised  hand  frequently  traces  the  boundaries 
of  the  stomach  accurately.  Simultaneously  the  proof  of  a  tumor  in  the 
jnloric  region  sometimes  complements  the  diagnosis  of  such  cases. 

Less  importance  is  to  be  attached  to  the  method  formerly  so  much  prac- 
tis(Hl— f)f  palpation  by  means  of  a  sound.  Although  it  is  true  that  we 
frociiioiitlv  succeed  in  feeling  the  end  of  the  sound  through  the  abdominal 


SYMPTOMATOLOGY  137 

walls,  we  find  at  most  only  the  lower  boundary  of  the  stomach,  and  noth- 
ing showing  its  total  extension;  moreover,  a  bend  in  the  sound  may  very 
readily  lead  to  errors. 

Another  symptom  that  may  be  determined  by  palpation  is  the  splash- 
ing sound  which  we  elicit  by  tapping  the  abdominal  coverings  with  the 
finger.  Splashing  sounds  only  permit  diagnostic  conclusions  when  we 
simultaneously  consider  the  time  and  the  extent  of  their  development.  In 
themselves  they  only  show  the  presence  of  fluid  and  air  in  a  hollow  organ. 
Splashing  sounds  may,  under  some  circumstances,  also  be  produced  in 
healthy  persons,  but  only  when  the  stomach  contains  air  and  fluid,  and 
even  when  this  is  the  case  not  beyond  the  normal  boundaries  of  the  stom- 
ach. If  we  find  splashing  sounds  extending  beyond  these,  if  we  find  them 
within  abnormal  limits  at  a  time  when  a  healthy  stomach  should  be  empty, 
that  is,  seven  hours  after  a  meal  or  in  the  morning  before  food  is  taken, 
diagnostic  significance  may  be  attached  to  them. 

Such  a  splashing  sound  proves  that  the  stomach  still  contains  more 
or  less  profuse  amounts  of  fluid,  and  it  further  proves  that  the  stomach 
is  more  decidedly  dilated  than  the  normal.  Naturally,  if  the  latter  con- 
clusion is  justified,  gastroptosis  must  be  excluded. 

To  determine  the  boundaries  and  position  of  the  stomach  it  is  best 
to  inflate  it  by  means  of  air  or  carbonic  acid,  and  the  choice  between 
these  two  methods  has  been  much  discussed.  We  would  digress  too  far 
to  enumerate  all  the  objections  which  have  been  made  against  inflation 
by  carbonic  acid.  I  believe,  however,  that  these  objections  are  entirely 
unfounded.  I  have  never  seen  deleterious  effects,  or  even  danger  from  it, 
although  I  have  used  this  method  daily  for  many  years.  But  doses  suflB- 
eiently  large  must  be  given,  a  heaping  teaspoonful  of  sodium  bicarbonate 
and  a  correspondingly  large  dose  of  tartaric  acid;  less  than  this  is  in- 
sufficient. 

Distention  by  means  of  bellows,  and  autodistention,  such  as  has  lately 
been  advised  by  Spirack  ^  have  the  disadvantage  that  a  stomach-tube  is 
necessary.  The  administration  of  the  effervescing  mixture  is  easier  and 
more  readily  carried  out.  If  the  abdominal  walls  are  not  too  tense  and 
fat  we  usually  succeed,  without  more  ado,  in  tracing  the  contours  of  the 
stomach;  where  this  is  impossible,  its  boundaries  are  frequently  revealed 
by  the  uniformly  elastic  sensation  and  by  percussion.  In  stenosis  of  the 
pylorus,  after  the  administration  of  an  effervescing  mixture,  the  peristaltic 
movements  of  the  stomach  usually  show  a  marked  increase  in  activity. 

Percussion  of  the  stomach  serves  to  confirm  and  emphasize  the  pre- 
viously mentioned  results;  primarily  it  only  aids  us  in  tracing  the  boun- 
daries of  the  stomach,  therefore  in  gauging  its  size,  but  does  not  prove  a 
simultaneously  existing  motor  insufficiency.     But  it  does  confirm  the  lat- 

^  Deutsche  mcd.  Wochenschr.,  1900,  Nr.  23. 


138         DIAGNOSIS  AND  TREATMENT   OF   GASTRIC   DILATATION 

ter  if  we  succeed  in  ascertaining  the  presence  of  fluid  in  the  stomach  at 
a  time  when  it  should  be  empty.  For  this  purpose  it  is  advisable  to 
examine  the  patient  while  in  the  erect  and  the  recumbent  postures  alter- 
nately. If,  when  standing,  we  percuss  downward,  and  if  the  upper  areas 
of  the  stomach  are  first  filled,  we  find  a  tympanitic  zone  which  is  bounded 
at  the  height  of  the  navel,  or  somewhat  below  or  even  somewhat  higher, 
by  a  horizontal  dull  line,  which  lower  down  terminates  in  a  more  or  less 
convex  curve,  but  which  in  the  recumbent  posture  again  clears  up.  To 
guard  against  errors,  it  is  advisable  in  such  cases  to  evacuate  the  stomach 
and  thus  control  it.  An  evacuation  of  this  kind  is,  eo  ipso,  advisable  in 
all  cases  where  there  is  the  slightest  suspicion  of  disturbance  of  the  motor 
activity  of  the  stomach. 

The  Penzoldt-Dehio  method,  which  consists  in  administering  to  the 
patient  early  in  the  morning  upon  an  empty  stomach  two  or  three  glasses 
of  water  in  succession,  and  determining  after  each  glass  the  extent  of  the 
gastric  dulness  while  the  patient  stands  erect,  is  more  useful  for  ascertain- 
ing the  lower  border  of  the  stomach  and  its  tonus  than  for  the  proof  of 
dilatation.  It  may  be  dispensed  with  in  cases  of  high-graded  ectasis  in 
which  the  stomach  is  never  entirely  empty.  Only  in  mild  grades  of  motor 
insufficiency  is  it  worthy  of  trial,  and  even  here  it  is  superfluous  since  a 
diagnostic  evacuation  will  give  us  much  more  positive  proof  of  the  exist- 
ence of  motor  insufficiency,  and,  at  the  same  time,  acquaints  us  with  the 
degree  of  the  same. 

Some  of  the  other  numerous  methods  for  determining  the  size  and 
capacity  of  the  stomach  are  very  complicated,  have  no  advantage  over 
those  just  mentioned,  and,  for  this  reason,  may  be  ignored.  The  same 
is  true  of  the  method  recently  proposed  by  Queirolo.^ 

If  the  methods  of  examination  described  have  given  any  evidence  of 
the  existence  of  a  dilatation  of  motor  insufficiency  of  mild  degree,  we 
produce  a  diagnostic  evacuation.  This  evacuation,  a  definite  time  after 
a  meal,  enables  us  to  decide  whether  or  not  the  stomach  has  fulfilled  its 
task  of  propelling  the  food  at  the  right  time  into  the  intestine.  As  a  test 
of  motor  activity,  the  test-meal  is  unquestionably  more  satisfactory  than 
the  test  breakfast,  for  the  reason  that,  in  consequence  of  the  greater  labor 
put  upon  the  stomach,  we  get  a  better  idea  of  its  activity.  However,  the 
trial-breakfast  may  also  be  utilized  to  test  the  motor  activity. 

A  healthy  stomach  is  empty  six  to  seven  hours  after  the  intake  of  a 
test-meal.  If,  after  this  time,  remains  of  food  are  present,  its  motor 
activity  is  impaired. 

The  greater  the  amount  of  food  still  present  in  the  stomach,  the  greater 
the  degree  of  motor  insufficiency.  We  may,  of  course,  differentiate  vary- 
ing degrees  of  motor  insufficiency  according  to  the  amount  of  the  residue 

*  VerhamUungen  dea  XVIII.  Congresses  fur  innere  Medicin,  1900. 


SYMPTOMATOLOGY  139 

and  the  time  it  remains  in  the  stomach.  Usually  it  is  sufficient  to  difiEer- 
entiate  two  degrees^  in  one  of  which  the  stomach  is  not  yet  empty  seven 
hours  after  a  test-meal  but  is  so  in  the  morning;  in  the  second,  a  more 
advanced  stage,  in  which,  after  a  simple  evening  meal,  the  stomach  is  not 
empty  on  the  following  morning. 

My  usual  method  is  this :  In  the  evening,  seven  hours  after  the  midday 
meal,  I  evacuate  the  stomach.  If  there  are  profuse  remains  of  food  motor 
insufficiency  is  proven.  I  then  wash  out  the  stomach  and  permit  the 
patient  to  take  a  simple  evening  meal.  The  stomach  is  evacuated  the  next 
morning  before  any  food  is  taken.  If  it  is  empty,  this  shows  that  the 
stomach  which  was  unable  to  digest  a  test-meal  in  seven  hours  is,  never- 
theless, able  to  digest  a  smaller  meal,  the  evening  meal,  in  a  longer  period 
— in  about  twelve  hours.  If  the  stomach  is  not  empty  upon  the  succeed- 
ing morning,  a  higher  grade  of  motor  insufficiency  is  evident. 

Another  method  is  to  wash  the  stomach  clean  in  the  evening,  after 
which  the  patient  is  permitted  to  take  the  evening  meal,  and  the  stomach 
is  evacuated  the  next  morning  before  any  food  is  taken.  The  next  day, 
without  a  previous  evening  washing,  the  supper  is  eaten,  and  the  follow- 
ing morning  the  stomach  is  again  washed  out  before  any  food  is  taken.  In 
the  latter  case  we  will  often  see,  before  food  is  taken,  that  the  stomach  still 
contains  remains  of  food,  while,  upon  the  day  before,  when  an  evening 
washing  preceded,  it  contained  none.  This  shows  that  the  evening  washing 
has  benefited  the  condition  of  the  stomach.  Naturally  this  method  may 
be  modified  in  various  ways. 

Higher  grades  of  motor  insufficiency  wherein  the  stomach,  even  over- 
night, cannot  completely  get  rid  of  its  contents,  as  a  rule  are  associated 
with  an  increase  in  size,  and  this  is  not  surprising.  Evidently,  the  dura- 
tion of  the  motor  insufficiency  has  a  causative  influence  in  the  development 
of  this  increase. 

In  connection  with  gastric  evacuation,  there  must  be  an  exact  examina- 
tion of  the  gastric  contents.  This  also  occasionally  aids  us  in  the  diagnosis 
of  motor  disturbance,  for,  very  frequently,  remains  of  ingesta  which  had 
been  consumed  days,  even  weeks,  prior,  are  evacuated, — substances  such  as 
cherry-stones,  seeds  of  cranberries,  of  cucumbers,  of  pears,  currants,  etc. 
Marked  gas  fermentation  also  presupposes  a  prolonged  stagnation.  The 
three  characteristic  layers  of  the  gastric  contents  (the  upper  or  foamy 
layer,  the  medium  or  fluid  laj^er,  the  lower  or  finely  distributed  starchy  sedi- 
ment) proves  stagnation  and  at  least  a  sufficient  HCl  secretion.  For  an 
exact  estimation  of  slight  disturbance  in  less  developed  cases  Strauss  ^  gives 
valuable  advice,  which  is  to  take  the  unfiltered  gastric  contents,  place  them 
in  a  fermentation  tube  with  grape  sugar,  and  permit  them  to  stand  for 
some  time;  by  this  means  we  get  an  idea  of  the  rapidity  and  intensity  of 

*  Zeitschrift  fur  praktische  Aerste,  1896,  Nr.  6. 


140        DIAGNOSIS  AND  TREATMENT  OF  GASTRIC  DILATATION 

the  gas  formation,  of  the  retained  causes  of  fermentation.  The  further 
examination  of  the  gastric  contents  does  not  aid  so  much  in  the  exact 
estimation  of  motor  insufficiency  as  in  the  question  of  the  nature  and  final 
cause  of  the  dilatation,  that  is,  of  the  underlying  affection.  Although  by 
this  process  only  can  we  understand  the  nature  of  the  transformation  of 
the  ingesta,  and  from  the  gastric  juice  only  can  draw  conclusions  regard- 
ing the  underlying  affections  which  have  caused  the  dilatation  and  motor 
insufficiency,  nevertheless  we  obtain  from  this,  particularly  when  taken 
in  connection  with  the  other  symptoms,  important  points  of  support. 
Thus  coarse  undigested  remains  of  food,  particularly  of  meat,  absence  of 
free  HCl  and  profuse  amounts  of  lactic  acid  primarily  indicate  carcinoma, 
while  a  profuse  residue  consisting  only  of  fluid  and  remains  of  starch 
with  decided  yeast  fermentation,  the  presence  of  large  amounts  of  yeast 
cells  which  are  beginning  to  germinate,  as  well  as  sarcinae  and  an  abundant 
amount  of  hydrochloric  acid,  favor  benign  dilatation. 

A  constant  admixture  of  bile  in  the  material  vomited  or  evacuated  from 
the  stomach  points  to  a  deeper  seat  of  the  obstruction,  to  an  infrapapillary 
duodenal  stenosis. 

In  the  majority  of  cases,  we  may  content  ourselves  with  testing  the 
motor  activity  by  simple  lavage,  and,  perhaps,  as  a  control,  a  subsequent 
lavage  may  be  performed.  If,  one  hour  after  a  test  breakfast,  and  six  to 
seven  hours  after  a  test-meal,  a  plentiful  residue  of  half  a  liter  and  more 
is  found,  motor  insufficiency  is  certainly  present. 

This  method  is  satisfactory  in  practice.  For  exact  estimation  and 
scientific  purposes  it  is  insufficient.  Here  the  method  must,  at  the  same 
time,  show  us  what  residue  remains  in  the  stomach.  Formulas  for  deter- 
mining the  residue  have  been  given  by  Mathieu  and  Remond,^  Strauss,^ 
Goldschmidt,^  Sorensen  and  Brandenburg.*  We  cannot  enter  into  the  de- 
tails of  these  processes.     In  practice  they  may  all  be  dispensed  with. 

Any  one  who  desires  to  employ  still  other  methods  of  examination  for 
purposes  of  control  finds  a  number  of  such  at  his  service.  One  is  Strauss' 
currant  test,  in  which  the  patient  is  given  in  the  evening  a  table^poonful 
of  currants  or  cranberry  jelly,  and  upon  the  succeeding  morning,  the 
stomach  is  evacuated  after  a  test  breakfast  or  a  test-meal,  and  an  exam- 
ination is  made  to  determine  whether,  and  how  many,  seeds  are  still  present 
in  the  evacuated  contents.  In  a  normal  person  these  are  no  longer  found. 
Other  tests  are  by  the  salol  method  and  Klemperer's  oil  method.  These 
tests  are  all  inferior  to  the  old  process,  first  employed  by  Leube,  for 
testing  the  duration  of  digestion.     The  iodipin  method,  lately  advised, 


*  Soc.  de  biolog.,  1890. 

'  Therapeutische  Monatshefte,  1895. 

'  Miinchener  mrd.  Wochenschrift,  1897,  Nr.   13. 

*  Archiv  f.  Verdauuvnskrankheiten,  Bd.  III. 


SYMPTOMATOLOGY  141 

which  depends  upon  the  fact  that  the  gastric  juice  is  incapable  of  freeing 
iodin  from  the  iodin  fat,  and  that  the  iodin  is  first  set  free  in  the  intes- 
tine, can,  if  necessary,  be  employed  as  a  substitution  method,  which  is  not 
quite  free  from  objection  in  those  eases  in  which  absolutely  no  use  can 
be  made  of  the  stomach-tube.  This  method  has  the  disadvantage  that  it 
consumes  more  time  than  lavage,  while  the  latter  is  superior  in  that  it 
enables  us  to  form  conclusions  in  regard  to  the  motor  activity,  and  also 
shows  us  the  secretory  condition. 

These  are  the  objective  signs  which  indicate  gastric  dilatation  and 
motor  insufficiency. 

Before  we  ask  what  aids  we  have  at  command  to  assist  us  in  determin- 
ing the  nature  of  the  dilatation  and  the  motor  insufficiency,  a  few  symptoms 
may  be  briefly  mentioned  which  are  directly  connected  with  the  disturbed 
motor  activity  of  the  stomach. 

That  disturbances  of  intestinal  activity  are  not  rarely  observed  in  dila- 
tation of  the  stomach  is  not  surprising.  Patients  with  this  affection  fre- 
quently have  a  tendency  to  constipation;  much  more  rarel}'^  they  suffer 
from  diarrhea.  This  constipation  may,  to  a  great  extent,  be  due  to  insuffi- 
cient absorption  of  water;  the  excretion  of  water  from  the  stomach  and 
the  difficult  propulsion  of  the  ingesta  into  the  intestine  may  be  the  cause 
of  this.  In  cases  of  high-graded  dilatation  the  dryness  of  all  the  tissues 
is  the  reason  why  more  water  is  withdrawn  from  the  intestinal  contents 
than  in  the  norm.  This  readily  explains  the  conspicuously  hard  and 
dry  composition  of  the  feces  so  often  observed,  and  the  difficulty  of  their 
propulsion. 

The  diminution  in  the  amount  of  urine  noted  in  extreme  dilatation  is 
due  to  the  decreased  absorption  of  water.  The  amount  of  urine  voided  is 
a  fair  measure  of  the  activity  of  the  stomach.  In  very  marked  cases,  the 
daily  excretion  of  urine  is  often  decreased  to  a  few  cubic  centimeters. 
An  increase  in  the  amount  of  urine  is  an  infallible  sign  of  improvement; 
the  slighter  the  amount,  the  more  concentrated  it  naturally  is,  and  the 
higher  its  specific  gravity.  In  dilatation  with  a  plentiful  HCl  production, 
the  urine  often  shows  a  neutral  or  alkaline  reaction,  and  also  when,  in 
consequence  of  profuse  vomiting  or  by  frequently  repeated  lavage,  much 
acid  gastric  juice  is  removed. 

Occasionally  we  note  an  action  upon  the  heart  shown  by  a  slowing  of 
the  heat.  However,  this  occurs  not  only  in  dilatation,  but  also  in  many 
other  gastric  affections,  and,  therefore,  may  in  nowise  be  designated  a 
pathognomonic  peculiarity  of  dilatation. 

More  important  than  the  previously  mentioned  effects  are  certain  de- 
rangements of  the  nervous  system.  Among  these  the  symptom-complex 
designated  as  tetany  is  especially  interesting.  This,  as  is  well  known, 
manifests  itself  particularly  by  tonic  muscular  spasms  in  the  hands  and 
arms,  occurring  intermittently,  and  an  increased  irritability  of  the  nerves. 


142        DIAGNOSIS   AND  TREATMENT   OF   GASTRIC   DILATATION 

Fortunately,  tetany  is  not  among  the  frequent  sequels  of  dilatation.  Most 
cases  of  tetany  in  gastric  dilatation  observed  up  to  the  present  have  occurred 
in  benign  pyloric  stenoses,  mostly  in  such  as  were  accompanied  by  hyper- 
acidity and  acid  fermentation;  however,  cases  of  tetany  have  also  been 
observed  in  carcinomatous  pyloric  stenosis,  in  absence  of  HCl  secretion,  and 
in  lactic  acid  fermentation.  How  tetany  is  produced  in  these  cases  is  still 
a  mooted  question.  With  Kussmaul,  some  attribute  it  to  a  deficiency  of 
water  in  the  organism;  in  another  theory,  the  development  of  the  attacks 
of  spasm  is  attributed  to  a  reflex  irritation  of  the  nerve  center  from  the 
irritated  nerves  of  the  gastric  mucous  membrane;  in  a  third  theory,  gastric 
tetany  is  regarded  as  the  consequence  of  an  intoxication  of  the  organism 
by  abnormal  products  of  metabolism  in  the  diseased  gastrointestinal  canal. 
So  far  as  I  am  able  to  judge,  the  last  theory  has  found  the  most  adherents. 
A  discussion  of  these  various  theories  would  lead  us  too  far  from  our  sub- 
ject; and,  naturally,  I  must  decline  to  enter  upon  a  special  description  of 
the  symptoms  of  tetany.     (See  volume  "  Diseases  of  the  Nervous  System.") 

Headache  and  vertigo  are  not  rarely  the  sequels  and  accompanying 
symptoms  of  dilatation;  usually  these  are  not  very  intense.  In  the  ter- 
minal stages  of  marked  dilatation  the  patients  are  sometimes  observed  to 
become  soporose,  and  finally  succumb  to  coma.  Such  a  case,  in  which  sopor 
and  general  spasms  occurred  and  terminated  fatally  after  a  few  days,  has 
recently  been  reported  by  Jiirgensen.^  In  this  case  the  fact  was  note- 
worthy that  during  the  soporose  condition  the  secretion  of  urine  ceased 
entirely.  The  supposition  of  an  autointoxication  in  such  cases  is  certainly 
very  reasonable. 

The  appearance  of  curious  drumstick-like  changes  in  the  fingers  and 
toes  in  a  case  of  gastrectasis  due  to  benign  pyloric  stenosis  must  be  men- 
tioned. This  case,  recently  reported  by  Dennig,^  is  interesting  for  the 
reason  that  after  a  successful  operation  (pyloric  resection)  there  was  a 
complete  retardation  of  the  drumstick-like  changes. 

If,  after  an  examination  by  the  methods  detailed,  gastrectasis  and 
motor  insufficiency  have  been  determined,  we  then  inquire  what  has  pro- 
duced the  condition,  whether  a  mechanical  obstruction  at,  or  in  the  neigh- 
borhood of,  the  pylorus,  or  simple  flaccidity.  The  question  may  sometimes 
be  decided  at  a  glance,  or  immediately  upon  palpating  the  abdomen,  in 
other  cases  only  after  minute  consideration  of  all  the  symptoms  and  after 
prolonged  observation.  If  the  condition  were  as  simple  as  has  recently 
Ijeen  maintained,  that  every  chronic  dilatation  is  due  to  a  hindrance  in 
passage  or  to  a  local  process  at  the  outlet  of  the  stomach,  the  diagnosis  of 
cctasis,  and  also  of  "  pyloric  stenosis  "  could  be  at  once  made.  But  the 
conditions  are  not  so  simple,  although  it  is  true  that  the  most  marked 

•  Deutsches  Archiv  f.  klin.  Medicin,  Bd.  LX. 
'  Miinchener  med.  Wochenschrift,  1901,  Nr.  10. 


DIFFERENTIAL   DIAGNOSIS  143 

grades  of  dilatation  occur  in  pyloric  stenosis.  In  practice,  however,  we 
must  diagnosticate  not  only  the  marked  grades  of  ectasis,  but  also  the 
milder  grades,  the  earlier  stages. 

Such  forms  are  due  to  an  atonic  condition.  But  spastic  processes  also, 
without  an  organic  stenosis  being  present,  occasionally,  as  we  have  before 
stated,  play  a  role  in  the  etiology  of  dilatation. 

Atony,  as  we  have  seen,  occurs  in  persons  whose  nutrition  has  suffered, 
and  in  those  with  flaccid  abdominal  walls;  not  rarely,  gastroptosis  and 
enteroptosis  exist  simultaneously.  Such  an  atonic  stomach,  as  a  rule,  has 
a  flaccid  feeling  with  but  little  tension.  In  spite  of  a  sufficient  secretion 
of  gastric  juice,  as  shown  by  lavage,  we  frequently  find  coarse  particles  of 
food,  especially  fibers  of  meat.  The  latter  are  probably  due  to  a  loss  of 
energy  of  the  muscularis  which  prevents  an  intimate  admixture  of  the 
ingesta  with  the  gastric  juice. 

A  successful  treatment,  in  such  cases,  often  confirms  the  diagnosis.  If, 
by  suitable  diet  and  by  improving  the  nutrition, — briefly,  by  methods  which 
strengthen  the  tonus  of  the  muscularis  and  improve  the  general  nutrition, — 
we  can  remove  the  symptoms  of  motor  insufficiency,  this  result  favors 
the  view  that  we  are  not  dealing  with  an  organic  stenosis. 

DIFFERENTIAL    DIAGNOSIS 

In  the  differential  diagnosis  between  atonic  and  mechanical  dilatation, 
the  history  is  important.  When  symptoms  of  ulcer  have  previously  existed, 
when  in  connection  with  this  the  picture  of  dilatation  has  gradually  devel- 
oped, our  first  thought  is  that  a  cicatrix  of  the  pylorus  has  produced 
stenosis.  If  examination  reveal  a  uniform  resistance  in  the  pyloric  region, 
if  the  secretion  of  gastric  juice  be  normal  or  increased,  if  we  observe  active 
peristaltic  movements,  a  cicatrix  from  ulcer  is  indicated.  When,  upon  in- 
flation, we  find  that  the  thickened  area  remains  immobile  at  the  same  place 
in  which  it  appeared  while  the  stomach  was  empty,  this  we  assume  to  indi- 
cate a  simultaneous  perigastric  adhesion. 

The  diagnosis  is  more  difficult  in  cases  in  which  hypersecretion  and 
dilatation  exist  simultaneously.  I  have  already  discussed  the  varying  pos- 
sibilities of  this  combination.  Active  peristalsis  favors  a  mechanical  ob- 
struction, although  not  necessarily  an  organic  hindrance.  Preceding  gas- 
tric hemorrhage  favors  ulcer,  and,  possibly,  a  cicatricial  stenosis,  although 
this  is  by  no  means  absolutely  proven.  The  results  of  therapy  often  indi- 
cate that  the  cause  which  brought  about  the  dilatation  could  not  well  have 
been  an  organic  stenosis. 

Probably  the  most  positive  sign  of  mechanical  obstruction  at  the  pylorus 

is  active  peristalsis.     It  is  never  absent  except  in  the  terminal  stages  and 

in  those  instances  in  which  secondary  degeneration   of  the  hypertrophic 

musculature  has  occurred.     Yet  the  obstruction  is  not  necessarily  an  organic 

11 


144         DIAGNOSIS   AND  TREATMENT   OF   GASTRIC   DILATATION 

one.  As  is  well  known,  spasms  of  the  pylorus  play  a  part  in  many  forms 
of  disease  of  the  stomach  as  well  as  in  dilatation,  and  are  particularly  prom- 
inent in  those  which  run  their  course  with  increased  secretion  of  gastric 
juice.  According  to  Serejukow,  acids  cause  the  sphincter  muscle  to 
contract. 

A  factor  not  without  significance  in  the  differential  diagnosis  between 
these  forms  of  dilatation  is  the  rapidity  of  the  influx  and  outflow  of  the 
gastric  contents;  that  is,  of  the  water  used  for  lavage.  The  stronger  the 
tonus  of  the  stomach,  the  more  powerful  the  musculature  in  an  obstruction 
at  the  outlet  of  the  stomach,  the  greater  the  force  with  which  the  organ 
will  empty  itself.  The  more  slowly  the  water  used  for  lavage  flows  in, 
the  more  rapidly  will  it  flow  out.  The  conditions  are  the  reverse  of  this 
witli  very  flaccid,  thin,  atrophic  gastric  walls.  Here  the  gastric  contents 
are  discharged  very  slowly  and  incompletely;  the  water  poured  in,  however, 
rushes  with  force  through  the  tube,  so  that  swirls  develop,  and  air  is  readily 
aspirated  into  the  stomach. 

An  admixture  of  bile  is  not  infrequently  observed  at  the  termination 
of  a  washing  of  the  stomach,  especially  in  atonic  dilatation.  If  other  signs 
of  stenosis  exist,  the  permanent  regurgitation  of  bile  favors  an  infrapapil- 
lary  seat  of  the  stricture. 

The  most  important  sign  of  stenosis,  however,  is  always  the  demonstra- 
tion of  a  tumor  at,  or  in  the  vicinity  of,  the  pylorus.  The  tumor,  in  itself, 
does  not  prove  a  stenosis,  for  we  must  be  certain  that  it  belongs  to  the 
stomach  or  to  the  adjacent  portion  of  the  duodenum. 

When  a  tumor  has  been  diagnosticated,  the  question  to  be  next  decided 
is  wliether  it  be  benign  or  malignant.  We  would  digress  too  far  if  we 
entered  uj)on  this  differential  diagnosis.  This  point  can  only  be  established 
liy  considering  the  duration  of  the  disease,  the  condition  of  the  gastric 
contents,  the  secretion  of  the  gastric  juice  and  the  like. 

That  the  results  of  treatment  may  be  utilized  to  a  certain  extent  in 
diagnosis,  particularly  in  differential  diagnosis,  whether  stenosis,  or  atony, 
()]•  only  functional  spasm  be  present,  is  clear.  Rapid  relief  of  the  dilata- 
tion by  suitable  treatment  favors  the  atonic  form  or  spastic  stenosis. 
Xaturally,  in  a  temporary  improvement,  we  should  not  at  once  permit  our- 
selves to  make  this  diagnosis.  Ectases  due  to  organic  stenosis  are  also 
ameliorated  Ijy  methodical  lavage,  by  diet,  and  other  remedies;  but  this 
improvement  is  not  permanent. 

COURSE    OF   THE    DISEASE 

Having  described  the  symptoms  of  motor  insufficiency  and  dilatation, 
it  is  next  ex))edient  to  describe  their  course.  In  the  majority  of  cases  the 
elinieal  ])ieture  of  dilatation  develops  gradually;  rarely  does  it  happen  that 
a  single  deleterious  effect,  brief  in  duration,  suddenly  causes  dilatation. 


COURSE  OF  THE  DISEASE  145 

In  the  course,  as  in  the  development,  we  must  differentiate  between  acute 
and  chronic  dilatation.  The  acute  varieties,  as  a  rule,  are  rapidly  cured 
by  appropriate  treatment;  yet,  repeatedly,  cases  with  a  fatal  termination 
have  been  observed.  In  explanation  of  these,  Albrecht's  previously  men- 
tioned investigation  of  arterio-mesenteric  intestinal  occlusion  at  the 
duodeno-jejunal  boundary  might  well  be  considered. 

Whether,  in  all  cases  of  acute  gastric  dilatation  running  a  fatal  course, 
mechanical  factors  of  this  kind  play  an  important  role,  cannot,  naturally, 
be  subsequently  decided.  The  symptoms  of  severe  acute  dilatation  have 
several  times  appeared  without  any  demonstrable  cause.  In  a  few  cases 
the  clinical  picture  developed  directly  after  anesthesia;  in  several  cases 
a  severe  infectious  disease  immediately  preceded  the  condition.  It  is  worthy 
of  note  that  in  a  number  of  these  cases  vomiting  was  absent  during  the 
entire  course;  this  is  probably  to  be  explained  by  the  high-graded,  over- 
distention  and  loss  of  tonicity  of  the  walls  of  the  stomach. 

Such  severe,  rapidly  fatal  cases  are  very  rare.  Much  more  frequently 
mild  and  moderately  severe  forms  are  observed,  the  origin  of  which  is  traced 
to  gross  errors  in  diet.  A  marked,  painful  swelling  of  the  abdomen  soon 
occurs  and  is  associated  with  nausea,  vomiting,  and  great  thirst.  In  mild 
cases  the  symptoms  disappear  in  a  few  days,  particularly  if  thorough  lav- 
age is  performed,  and  we  must  be  careful  to  see  that  the  stomach  is  abso- 
lutely emptied.  In  other  cases  the  symptoms  do  not  yield  so  readily.  The 
earlier  and  more  energetic  the  treatment,  the  more  favorable  and  rapid,  as 
a  rule,  is  the  course. 

In  private  practice,  we  more  frequently  deal  with  chronic  cases — dila- 
tation which  develops  gradually.  The  course  of  these  varies  greatly,  and 
depends  upon  different  factors :  the  underlying  cause,  the  mode  of  life,  and 
numerous  other  conditions.  Not  infrequently  we  notice  a  change  in 
the  symptoms,  sometimes  amelioration,  at  other  times  aggravation;  this  is 
observed,  above  all,  in  cases  of  non-organic  stenosis.  Organic  stenosis,  on 
the  other  hand,  generally  shows  a  progressive  increase  in  the  symptoms. 
The  most  marked  degrees  of  dilatation  are  met  with  in  pyloric  stenosis; 
atonic  dilatation,  in  the  majority  of  cases,  is  extremely  slight.  Yet  it 
appears  to  me  that  we  are  not  justified  in  denying  absolutely  the  occur- 
rence of  atonic  dilatation,  as  some  writers  do.  At  all  events,  it  is  rare, 
and  usually  not  of  marked  extent. 

It  is  unfortunate  that  the  test  by  physicians  of  the  motor  activity  has 
not  everywhere  been  regarded  as  of  equal  value  with  the  test  of  the  secre- 
tory activity.  Nevertheless,  we  must  admit  that  the  disturbances  of  motor 
activity  are  often  of  the  greatest  importance,  even  more  so  than  the  varia- 
tions in  the  secretion  of  the  gastric  juice.  If  in  every  serious  gastric 
disturbance  the  same  importance  were  attached  to  the  motor  as  to  the 
secretory  activity,  many  a  case  wliich  is  now  recorded  under  the  name 
"  chronic  catarrh  "  or  "  nervous  dyspepsia  "  would  be  recognized  as  motor 


146         DIAGNOSIS  AND  TREATMENT   OF   GASTRIC   DILATATION 

insufficiency  or  as  dilatation,  although  not  of  extreme  degree.  I  have 
met  with  a  considerable  number  of  such  moderate  dilatations  which,  under 
appropriate  treatment,  proper  diet,  rest,  forced  feeding,  methodical  lavage 
and  the  like,  were  entirely  cured.  These  patients  with  atony,  even  after 
relatively  light  meals,  have  a  sensation  of  satiety,  of  pressure  or  fulness 
in  the  stomach;  they  feel  indisposed  to  follow  their  occupations;  they 
are  listless.  As  a  rule  there  is  no  complaint  of  actual  pain.  If  gas- 
troptosis  goes  hand  in  hand  with  atony,  as  it  frequently  does,  the  dis- 
turbances are  increased.  The  patients,  after  eating  only  a  little  food,  have 
very  disagreeable  sensations,  they  lose  their  appetite,  and  gradually  the 
nutrition  suffers.  Such  atonies  are  very  often  disregarded,  or  erroneously 
diagnosticated,  and  if  they  do  not  early  come  under  suitable  treatment  they 
rapidly  increase  in  severity.  Only  a  minute  objective  examination  and 
the  aid  of  an  accurate  history  make  an  early  diagnosis  possible.  The  more 
promptly  suitable  treatment  is  instituted,  the  easier  is  the  cure.  It  can 
be  readily  understood  that  these  forms  show  frequent  changes,  a  tendency 
to  relapse,  and  that  periods  of  amelioration  and  aggravation  alternate. 

A  much  more  uniform  course  is  generally  observed  in  motor  insufficiency 
and  dilatation  due  to  organic  stenosis.  Here,  also,  transitory  improve- 
ment may  occur;  but  it  cannot  last  long  unless  we  succeed  in  remov- 
ing the  obstruction  which  causes  the  stenosis;  however,  this  is  hardly  possi- 
ble except  by  surgical  interference.  We  cannot  enter  into  details  of  the 
modifications  of  these  forms  on  account  of  the  great  variety  of  their  causes. 

DIAGNOSIS 

In  discussing  the  diagnosis  of  motor  insufficiency  in  dilatation,  I  may 
be  brief.  This  is  based  solely  upon  the  objective  examination,  upon  the 
proof  of  prolonged  digestion,  and  upon  an  increase  in  the  size  of  the 
stomach.  Among  the  methods  that  have  been  mentioned,  the  most  certain 
one  for  determining  motor  insufficiency  is  to  wash  out  the  stomach  six 
to  seven  hours  after  a  test-meal,  or  two  hours  after  a  test  breakfast.  Splash- 
ing sounds  heard  at  a  period  in  which  the  stomach  should  be  empty  assist 
the  diagnosis,  but  never  render  the  diagnostic  washing  out  unnecessary. 
The  latter  has  the  advantage  that  it  simultaneously  enables  us  to  form 
conclusions  in  regard  to  the  secretory  activity,  and  also  to  determine  what 
processes  cause  the  dilatation. 

The  degree  of  motor  insufficiency  is  readily  estimated  from  the  amount 
of  retained  material  and  the  period  of  its  retention  in  the  stomach. 

Considering  the  diagnostic  criteria  which  have  been  mentioned,  con- 
fusion with  other  affections  is  hardly  possible.  Megalogastria  could  only 
be  mistaken  for  dilatation  if  we  should  neglect  the  washing  out  of  the 
stoniiK  li  which  is  absolutely  necessary  to  test  the  motor  activity.  Still 
loss  would  it  be  possible  to  confound  the  condition  with  chronic  gastritis 


DIAGNOSIS  147 

or  with  nervous  dyspepsia.  This  confusion  is  impossible  if  diagnostic 
lavage  be  performed.  However,  atony  and  motor  insufficiency  may  occur 
simultaneously  with  chronic  gastritis  and  nervous  dyspepsia;  motor  insuffi- 
ciency is  only  a  disturbance  of  function  which  may  develop  in  various  ways. 

In  practice  confusion  of  gastrectasis  with  gastroptosis  occurs.  This 
error  is  not  rare,  for  the  reason  that  with  a  low  position  of  the  greater 
curvature  of  the  stomach  and  a  succussion  sound  developed  below  the  navel 
dilatation  is  assumed  without  further  investigation.  This  is  not  justified 
by  the  facts.  The  proof  of  displacement  of  the  lower  boundary  of  the 
stomach  is  not  sufficient  to  determine  dilatation;  its  total  extension  must 
be  determined,  not  only  that  of  the  lower,  but  also  of  the  upper  and 
the  lateral  borders.  The  investigation  of  the  latter  is  interesting.  As 
Michaelis  ^  has  shown  in  cases  of  enlargement  of  the  stomach  in  which  the 
gastric  motility  was  severely  disturbed,  the  right  border,  as  a  rule,  is  found 
much  farther  removed  from  the  median  line  than  in  a  stomach  with  normal 
motility. 

On  the  other  hand,  we  must  remember  that  motor  insufficiency  and  dila- 
tation are  often  combined  with  gastroptosis.  It  is  quite  natural  that  a 
permanent  over-weighting  of  the  stomach  should  lead  to  a  sinking,  to 
gastroptosis.  In  fact,  in  almost  all  extreme  dilatations,  we  find  more  or 
less  sinking  of  the  lesser  curvature.  An  extreme  case  of  decidedly  low 
position  of  the  stomach  which  may  readily  be  recognized  (with  a  high 
grade  of  dilatation)  may  be  seen  in  the  accompanying  illustration  (Fig.  10) 
in  the  case  of  a  woman,  aged  59,  who  had  carcinomatous  stenosis  of  the 
pylorus. 

Simple  atonic  dilatations  very  frequently  are  combined  with  gastrop- 
tosis. This  combination  is  not  difficult  to  recognize,  provided  we  make 
use  of  the  previously  mentioned  diagnostic  aids. 

By  what  means  atonic  dilatation  is  to  be  distinguished  from  that  caused 
by  mechanical  obstruction  has  been  stated.  This  question  can  often  only 
be  decided  after  prolonged  observation,  under  some  circumstances  only  by 
studying  the  results  of  treatment. 

Much  more  difficult  is  it  to  decide  as  to  the  nature  of  the  constriction. 
Whether  we  are  dealing  with  benign  or  malignant  stenosis  is  a  most  im- 
portant question,  and,  in  the  majority  of  cases,  not  difficult  to  decide.  A 
hard,  nodulated  tumor  in  the  pyloric  region,  abundant  coarse  residue  with 
frequent  hemorrhagic  admixture  in  the  form  of  coffee-ground  masses,  ab- 
sence of  free  HCl,  lactic  acid  fermentation,  and  rapidly  increasing  cachexia, 
naturally  favor  malignant  stenosis.  But.  in  malignant  stenosis,  particu- 
larly in  such  as  develops  from  an  ulcer,  we  often  find  a  normal  secretion 
of  gastric  juice.  It  must  be  borne  in  mind  that  no  single  symptom  is 
decisive,  but  the  combination  of  all  the  symptoms  is  necessary  to  a  diag- 

^Zeitschr.  f.  klin.  Med.  XXXIV. 


Fig.  10. 


TREATMENT  149 

nosis;  whether  one  or  the  other  is  absent  is  not  conclusive.  But  a  diag- 
nosis can  never  be  looked  upon  as  certain  which  does  not  combine  all 
the  symptoms. 

PROGNOSIS 

As  has  been  shown,  the  importance  of  motor  insufficiency  and  dilata- 
tion varies  greatly  in  th,e  individual  case ;  it  may  run  an  acute  or  a  chronic 
course.  At  one  time  it  represents  a  transitory  atonic  condition,  at  another 
time  it  depends  upon  a  mechanical  obstruction,  which  in  one  case  may 
be  benign,  and  in  the  other  malignant.  The  prognosis  of  motor  insuffi- 
ciency in  dilatation,  therefore,  also  varies  strikingly  in  the  individual  case. 
Some  forms  are  cured  in  the  briefest  time  by  proper  management,  others 
only  after  months  or  even  years  of  treatment;  some  in  the  briefest  time 
terminate  fatally,  others  again  are  not  susceptible  to  internal  treatment, 
and  surgical  measures  alone  will  cure  the  affection  or  moderate  its  con- 
sequences. 

The  earlier  treatment  is  begun,  and  the  more  systematically  it  is  car- 
ried out,  the  more  rapidly  do  acute  dilatations  improve.  Under  some  cir- 
cumstances threatening  symptoms  may  intervene,  and  the  cases  even  ter- 
minate fatally.  Generally  no  prognosis  is  possible  in  chronic  dilatation. 
Many  factors  influence  the  prognosis  in  a  given  case;  thus,  the  duration 
of  the  affection  and  the  degree  of  motor  insufficiency.  Moderate  degrees 
of  motor  insufficiency  which  have  not  existed  for  a  long  time  naturally 
lead  to  a  more  favorable  prognosis  than  long-existing,  high-graded  dilata- 
tions. But,  above  all,  the  prognosis  depends  upon  the  underlying  cause 
of  the  dilatation.  If  we  succeed  in  removing  the  causative  factor,  as  a 
rule  we  also  succeed  in  ameliorating  the  dilatation.  Mild  and  medium 
grades  of  atony  under  suitable  treatment  are  often  cured  in  the  briefest 
time.  Where  the  cause  of  the  dilatation  is  an  organic  obstruction  in  the 
pylorus  or  its  vicinity,  improvement  can  only  be  brought  about  by  surgical 
means.  Internal  treatment  in  such  cases  produces  apparent,  but  in  reality 
transitory,  results.  Unfortunately  many  cases  are  no  longer  suitable  for 
operative  interference,  such  as  extensive  carcinomata,  or  those  in  which 
metastases  are  present  and  the  like.  The  dilatation  alone  does  not  per- 
mit a  positive  prognosis,  but  this  depends,  above  all,  upon  the  underlying 
affection ;  that  is,  upon  the  cause  which  has  produced  the  dilatation. 


TREATMENT 

We  now  come  to  the  main  question:  How  shall  we  treat  dilatation? 
Naturally  it  is  not  my  object  to  explain  here  all  the  methods  of  treatment 
and  the  other  procedures  which  may  be  necessary  on  account  of  the  causa- 
tive factor,  carcinoma,  cicatrix  from  ulcer,  perigastric  adhesions,  and  sim- 
ilar conditions;  we  should  digress  too  far  from  our  actual  theme.     But 


150         DIAGNOSIS   AND  TREATMENT   OF  GASTRIC   DILATATION 

we  shall  consider  only  the  treatment  of  motor  insufficiency  and  dilatation 
as  such. 

Acvte  dilatations  which  have  been  brought  about  by  over-loading  the 
stoniacli  with  food  difficult  to  digest  require  immediate  and  thorough  empty- 
ing of  the  stomach  and  an  absolute  rest  of  the  organ  for  some  time.  When 
debility  necessitates  the  administration  of  food  or  fluid,  rectal  alimentation 
should  be  resorted  to.  Under  all  circumstances,  however,  the  stomach 
must  have  absolute  rest  in  the  days  succeeding.  How  long  this  treatment 
is  to  be  pursued  naturally  depends  upon  the  severity  of  the  symptom- 
complex.  In  acute  dilatation  in  which  symptoms  of  obstruction  appear, 
it  is  not  enough  merely  to  empty  the  over-filled  stomach,  and  to  suspend 
for  some  time  the  administration  of  food  and  fluid  by  the  mouth ;  we  must 
also  attempt  to  relieve  the  coils  of  the  small  intestines  at  their  mesenteric 
roots,  which,  by  a  drawing  process,  have  been  forced  down  into  the  pelvis. 
For  this  purpose,  the  patient  must  be  placed  in  such  a  position  that  the 
small  intestine  may  find  its  way  out  of  the  pelvis,  and  the  tension  of  its 
mesentery  be  quickly  relieved.  Therefore  the  knee-elbow  position,  or  lying 
prone  upon  the  stomach,  is  most  effective.  Cases  of  this  kind  ending  in 
recovery  have  recently  been  reported  by  Miiller.^  Where  this  method  does 
not  bring  relief,  eventually  surgical  measures  only  can  avail. 

The  conditions  are  different  in  the  much  more  frequent  chronic  forms 
of  dilatation  and  motor  insufficiency  with  which  the  physician  must  chiefly 
concern  himself.  Although  our  object  varies  according  to  whether  we  are 
dealing  with  simple  atony,  with  atonic  dilatation,  or  with  dilatation  caused 
by  a  mechanical  obstruction,  nevertheless,  certain  therapeutic  rules  are 
equally  operative  in  all  these  forms.  In  these  groups,  prolonged  stagna- 
tion, and  all  abnormal  weighting  of  the  stomach,  must  be  avoided  as  much 
as  possible,  that  is,  combated,  and  the  diet  must  be  so  ordered  that  it  will 
necessitate  the  least  possible  exercise  of  the  motor  activity  of  the  stomach, 
and  can  by  no  possibility  be  injurious. 

Our  primary  object  in  dilatation  is  to  regulate  the  diet.  We  must  in- 
variably consider  first,  the  kind  of  food,  and,  secondly,  much  more  impor- 
tant ill  dilatation,  the  form  in  which  it  is  administered.  In  modern  prac- 
tice tlu"  majority  of  physicians  advise  a  dry  diet  in  dilatation;  fluids  are 
to  1)0  refrained  from  as  much  as  possible,  for  they  load  the  stomach  by 
their  weight,  are  badly  absorbed,  and,  in  pyloric  stenosis  are  expelled  from 
the  stomach  with  difficulty  as  is  proven  by  the  over-distention  of  the  stomach 
wilb  fluid.  A  dry  diet,  therefore,  with  the  greatest  possible  limitation  of 
iluids.  is  advisable. 

In  every  form  of  dilatation,  whether  it  depend  upon  atony  or  upon 
mechanical  obstruction,  the  motor  activity  of  the  stomach  is  insufficient, 
eitli(M-  absolutely  or  relatively  insufficient,  according  to  the  amount  of  labor 

*  Deutsche  Zeitschrift  fur  Chirurgie,  Bd.  LVI. 


TREATMENT  151 

required  of  it.  We  must  reckon  with  this  motor  weakness ;  i.  e.,  we  must 
choose  a  diet  which  necessitates  but  slight  exertion  on  the  part  of  the 
motor  power,  which  does  not  require  over-exertion,  but  one  that  prevents 
it.  For,  by  means  of  the  motor  power,  the  fragments  of  ingesta  are  split 
up  in  the  stomach,  reduced  in  size,  liquefied,  and,  finally,  propelled  from 
the  stomach  into  the  intestines. 

V,  Mering,  by  his  well  known  researches,  has  proven  that  the  healthy 
stomach  possesses  only  very  slight  power  of  absorption,  and  that  its  labor 
consists  chiefly  in  propelling  the  fluid  gastric  contents  into  the  intestines. 
Moritz,  too,  has  demonstrated  by  investigations  that  fluid  food  is  more 
rapidly  propelled  into  the  intestine  than  pappy  food,  and  this  again  in  a 
shorter  time  than  solids. 

Therefore,  above  all,  in  motor  insufficiency  and  dilatation  we  must 
choose  a  diet  which  is  readily  forced  onward  into  the  intestine.  This  is 
true,  however,  only  of  fluid  and  pappy  food. 

In  opposition  to  the  almost  universal  practice  of  emplo3ring  a  dry  diet, 
I  have  for  years  advised  fluid  and  pappy  forms  of  food  in  dilatation.  This 
method  appears  to  have  recently  gained  many  adherents.  In  the  choice 
of  the  diet  we  must  always  reckon  with  the  weakened  motor  power,  and, 
therefore,  so  far  as  possible,  choose  a  food  that  may  be  broken  up  into  fine 
particles. 

One  objection  has  been  raised  to  fluid  diet,  namely,  that  the  nutritive 
value  of  fluid  food,  in  proportion  to  its  volume,  is  but  slight.  This  argu- 
ment may,  however,  be  met  by  choosing  a  food  as  nutritious  as  possible. 
Such  a  nutriment  is  represented  by  milk,  which  may  be  given  pure,  or  as 
buttermilk,  as  cream,  as  milk-custard,  and  as  gruel  with  various  additions 
of  grits,  rice,  and  the  like.  The  taste  may  be  varied  by  the  addition  of 
aromatic  substances — by  brandy,  lime-water,  by  the  addition  of  cocoa, 
vanilla,  cinnamon,  lemon,  etc.  We  can  generally  succeed,  in  almost  all 
patients,  in  administering  larger  or  smaller  amounts  of  milk,  even  when 
they  express  a  dislike  for  it. 

Eggs  may  be  variously  prepared  and,  in  addition  to  other  foods,  take 
a  place  in  the  diet  of  the  patient.  The  addition  of  tropon,  nutrose,  plas- 
mon  and  similar  preparations  to  fluid  and  pappy  food  increases  their 
nutritive  value. 

Meat,  in  so  far  as  the  underlying  affection  permits  its  use,  had  best 
be  given  scraped  or  chopped.  Calves'  brains  and  sweetbreads,  on  account 
of  their  pulpy  consistence,  are  very  suitable  for  such  patients.  Game  must 
be  avoided,  as  well  as  goose,  duck,  and  fat  pork.  Of  fish  the  most  suitable 
are  giant  pike,  pike,  per5h,  and  shell  fish.  Vegetables  are  to  be  given  only 
very  finely  split  up  or  in  the  form  of  puree, — of  asparagus  the  heads,  of 
cauliflower  the  tops,  and  mashed  potatoes. 

Fat,  especially  milk-fat,  is  also  suitable  for  patients  with  disturbances 
of  the  gastric  motility,  particularly  for  such  forms  as  are  combined  with 


152         DIAGNOSIS   AND  TREATMENT   OF   GASTRIC   DILATATION 

hyperacidity.  Formerly  the  opinion  prevailed  that  large  amounts  of  fat 
lie  heavy  in  the  stomach  ^  and  that  in  disturbances  of  its  motility  they 
should  be  avoided.  The  researches  of  Strauss,^  Bachmann,*  Wolkowitsch  * 
and  others,  show  that  too  much  cream  will  diminish  the  secretory  power 
of  the  stomach,  and  even  in  the  stomach  showing  motor  insufficiency  it 
is  siii)jectively  better  borne  than  a  large  quantity  of  carbohydrates.  In 
liypersecretion,  and  particularly  when  disturbance  of  motility  is  simul- 
taneously present,  the  profuse  ingestion  of  undissolved  carbohydrates  in- 
creases hypersecretion.  For  these  cases  of  disturbance  of  motility  with  well 
maintained  HCl  secretion,  it;,  therefore,  seems  more  rational  to  substitute 
for  the  carl)ohydrates  as  far  as  possible  the  fats  which  are  readily  and  thor- 
ou<i:hly  broken  up.     Here  the  aJhumin  fat  diet  for  several  weeks  is  advisable. 

It  is  well  kno^vn  that  some  patients  cannot  digest  fat,  particularly 
cream.  In  these  cases  of  motor  insufficiency  and  dilatation,  the  opinion 
]ireviously  maintained  that  fat  must  be  prohibited  and  that,  at  most,  but 
small  ({uantities  of  butter  should  be  permitted,  is  no  longer  in  accordance 
with  our  clinical  experience. 

A  definite  diet  list  for  patients  with  dilatation  cannot  be  given;  it  is 
clear  that  wealthy  patients  may  have  a  more  varied  dietary  than  the  poor, 
but  for  both  the  rules  given  above,  which  primarily  enjoin  a  rest  for  the 
stomaoli,  arc  alike  operative. 

Another  self-evident  rule  is  that  such  patients  should  never  take  too 
much  food  at  one  time.  The  custom  of  eating  only  two  meals  a  day  is  not 
suitable  for  patients  with  gastrectasis.  The  meals  are  to  be  small,  but 
tliey  should  be  frequent.  Under  some  circumstances,  the  method  of  Albu  ^ 
of  giving  the  patient  fluid,  concentrated  food  through  the  stomach-tube 
immediately  after  the  morning  and  evening  stomach  washing  may  be 
adopted ;  but  this  would  come  into  consideration  only  in  the  nutrition  of 
very  debilitated  patients  with  marked  anorexia. 

In  very  emaciated  persons,  to  improve  the  nutrition  and'  to  rest  the 
stomach  as  much  as  possible,  a  portion  of  the  fluid  food  may  be  given  by 
the  rectum.  If  we  are  only  endeavoring  to  combat  the  decrease  of  water  in 
tlie  organism,  enemata  of  water  with  the  addition  of  salt  (1  teaspoonful 
of  table  salt  to  a  liter  of  water)  or  a  small  quantity  of  brandy,  or  wine 
bouillon  enemata  (  ^  bouillon  and  ^  Rhine  wine)  may  be  given.  It  is 
advisable  to  give  nutritive  substances  admixed  with  the  enema.     For  this 


'  In  ictrard  to  the  question  of  the  part  plaj'ed  by  the  stomach  in  the  digestion  of 
fats.  ]  refer  to  the  investigations  of  Volhard  upon  "  Absorption  and  Fat  Splitting  in 
tlie  Stomaoli."  recently  published  from  my  Clinic.  (Milnchener  med.  Wochenschrift, 
11)00.  Nr.  o  u.  6.  und  Zeitschr.  f.  klin.  Med.,  XLII.) 

-  Zritsrhrift  fiir  diiitetischc  und  physikalische  Therapie,  III. 

^  Archiv  fiir  Verdauungskrankheiten,  V, 

"  Wratsrh,  1898;,  Nr,  13,  in  Archiv  fiir  Verdauungskrankheiten. 

■'  Deutsche  vied.  Wochenschr.,  1900,  Nr.  11. 


TREATMENT  153 

purpose  a  peptone-enema  (50  to  60  of  peptone  to  300  of  milk),  milk  and 
egg  enemata  (3  eggs  with  the  addition  of  3  grams  of  table  salt,  in  300  of 
milk)  and  starch  enemata  (50  starch  to  300  of  milk)  may  be  employed. 
Solutions  of  sugar  are  liable  to  produce  irritation  of  the  mucous  mem- 
brane of  the  rectum.  If  they  must  be  employed,  not  more  than  15  or  20 
grams  of  sugar  to  300  of  fluid  should  be  used.  Nutritive  enemata  of  this 
kind  must  of  course  only  be  given  in  extreme  dilatation,  and  for  a  short 
time;  as  complete  substitutes  for  the  administration  of  food  by  the  mouth, 
they  naturally  fail.  Subcutaneous  injections  of  fat  may,  under  some  cir- 
cumstances, be  given  for  nutritive  purposes. 

Alcohol  is  generally  to  be  avoided  in  dilatation.  It  is  true  the  stom- 
ach will  absorb  alcohol,  but,  with  its  absorption,  a  plentiful  excretion  of 
water  from  the  stomach  occurs,  which  is  the  greater  the  larger  the  amount 
of  alcohol  absorbed. 

Although  these  diet  rules  apply  in  general  to  every  form  of  dilatation, 
whether  it  run  its  course  with  normal  or  defective  secretion  of  gastric 
juice,  nevertheless,  this  secretion  of  gastric  juice  should  be  considered 
in  the  choice  of  food.  Where  it  is  more  or  less  decreased,  milk  foods, 
strong  soups,  and  the  most,  tender  meats  are  indicated,  the  meat  to  be 
finely  chopped  or  divided.  But  in  hypersecretion  and  hyperacidity,  the. 
carbohydrates  must  be  limited,  and  a  meat-fat  diet  is  preferable.  In  cases 
of  this  kind  where  the  secretion  of  gastric  juice  is  due  to  pyloric  stenosis, 
where,  therefore,  notwithstanding  dilatation,  gastric  peristalsis  is  still 
active,  it  may  be  expected  that  the  stomach  is  still  able  to  digest  meat 
divided  less  finely.  At  all  events  we  need  not  be  so  careful  in  this  respect 
as  in  the  cases  with  diminished  secretory  power  and  simultaneous  atony. 

As  with  every  damaged  or  weakened  organ,  so  in  the  case  of  the  stom- 
ach it  must  be  our  first  object  to  give  it  rest.  The  diet  should  be  light, 
but,  nevertheless,  sufficient  food  must  be  taken.  Rest  of  the  organ  is 
facilitated  if  the  patient  with  dilatation  is  kept  as  much  as  possible  in  a 
recumbent  posture. 

That  an  upright  position  of  the  body  is  more  unfavorable  for  the 
dilated  stomach  than  a  recumbent  one  is  clear.  After  eating,  the  patient 
should  lie  down  for  a  long  time.  Lying  upon  the  right  side  after  eating 
lias  frequently  been  recommended  to  facilitate  the  propulsion  of  the  food 
mass  into  the  duodenum.  It  is  self-evident  that  such  patients  must  eat 
slowly  and  masticate  thoroughh/. 

If  the  dilatation  and  the  motor  insufficiency  are  due  to  the  difficulty 
of  expelling  the  gastric  contents,  we  must  resort  to  measures  that  will 
assist  in  this  expulsion.         ^ 

For  this  purpose  systematic  massage  has  been  advised.  Massage  of  the 
stomach,  however,  also  serves  the  further  purpose  of  strengthening  the 
gastric  musculature.  If  we  intend  the  massage  merely  to  produce  a  more 
rapid  propulsion  of  the  ingesta  into  the  intestine,  it  should  not  be  given 


154         DIAGNOSIS  AND  TREATMENT  OF  GASTRIC  DILATATION 

immediately  after  a  meal  but  a  considerable  time  later.  Massage  is  con- 
traindicated  in  cases  of  decided  fermentation,  which  must  first  be  re- 
moved. In  the  majority  of  cases  the  results  of  massage  are  not  very 
satisfactory.  We  cannot  describe  the  technic.  Massage  of  the  stomach, 
however,  should  always  be  given  by  the  physician. 

In  atony  the  faradic  current  is  useful  to  strengthen  the  muscularis 
of  the  stomach ;  this,  as  a  rule,  is  employed  extraventricularly,  more  rarely 
intra ventricularly.  Certain  hydropathic  procedures,  douches,  the  fan- 
douche,  and,  particularly,  the  so-called  Scotch  douche,  are  beneficial. 
From  my  experience  I  cannot  advise  internal  douches;  in  extreme  dilata- 
tion I  do  not  consider  them  free  from  danger,  and  in  milder  forms  more 
simple  methods  may  be  substituted. 

To  promote  more  rapid  propulsion  of  the  gastric  contents  into  the 
intestine  in  cases  of  organic  or  spastic  stenosis  of  the  pylorus,  the  use  of 
olive  oil  has  recently  been  recommended.  Cohnheim  ^  advises  50  grams 
one  hour  before  meals  three  times  daily.  Not  only  in  cases  of  spasm 
of  the  pylorus,  but  also  in  cicatricial  stenoses  of  the  same,  he  claims  to 
have  had  good  results.  In  several  of  these  cases,  there  was  scarcely  a 
hope  of  recovery  except  by  surgical  interference. 

All  of  these  methods  are  designed  to  rest  and  strengthen  the  stomach; 
they  may  suffice  in  mild  grades  of  motor  insufficiency  and  atony,  but 
not  in  the  severe  forms  of  dilatation  in  which  the  stomach  is  never  per- 
fectly empty,  but  even  in  the  morning,  before  taking  food,  portions  of  that 
consumed  the  previous  day  are  still  present.  Here  it  is  necessary  to  re- 
lieve the  stomach  of  its  abnormal  contents  by  gastric  lavage.  In  all  severe 
forms  of  motor  insufficiency  and  dilatation,  gastric  lavage  is  an  extremely 
valuable  and  indispensable  aid. 

The  degree  of  motor  insufficiency  which  necessitates  methodic  lavage 
is  a  disputed  point.  All  authors  are  unanimous  that,  in  the  extreme 
forms  in  which  the  stomach  in  the  morning  before  breakfast  contains  food 
from  the  day  previous,  it  should  be  washed  daily.  It  is  different  in 
slighter  dilatation.  In  my  opinion,  even  mild  forms  of  dilatation  indicate 
regular  lavage.  The  normal  stomach  acts  only  periodically,  not  continu- 
ously. Six  to  seven  hours  after  the  midday  meal  it  is  empty,  and  four  to 
five  liours  after  a  simple  evening  meal  it  should  no  longer  contain  food. 
In  conso(|uence  of  this,  the  stomach  has  certain  periods  of  rest.  The  dis- 
easefl  stomach  with  motor  insufficiency  should  have  no  greater  work,  and 
no  longer  hours  of  labor,  than  correspond  to  the  norm.  If  the  stomach 
in  the  evening,  before  supper,  still  contains  larger  or  smaller  quantities 
of  food,  it  must  be  washed  out.  If  this  is  not  done  it  is  abnormally  taxed, 
and  if  the  debilitated  and  distended  stomach  with  motor  insufficiency  is 
not  to  be  still  further  stretched  and  taxed,  naturally  no  more  labor  must 

*  Archiv  fiir  Verdauungskrcmkheiten,  Bd.  V. 


TREATMENT  165 

be  exacted  from  it  than  from  a  normal  organ.  This  would,  however,  be 
the  ease,  if  we  expect  an  evening  meal  to  be  digested  besides  the  remains 
of  the  midday  meal  which  is  still  in  part  undergoing  fermentation.  This 
would  not  ensure  to  the  diseased  organ  the  rest  which  is  of  such  primary 
importance. 

If  the  stomach  that  has  been  washed  before  supper  is  empty  upon 
the  following  morning,  this  evening  lavage  alone  will  be  sufficient;  if  not, 
it  must  be  performed  in  the  morning  in  addition.  This  is  not  only  neces- 
sary to  relieve  the  stomach,  but  because  abnormal  fermentation  and  decom- 
position occur  upon  prolonged  stagnation  of  the  ingesta. 

Many  recommend  lavage  in  the  morning  before  breakfast.  They  be- 
lieve that  if  the  stomach  is  not  empty  at  this  time  it  should  be  washed 
out,  and  that  this  is  the  best  time  for  the  procedure.  They  also  believe  that 
at  this  hour  the  washing  can  be  most  rapidly  performed,  and  is  the  least 
exhausting.  I  do  not  coincide  with  this  reasoning.  Lavage  should  relieve 
the  stomach  by  removing  its  decomposed  products  of  abnormal  fermenta- 
tion. 

It  is  undeniably  true  that  lavage  is  most  easily  performed  in  the  morn- 
ing, and  more  rapidly  because  the  stomach  before  breakfast  contains  rela- 
tively the  slightest  residue  of  food.  But  this  method  gives  little  relief 
to  the  stomach;  it  has  no  periods  of  rest  as  in  the  norm.  It  is  better,  as 
others  advise,  to  carry  out  the  lavage  late  in  the  evening  between  9  and 
10  o'clock.  This  gives  absolute  relief  and  an  actual  period  of  rest  follows. 
To  me  it  appears  most  rational  to  use  lavage  immediately  before  the 
evening  meal.  If,  after  seven  hours,  much  residue  is  still  present,  which 
must,  under  any  circumstances,  have  begun  to  ferment,  it  is  wiser  to  remove 
this  and  to  introduce  fresh  food  into  the  cleansed  stomach  than,  as  the 
exponents  of  lavage  in  the  late  evening  recommend,  to  add  an  even- 
ing meal  to  the  fermenting  remains  and  evacuate  the  stomach  two  or 
three  hours  later.  If,  after  evening  lavage,  the  stomach  is  not  empty 
upon  the  following  morning,  it  must,  in  addition,  be  washed  in  the 
morning. 

Therapeutic  washings  should  be  as  thorough  as  possible,  not  only  to 
empty  the  stomach,  but  to  remove  as  well  the  causes  of  fermentation.  This 
should  be  done  first  with  lukewarm  water;  medications  may  be  necessary 
in  subsequent  washings  on  account  of  special  individual  conditions,  because 
of  acid,  abnormal  fermentation,  and  the  like.  The  latter,  especially,  often 
renders  the  use  of  drugs  necessary,  such  as  salicylic  acid  (1-1000),  boric 
acid,  resorcin,  and  similar  antiferments. 

A  thorough  cleansing  of  the  stomach  is  more  rapid  when  there  is  rela- 
tively increased  gastric  tonu^,  such  as  we  meet  with  in  pyloric  stenosis 
rather  than  in  the  atonic  forms.  Naturally,  lavage  must  be  continued 
until  the  stomach  is  thoroughly  cleansed,  or  until  we  have  convinced  our- 
selves of  the  uselessness  of  further  effort. 


156         DIAGNOSIS   AND  TREATMENT   OF   GASTRIC   DILATATION 

To  tlie  physical  aids  which  play  but  an  indirect  role  in  the  therapy 
of  dilatation,  bandages  may  be  added.  They  do  not  reduce  the  dilata- 
tion, but  they  give  the  dilated  stomach  a  firm  support;  they  not  only 
assist  in  producing  subjective  amelioration,  but  to  a  certain  extent  they 
i-clieve  the  condition.  They  are  particularly  valuable  in  those  numerous 
cases  in  which,  besides  dilatation,  there  is  also  gastroptosis,  or  where 
there  is,  at  the  same  time,  a  marked  degree  of  flaccidity  of  the  abdominal 
walls. 

These  are  the  chief  remedies  and  methods  to  which  we  resort  in  dila- 
tation of  the  stomach.  Actual  drug  medication  for  dilatation  does  not 
come  into  question.  It  has  been  maintained  of  some  remedies,  such  as 
slnjchnin,  that  they  stimulate  the  tonus  and  peristalsis  of  the  stomach, 
wliich  has  also  been  claimed  for  creosote,  orexin  and  other  drugs.  But 
I  have  observed  no  remarkable  action  of  this  kind  from  any  of  the  remedies 
api)lied. 

A  few  words  must  be  devoted  to  the  belladonna  preparations  and 
to  alropin  since  these  remedies  have,  to  a  high  degree,  an  antispasmodic 
t'UV'ct.  S])asm  of  the  pylorus,  however,  often  exerts  an  influence  in  dila- 
tation, particularly  in  those  varieties  running  their  course  with  hyper- 
acidity and  hypersecretion.  As  I  have  shown,  the  belladonna  prepara- 
tions not  alone  inhibit  the  secretion  of  gastric  juice,  but  are,  at  the  same 
time,  antispasmodic.  On  account  of  these  properties,  they  may  be  em- 
]>l()y('d  with  advantage  in  the  two  forms  of  gastrectasis  even  though  only 
as  syiiiptoinatic  remedies. 

Tlie  alkaHes  also,  even  if  only  indirectly,  are  useful  in  certain  forms  of 
dilatation,  especially  in  those  varieties  in  which  there  is  hypersecretion, 
llcie  tliey  prevent  the  abnormal  production  of  acids,  and  assist  in.  the 
(litest ion  of  starches  as  well  as  the  propulsion  of  the  gastric  contents, 

I  cannot  enter  minutely  into  an  enumeration  of  drugs  for  the  relief 
of  individual  symptoms',  they  do  not  affect  the  dilatation  as  such,  but 
only  certain  symptoms  caused  by  the  underlying  condition. 

Teldiiy,  a  symptom-complex  closely  related  to  ectasis,  shall  be  briefly 
discussed.  Views  regarding  the  origin  of  tetany  and  gastrectasis  are 
diverse.  The  majority  of  authors  adhere  to  the  intoxication  theory,  and 
iciiard  tetany  as  the  consequence  of  an  intoxication  of  the  organism  with 
abnormal  products  of  metabolism  from  the  diseased  gastrointestinal  canal. 
If  this  theory  be  correct,  the  therapeutic  indication  is  that  prolonged  stag- 
nation must  be  prevented.  The  active  treatment  of  stagnation  is,  accord- 
inirly.  the  prophylaxis  of  tetany.  Remedies  which  relieve  attacks  of 
tit  any.  or  prevent  its  occurrence,  are  unknown. 

('nfortniuitely,  the  number  of  cases  of  dilatation  in  which  the  reme- 
dies just  mentioned  do  not  bring  relief  is  very  great,  and  in  the3e  the 
(inly  hope  of  improvement  or  cure  is  in  surgical  measures.  These  may 
seivt    I  wo  purposes,  either  in  removing  the  actual  cause  of  the  dilatation, 


TREATMENT  157 

or  in  some  maimer  bringing  about  the  compensation  of  the  damaged  motor 
power. 

By  far  the  most  frequent  indication  for  surgical  interference  is  seen  in 
pyloric  stenosis,  immaterial  whether  the  stenosis  be  due  to  a  cicatricial 
narrowing,  to  a  carcinoma,  to  compression  from  without  or  elsewhere. 
Where  it  is  possible  entirely  to  remove  the  stenotic  obstruction,  this  should 
always  be  the  primary  aim. 

When  the  surgical  operation  is  decided  upon,  •  the  proper  time  for 
it  should  be  determined  by  a  full  consideration  of  all  the  conditions.  Ma- 
lignant stenosis  should  be  operated  upon  as  early  as  possible.  Kadical 
removal  of  a  carcinoma  is  most  desirable.  Benign  stenosis  also  necessi- 
tates surgical  interference,  but  here  we  must  usually  wait  until  the  use- 
lessness  of  internal  remedies  has  been  proven.  .Where  the  internal  clinician 
cannot  ameliorate  the  condition  with  the  remedies  at  his  command,  where, 
in  spite  of  all  the  described  methods  it  is  impossible  to  introduce  sufficient 
nourishment  into  the  organism,  the  surgeon's  art  must  be  called  into  play. 

If  the  radical  removal  of  the  stenosed  area  be  impossible,  prevention 
of  the  stenosis  and  compensation  may  be  brought  about  by  the  formation 
of  new  outlets.     Gastroenterostomy  answers  this  purpose. 

There  are,  however,  also  relative  indications  which  are  the  result  of 
special  circumstances.  Thus,  we  occasionally  see  patients  whose  condition 
is  endurable  so  long  as  they  remain  in  a  hospital  where  proper  diet  and 
other  auxiliary  remedies  are  at  hand  to  maintain  them,  and  where  they 
are  able  to  help  themselves.  If  they  return  to  their  former  unfavorable 
surroundings,  are  compelled  to  work  hard,  and  are  unable  to  spare  them- 
selves, aggravation  at  once  occurs.  Here,  the  unfavorable  circumstances 
of  life,  not  the  severity  of  the  disease,  compel  operative  interference  which, 
undor  other  circumstances,  might  have  been  postponed.  Without  an  oper- 
ation such  patients  as  these  would  succumb  in  a  very  brief  time.  Here 
the  operation  is  not  absolutely  indicated,  but  relatively,  on  account  pf  the 
special  environment  of  the  case  in  question. 

What  operation  (resection,  pyloroplasty,  gastroenterostomy,  digital 
diviilsion  of  the  pylorus,  etc.)  is  to  be  performed  in  the  given  case,  can 
only  be  determined  after  opening  the  abdominal  cavity.  Radical  removal 
of  the  obstruction  which  causes  stenosis  is  primarily  the  aim,  even  though 
this  very  frequently  cannot  be  attained. 

Atonic  dilatation  also  may,  under  some  circumstances,  although  much  ^ 
more  rarely,  require  surgical  relief;  this  does  not  affect  the  atony,  as  such, 
but  serves  to  facilitate  the  outflow. 

(rastroplication  cannot  restore  the  tonus,  but  only  decreases  the  vol- 
ume of  tlie  organ,  and  in  atoffy'  with  this  alone  very  little  is  attained. 
On  tlie  otlier  hand,  gastroenterostomy,  while  it  does  not  remove  the  atony, 
prevents  stasis,  and  under  some  circumstances  restores  the  tonus  of  the 
organ.     But,  with  the  early  recognition  and  proper  treatment  of  atony. 


158         DIAGNOSIS   AND  TREATMENT  OF  GASTRIC   DILATATION 

as  a  rule  it  rarely  attains  such  a  high  degree  of  development  that  surgical 
intervention  becomes  necessary. 

It  is  not  our  object  to  enumerate  the  individual  surgical  operations; 
the  internal  clinician  must  perceive  the  indications  for  surgery;  the  choice 
of  the  method  must  be  left  to  the  surgeon. 


GASTRIC    ULCER    AND    GASTRIC 
HEMORRHAGE 

Bt  C.  a.  EWALD,  Berlin 

ETIOLOGY 

In  no  other  form  of  gastric  disease  is  our  insight  into  the  finer  path- 
ologic processes  and  the  methods  which  must  be  adopted  for  their  cure  so 
clear  as  in  gastric  ulcer,  round  ulcer  of  the  stomach,  or  peptic  ulcer,  as  the 
affection  has  been  designated  according  to  its  peculiar  features. 

My  actual  experience  regarding  this  disease  cannot  be  questioned  when 
I  state  that,  in  the  last  twelve  years,  I  have  seen  and  treated  1250  cases 
either  in  the  Hospital,  the  Clinic,  or  in  my  private  Clinic  (not  including 
my  office  practice).  At  this  point,  however,  I  do  not  intend  to  give  a 
text-book  description,  but  I  shall  consider  chiefly  the  clinical  aspect  of 
the  pathologic  picture,  and  shall  limit  myself  to  the  experiences  of  the 
last  few  years. 

We  differentiate  the  acute  and  chronic  forms  of  gastric  ulcer,  not, 
however,  by  the  different  nature  of  the  process,  but  by  the  rapid  or  slower 
course,  and  under  this  the  various  symptoms  will  be  included. 

Since  Cruveilhier  first  gave  us  such  a  minute  and  comprehensive  de- 
scription of  gastric  ulcer  (which  had  formerly  been  looked  upon  as  a  post 
mortem  curiosity)  that  it  constitutes  a  well-defined  and  easily  recognized 
pathologic  picture,  clinical  observers  and  experimental  investigators  have 
vied  with  each  other  in  eagerly  studying  this  affection. 

However,  the  various  experiments  made  in  the  course  of  time  to  dis- 
cover the  etiology  of  gastric  ulcer  cannot  all  be  enumerated  here.  It  must 
suffice  to  call  attention  to  the  fact  that  in  the  development  of  ulcer  we  are 
dealing  either  with  the  consequences  of  a  mechanical,  a  chemical,  or  a 
thermic  lesion  of  the  mucous  membrane,  with  a  disturbance  of  the  circu- 
lation at  the  point  of  lesion,  or  else  such  disturbances — and  this  is  more 
frequently  the  case — have  arisen  without  a  preceding  coarse  lesion  in  a  cir- 
cumscribed, vascular  area.  A  limited  destruction  of  the  tissue  follows 
because  the  gastric  juice  attacks  those  areas  which  are  no  longer  normally 
nourished,  just  as,  to  a  fuller  extent,  it  consumes  the  stomach  after  death, 
and  under  favorable  conditions  it  produces  softening.  There  is  always, 
however,  a  pathologic  disproportion  between  the  composition  of  the  gas- 
tric juice  and  the  nutrition  of  the  gastric  mucous  membrane,  and  the 
12  159 


160  GASTRIC   ULCER   AND  GASTRIC   HEMORRHAGE 

changed  nutrition  may  be  the  consequence  of  an  altered  composition  of 
the  blood  as  well  as  of  a  change  in  the  circulation.  As  this  has  been 
touched  upon  in  a  discussion  which  shows  conspicuously  the  present  status 
of  our  science,  we  shall  not  here  enter  upon  a  historic  retrospect.  Up  to 
the  present  time  the  view  has  been  generally  held  that  both  of  these  causes 
have  been  decisive,  first,  tlie  increased  production  of  acid  (hyperchlorhydria) 
and,  secondly,  the  circumscribed  tissue  lesion  of  the  mucosa  due  to  such 
causes  as  have  been  mentioned.  But  there  is  no  unanimity  of  opinion  as 
to  whether  the  hyperacid  gastric  juice  which  produces  tissue  necrosis  by 
injury  or  otherwise  is  first  present  and  thus  causes  destruction,  or  whether, 
inversely,  a  primary  lesion  of  the  gastric  mucous  membrane  exerts  a  sec- 
ondary reflex  action  upon  the  secreting  elements  of  the  entire  gastric 
mucous  membrane,  so  that  in  consequence  there  is  subsequently  an  in- 
creased production  of  acid. 

In  fact  the  view  that  this  factor  alone  is  operative  is  no  longer  tenable, 
smce  it  has  been  shown,  as  we  shall  later  see,  that  ulcer  of  the  stomach 
is  not  invariably  combined  with  increased  excretion  of  hydrochloric  acid, 
but  that  even  a  marked  decrease  may  be  observed.  Therefore  the  develop- 
ment of  the  affection  must  primarily  be  attributed  to  the  circulatory  dis- 
turbance always  produced,  and  to  the  circumscribed  tissue  necrosis  result- 
ing therefrom. 

Unquestionably  many  gastric  ulcers  are  the  direct  result  of  vascular 
lesions  and  their  consequences, — the  hemorrhagic  infarct, — and  the  pri- 
mary cause  is  either  an  occlusion  of  the  smallest  arterial  vessels  arising 
from  the  submucosa  between  the  tubules  of  the  mucosa,  or  atheromatous, 
amyloid,  or  aneurysmal  disease  of  the  walls  of  the  vessels,  or  even  simple 
stasis  and  spasmodic  contractions  of  the  muscles  may  lead  to  rupture  of 
the  vessels.  In  some  cases  v.  Openchowski  found  hyaline  degeneration 
of  the  walls  of  the  finest  vessels  in  the  hemorrhagically  infiltrated  areas  of 
the  mucosa,  and  this  he  holds  responsible  for  the  development  of  the 
latter.  Lepine  and  Bret  have  described  a  stomach  which  at  the  autopsy 
was  completely  filled  with  blood.  The  patient,  a  man  aged  65,  had  repeat- 
edly suffered  from  hemorrhages  (due,  as  was  shown,  to  small  ulcerations 
produced  by  an  endarteritis  of  the  smallest  vessels). 

l^ut  these  causes  alone  do  not  explain  the  numerous  cases,  particularly 
in  youthful  persons,  in  whom  disease  of  the  vessels  or  the  other  factors 
mentioned  do  not  exist.  In  some  of  these  it  must  be  assumed  that  the 
ulcers  develop  from  follicular  hemorrhages  and  the  hemorrhagic  ero- 
sions of  Ilokitansky,  which,  in  miniature,  disclose  a  condition  similar 
to  the  hemorrhagic  infarct,  namely,  small  areas  of  the  mucous  mem- 
brane suffering  from  insufficient  nutrition.  Insignificant  local  stasis  or 
sliglit  trauma  may  be  the  cause  of  such  hemorrhages.  They  develop  into 
hemorrhogic  erosions,  circular  losses  of  substance  from  the  size  of  a  millet 
seed  to  tliat  of  a  pea,  or  narrow,  striated  abrasions  iii  which  occasionally 


ETIOLOGY  161 

a  blackish-brown  extravasation  of  blood  appears  simultaneously  with  a 
loosening  of  the  mucous  membrane.  Their  number  varies  greatly.  Oc- 
casionally they  are  so  numerous  in  the  region  of  the  pylorus  that  the 
mucous  membrane  appears  to  be  covered  with  them.  From  this  erosion 
the  typically  chronic  ulcer  develops.  But  certainly  not  from  those  ero- 
sions which,  as  Langerhans  emphasizes,  in  my  opinion  most  justly,  by 
their  irregular  distribution  upon  the  mucous  membrane,  their  numbers, 
and  their  confluence,  differ  widely  from  the  typical  ulcer  with  its  char- 
acteristic appearance  and  its  solitary  seat.  Langerhans  states,  "  These 
hemorrhagic  erosions  usually  develop  from  spasmodic  contractions  and 
coincident  inflammatory  processes;  the  round  gastric  ulcer,  after  a  pri- 
mary affection  of  an  arterial  vessel.  Only  exceptionally  do  erosions  de- 
velop into  chronic  ulcers."  But  this  author,  and  D.  Gerhardt  as  well, 
accurately  describe  typical  examples  of  the  transition  of  such  erosions 
into  classical  ulcers,  and,  as  Gerhardt  has  shown,  the  small  ulcers  which 
develop  from  the  swelling  and  rupture  of  lymphatic  follicles  may  here  be 
included. 

According  to  the  descriptions  of  Nauwerk,  and  the  published  cases  of 
Letulle,  Dieulafoy,  Stokes  and  Krafft,  the  influence  of  bacteria,  that  is, 
of  bacterial  invasion,  in  the  development  of  gastric  ulcer,  appears,  on  the 
contrary,  to  be  of  mechanical  rather  than  of  a  true  toxic  nature,  and 
we  can  hardly  doubt  that  the  lesions  were  originally  bacterial  emboli 
of  the  smallest  vessels,  upon  the  base  of  which  the  ulcer  later  developed, 
and  this  was  the  primary  cause  of  a  limited  disturbance  of  nutrition  of  the 
mucous  membrane.  In  the  upper  layers  of  the  necrosed  mucous  mem- 
brane, various  microorganisms  collect. 

A.  Schmidt  claims  to  have  discovered  an  equally  important  factor  for 
the  development  as  well  as  for  the  cure  of  the  ulcer  in  the  possibility  of 
contraction  of  the  muscle  situated  below  the  lesion  in  the  mucous  mem- 
brane. Griffini  and  Vassale  had  already  demonstrated  that  the  healing 
of  erosions  of  the  gastric  mucous  membrane  in  animals  takes  place  by 
the  complete  approximation  of  the  edges  of  the  wound,  and  thus  further 
digestion  by  the  gastric  juice  is  prevented.  Schmidt  believes  that  the 
absence  of  such  contraction  accounts  for  the  production  of  an  ulcer  from 
superficial  losses  of  epithelium,  because  in  experimenting  upon  a  dog  he 
was  able  to  produce  deep  losses  of  substance  though  not  chronic  pro- 
gressive ulcers  whenever  by  suitable  measures  he  prevented  the  muscularis 
in  the  area  of  the  lesion  from  contracting.  The  conditions  are  similar 
in  the  human  being,  and  the  well  known  fact  that  gastric  ulcer  is  so 
frequent  in  chlorosis  and  anemia  might  be  attributed  to  the  flaccidity 
(atony)  of  the  gastric  muscles.  Admitting  the  latter  to  be  true — chlo- 
rosis, in  fact,  promotes  relaxation  also  in  other  organs,  the  heart,  the 
intestine,  the  uterus — Schmidt's  view  has  been  by  no  means  generally 
accepted.     Years  ago,  I  produced  the  same  deep  losses  of  substance  in 


162  GASTRIC   ULCER  AND  GASTRIC  HEMORRHAGE 

dogs,  and,  by  severing  the  medulla  oblongata,  circumscribed  hemorrhages 
into  the  stomach  without  the  contractile  power  of  the  muscularis  having 
suffered;  besides,  numerous  cases  are  observed  whose  entire  behavior  ex- 
cludes from  the  onset  a  flaccid  condition  of  the  stomach,  and  in  which 
there  was  neither  chlorosis  nor  anemia. 

The  relation  of  the  nervous  system  to  the  development  of  gastric  ulcer 
lias  been  repeatedly  studied.  Lately  Talma  and  his  pupil,  van  Yzeren, 
have  attempted  to  prove  by  clinical  and  experimental  research  that  a 
spasm  of  the  pylorus  due  to  nervous  influence  is  an  etiologic  factor. 
I  have  remarked  elsewhere  that  this  view,  for  several  reasons,  is  most 
impro])able;  above  all,  because  in  the  overwhelming  majority  of  ulcers 
tliore  is  not  the  slightest  indication  of  spasm.  In  my  opinion  van  Yzeren 
confounds  cause  and  effect,  for  he  bases  the  results  of  vagotomia  subdia- 
phragmatica  in  rabbits  upon  conclusions  arrived  at  in  man.  Spasm  of 
the  pylorus,  wherever  present,  is  not  the  cause  but  the  consequence  of  an 
ulcer.  We  have  long  known  that  conditions  induced  by  hyperacidity,  even 
where  they  run  their  course  without  producing  ulcer,  may  lead  to  occa- 
sional or  permanent  spasm  of  the  pylorus.  Dalla  Vedova  has  succeeded 
— as  well  as  other  authors  before  him — in  producing  necrotic,  hemor- 
rhagic, and  ulcerative  changes  in  the  wall  of  the  stomach  of  the  dog  by 
injuring  the  celiac  plexus  or  its  thoracic  roots  (splanchnic),  the  character- 
istic necrobiotic  lesion  closely  resembling  the  peptic  ulcer  of  man.  From 
the  nature  and  sequence  of  the  injuries  caused — hemorrhages  of  the  gas- 
tric mucous  membrane  from  the  size  of  a  pin's  head  to  that  of  a  lentil, 
hemoiihagic  erosions,  true  ulcers  and  typical  cicatrization — it  is  obvious 
that  ecchymosis  may  be  regarded  as  the  beginning  of  the  process  from 
which  other  conditions  arise. 

The  development  of  gastric  ulcer  from  trauma  has  lately  become  espe- 
cially interesting  to  us  because  the  laws  in  regard  to  accidents  frequently 
place  us  in  a  position  where  we  must  give  an  opinion  as  to  the  causal 
relation  between  trauma  and  ulcer.  Many  more  or  less  trustworthy  ob- 
servations are  distributed  throughout  literature  which,  in  their  totality, 
permit  no  doubt  that  gastric  ulcer  may,  indeed,  be  produced  directly  by 
a  l)low,  a  contusion,  a  fall,  or  the  like,  which  affects  the  gastric  region. 
A  com])rehensive  study  of  this  aspect  of  the  disease  will  be  found  in 
Stern's  book,  "  Ueber  traumatische  Entstehung  innerer  Krankheiten," 
Jena.  1900. 

I  have  repeatedly  been  called  upon  for  such  an  opinion,  and  the  fol- 
Idwiiii,^  considerations  have  been  my  guide.  First,  we  must  ascertain 
wlictluM-  immediately,  or,  at  least,  a  short  time  after  the  trauma,  an 
undoubted  gastric  hemorrhage  occurred,  for  this  is  the  only  positive  sign 
of  a  severe  injury  to  the  gastric  mucous  membrane.  Directly  following 
this,  nausea,  anemia,  syncope  and  localized  gastric  pain  may  occur;  but 
since,   as   is  well   known,   such   injuries  of  the  mucous  membrane  heal 


PATHOLOGICAL  ANATOMY  163 

rapidly  without  sequelae,  it  is  also  necessary  that,  following  this  hemor- 
rhage, the  typical  symptoms  of  ulcer  arise,  i.  e.,  gastric  pain,  particularly 
after  meals,  and  pain  upon  pressure  in  the  gastric  region.  The  latter 
symptoms  do  not  always  appear  immediately  after  the  trauma  but,  never- 
theless, they  must  show  a  certain  connection  with  it.  In  my  opinion  the 
diagnosis  is  best  founded  in  those  cases  in  which,  in  the  course  of  time, 
a  decided  gastric  dilatation  or  a  cancer  of  the  stomach,  particularly  about 
the  pylorus,  develops;  the  former,  because  it  points  to  a  stenosis  of  the 
pylorus,  which  in  the  given  case  may  be  the  consequence  of  a  traumatic 
ulcer  at  the  pylorus;  the  latter,  because  modern  experience  has  taught 
us  the  frequent  connection  between  ulcer  and  carcinoma.  (Upon  this 
occasion,  I  shall  only  remark,  parenthetically,  that  the  direct  relation 
between  trauma  and  cancer  does  not  appear  to  me  to  be  sufficiently  proven 
to  warrant  us  in  maintaining  this  association  without  the  connecting 
link  of  a  positive  or,  at  least,  very  probable  traumatic  ulcer  of  the  stomach.) 

Unquestionably  many  different  and  obscure  factors  assist  in  the  devel- 
opment of  peptic  ulcer.  Backmann,  who  investigated  the  distribution 
of  gastric  ulcer  in  Finland,  and  from  his  experience  also  described  the 
etiology,  maintains  that  "  except  for  a  few  cases  m  which  trauma  very 
likely  played  an  etiologic  role,  the  etiology  was  very  obscure."  In  passing 
it  may  be  remarked  that  Sohlern's  hypothesis,  repeatedly  combated,  ac- 
cording to  which  vegetable  food  confers  immunity  from  ulcer  of  the  stom- 
ach, is  not  supported  by  Backmann's  conclusions.  The  population  of 
Finland  subsist  chiefly  on  potatoes,  bread,  porridge,  and  peas.  Meat  is 
eaten  only  upon  Sundays  and  holidays,  nevertheless  gastric  ulcer  is  quite 
common. 

No  matter  in  what  manner  ulcer  may  develop,  in  a  pathologico- 
anatomical  respect  it  is  not  an  "  ulcer,"  but  a  "  progressive  tissue  necrosis," 
in  which  the  chief  characteristic  of  ulcer  is  entirely  absent,  namely,  "the 
proliferation  of  young  cellular  elements  which  persistently  invade  the  tissue 
more  deeply  and  invariably  cause  new  elements  to  appear  upon  the  sur- 
face." The  ulcer  does  not  grow  by  an  active  process  in  the  tissue  with 
subsequent  destruction,  but  by  a  passive  process.  The  tissue  only  becomes 
actively  involved  by  cellular  infiltration  which  leads  to  cicatrization. 

PATHOLOGICAL   ANATOMY 

In  regard  to  the  gross  anatomy  of  ulcer  and  its  consequences  a  few 
words  will  suffice.  Its  funnel-shaped  or  crater-like  structure,  corresponding 
to  the  ascending  vascular  tree,  is  well  known;  the  edges  are  at  first  clean 
cut,  later  becoming  thickened,  often  permeated  by  hemorrhages  which  are 
due  to  the  peptic  erosion  of  the  smallest  vessels.  Frequently,  especially 
in  the  acute  perforating  ulcer,  the  form  is  circular,  but  it  may  be  linear, 
oval,  or  terrace-shaped.    The  base  of  the  ulcer  is  usually  smooth,  or  it  may 


164  GASTRIC   ULCER  AND  GASTRIC   HEMORRHAGE 

show  a  few  uneven  points,  occasionally  it  is  covered  with  bloody  coagula 
or  a  greenish  or  brownish  tough  mucus.  The  size  varies  greatly,  generally 
from  that  of  a  dime  to  a  quarter  of  a  dollar,  but  it  may  be  very  much  larger, 
and  sometimes  may  entirely  cover  the  stomach.  Its  seat  is  preferably  at 
the  pylorus  and  on  the  greater  curvature,  which  are  the  lowest  portions 
of  the  stomach  when  in  the  erect  posture,  and  those  in  which  the  gastric 
juice  collects,  so  that  Nolte  has  given  the  following  scale  of  frequency: 
At  the  greater  curvature  22,  at  the  pylorus  13,  upon  the  anterior  wall  3, 
upon  tlie  posterior  wall  2,  at  the  cardia  1. 

According  to  Brinton  42  per  cent,  of  the  cases  are  upon  the  posterior 
wall,  26.8  per  cent,  at  the  lesser  curvature,  and  15  per  cent,  at  the  pylorus. 
These  reports  are  based  on  220  cases.  But  such  statistics  are  constantly 
modified  by  circumstances.  In  my  experience,  for  example,  ulcers  of  the 
pylorus  are  more  numerous  than  those  of  the  lesser  curvature,  and  these 
arc  more  frequent  than  those  of  the  greater  curvature.  Gluczinsky  coin- 
cides, for  in  95  autopsies  he  found  63  cases  of  ulcer  in  the  pyloric  region. 
In  the  majority  of  cases  there  is  but  one  ulcer;  several,  that  is,  three  or 
moie,  are  rare.  Lange,  however,  in  one  case  saw  so  many  "  that  he  was 
obliged  to  discontinue  counting  them." 

Occasionally  several  originally  distinct  ulcers  coalesce  and  form  one 
large  one. 

From  microscopic  sections  through  the  margin  of  a  fresh  ulcer  the 
glandular  tubules  are  seen  trough-shaped,  as  if  sharply  cut  off,  descending 
toward  the  floor  of  the  ulcer. 

They  are  digested  in  so  far  as  the  tissue  is  unable  to  resist  the  peptic 
power  of  the  gastric  juice.  In  older  ulcers  a  reactive  inflammation  sets 
in  at  the  periphery,  and  leads  to  the  formation  of  a  calloused  margin. 
Here  the  supporting  fibers  between  the  resisting  tubules  are  thickened,  and 
partially  formed  into  oblique  layers.  The  glandular  epithelium,  in  so  far 
as  it  is  still  present  in  the  fundus  of  the  glandular  nests,  has  suffered  a 
peculiar  change.  In  place  of  the  lab-cells,  cubical  or  cylindrical  epithelia 
have  appeared.  These  masses  are  contracted  so  that  they  are  separated 
from  the  membrana  propria  and  from  one  another.  Their  nuclei  cannot 
be  recognized  by  staining,  their  contents  have  a  friable,  light,  glassy  ap- 
pearance like  that  of  hyaline  degeneration.  The  individual  tubules  show 
cystic  degeneration.  The  submucosa  is  permeated  by  a  profuse  small  cell 
infiltration  and  a  strong  vascular  net.  The  layers  of  the  muscularis  are 
separated  by  a  fibrillary,  intermediate  tissue,  consisting  of  meshes  torn 
asunder,  some  of  which  have  been  destroyed.  We  see,  therefore,  that  the 
entire  necrotic  process  upon  borders  and  floor  is  surrounded  by  a  zone 
of  irritation,  which  in  its  further  development  leads  to  true  cicatrization, 
in  that  the  floor  of  the  ulcer  constantly  becomes  adherent  to  the  layer 
of  tissue  beneath,  and  the  mucous  membrane  of  the  border  of  the  ulcer 
retracts  into  its  floor. 


PATHOLOGICAL  ANATOMY  166 

In  the  interstices  of  the  glands,  not  only  in  the  immediate  vicinity 
of  the  ulcer,  but  also  in  those  more  distant,  the  mucosa  invariably  shows 
massive  small  cell  infiltration,  but  nothing  peculiar  to  ulcer,  only  what  is 
found  in  all  inflammatory  irritations  of  the  mucous  membrane  from  a 
mild  catarrh  to  an  acute  phlegmonous  gastritis,  I  have  rarely  examined 
a  gastric  mucous  membrane,  no  matter  whether  the  patient  suffered  from 
a  gastric  affection  or  some  other  chronic  disease,  without  discovering  here 
and  there  at  the  base  of  the  mucosa  disseminated  foci  of  small  cell 
infiltration  (not  lymph-follicles  by  any  means!)  which  had  separated  the 
glandular  tubules  from  each  other.  In  fact,  the  ulcer  subsequently  pro- 
duces an  irritation  in  the  surrounding  areas  of  the  mucous  membrane 
which  to  a  varying  extent  and  intensity  implicates  this  tissue. 

The  outcome  of  the  necrotic  process  is  especially  interesting.  We  must 
differentiate  between  the  following  conditions: 

1.  Cicatrization. — Here  there  is  a  marked  difference  from  the  cicatriza- 
tion produced  artificially  in  the  animal.  For  while  these  cicatrices,  as 
Cohnheim  reports,  and  as  I  also  found,  healed  by  the  restitution  of  the 
normal  mucous  membrane  tissue,  in  man  a  fibrous  cicatricial  tissue  with 
a  central  depression  and  the  well  known  tendency  to  contract  develops. 
Thus,  striated  cicatrices  form  and  produce  a  distortion  of  the  gastric  wall, 
particularly  when  the  cicatrix  is  fixed  in  position  by  a  preceding  adhesion 
with  neighboring  organs.  Girdle-like  constrictions  form  which  give  the 
organ  an  hour-glass  or  a  cucumber  shape.  Peculiar  cicatricial  bands  or 
bridges  develop,  and  form  a  many-celled  sac,  of  which  Cruveilhier  gives 
an  excellent  illustration  in  his  Atlas. 

2.  Progressive  Corrosive  Necrosis. — This  process,  provided  cicatriza- 
tion does  not  occur,  continues  as  long  as  peptic  gastric  juice  is  formed, 
and  finally  terminates  spontaneously,  i.  e.,  by  the  complications  which 
arise.    These  are: 

(a)  Erosion  of  Vessels. — According  to  the  seat  of  the  ulcer  and  its 
extent  and  depth,  sometimes  smaller,  sometimes  larger,  lumina  of  the  ves- 
sels are  eroded.  The  slight  tendency  to  permanent  thrombus  formation 
is  characteristic,  and  is  probably  due  to  the  corrosive  effect  of  the  gastric 
secretion.  Among  the  larger  vessels  the  pancreatic  artery,  the  gastric 
artery,  and  the  renal  arteries,  or  the  corresponding  veins,  are  attacked. 

Severe  hemorrhages  follow  which  are  only  terminated  by  thrombotic 
coagulation  of  the  blood.  If  the  thrombus  is  situated  in  the -splenic -vein 
it  may  produce  acute  enlargement  of  the  spleen. 

(b)  Adhesions  to  Neighboring  Organs  and  Perforation. — If  the  necrosis 
extends  to  the  serosa,  either  a  reactive  inflammation  and  adhesion  to 
neighboring  organs  with  consequent  implication  of  these,  a  perigastritis, 
or,  if  this  be  impossible,  direct  perforation  into  the  abdominal  cavity,  is 
produced.  Through  the  corresponding  intermediate  tissues  secondary  per- 
forations may  take  place  into  the  pleural  and  cardiac  cavities.    All  of  the 


166  GASTRIC   ULCER   AND  GASTRIC   HEMORRHAGE 

neighboring  organs,  the  liver,  the  gall-bladder,  the  pancreas,  the  spleen, 
the  diaphragm,  the  heart,  the  lungs,  and  the  intestines,  according  to  the 
seat  of  the  ulcer,  are  exposed  to  this  danger.  Occasionally  there  are  adhe- 
sions to  all  of  the  neighboring  organs  in  the  abdominal  cavity  without 
an  actual  perforation,  such  a  condition  having  been  described  by  Budd. 

Finally  the  tubercular  and  syphilitic  ulcers  are.  to  be  mentioned. 

Tubercular  ulcers,  which,  so  far,  have  always  been  found  in  combina- 
tion with  tubercular  lesions  of  others  organs,  are  characterized  by  their 
thickened,  infiltrated,  wall-like  edges.  Their  floor  is  usually  granular, 
and  of  a  light  yellow  color.  They  are  pale  and,  as  in  the  cases  of  Eppin- 
ger,  rise  sharply  from  the  darkly  stained  surrounding  areas. 

In  the  margin  and  upon  the  floor  we  find  tubercular  nodules  with 
characteristic  giant  cells.  The  ulcer  may  be  solitary  or  multiple,  and 
only  affect  the  mucous  membrane  and  mucosa,  or  also  the  muscularis. 
Microscopic  examination  shows  the  well  known  tuberculous  foci  with 
numerous  tubercle  bacilli.  In  some  cases  (Litten)  the  serosa  forming  the 
floor  of  the  ulcer  was  permeated  by  miliary  nodules.  In  Litten's  case  the 
ulcer  was  quite  large,  4.2  by  3.3  ccm.,  its  border  sharp  and  serrated, 
partly  swollen  and  hemorrhagically  infiltrated,  the  remaining  digestive 
tract  free  from  tuberculous  ulcerations,  but  these  were  present  in  the 
larynx,  bronchi  and  lungs.  Similar  cases  have  been  reported  by  Talamon- 
Balzor,  by  Giles  Saburin,  and  two  by  Eppinger.  An  excellent  description 
of  a  tubercular  ulcer  is  given  by  J.  H.  Musser.  The  case  was  that  of  a 
negro,  4-4  years  of  age,  suffering  from  pulmonary  tuberculosis  and  ill- 
defined  dyspeptic  symptoms.  At  the  autopsy  a  gastric  ulcer  was  found, 
1|  by  3|  inches,  and  undoubtedly  of  tuberculous  nature.  Many  miliary 
tubercles  and  much  caseous  material  were  found  upon  its  floor,  and  tuber- 
cles in  the  neighboring  submucosa.  In  this  caseous  mass  were  tubercle 
bacilli.  The  case  of  Bar-Bacci  is  similar:  Isolated,  tuberculous  ulcerations 
of  the  stomach  with  primary,  pharyngeal  tuberculosis. 

Musser  mentions  a  few  similar  cases,  mostly  in  children,  in  which 
also  tubercle  bacilli  were  found  in  the  ulcers.  Evidently  these  findings 
are  rare,  for  in  567  cases  of  tuberculosis  of  the  intestine  Eisenhardt  found 
gastric  tuberculosis  in  only  one  case,  and  in  nearly  2,000  autopsies  of 
tubercular  individuals  Simmonds  found  only  eight  cases.  Marfan,  in  a 
study  of  gastric  disturbances  in  pulmonary  phthisis,  mentions  but  a  few 
examples,  and  these  are  somewhat  doubtful. 

In  children  the  affection  appears  to  be  more  frequent,  for  in  297  tuber- 
cular children  0.  Miiller  and  Hecker  found  8  cases  of  tuberculosis  of  the 
stomach,  and  Biedert  collected  41  cases  of  which  one-third  occurred  in 
cliildren.  These  ulcerations  do  not  all  belong  to  the  type  of  the  corrosive 
ulcer;  on  the  contrary,  some  are  due  to  true  tuberculous  foci  or  softening 
with  a  caseous  decomposition  of  the  tubercle,  or,  at  all  events,  to  their 
combination  with  the  corrosive  action  of  the  gastric  juice  upon  the  ne- 


PATHOLOGICAL  ANATOMY  167 

crosed  tissue  elements.  Their  point  of  preference  is  the  pyloric  region, 
and  their  development  may  certainly  in  most  cases  be  attributed  to  the 
deglutition  of  sputum  containing  bacilli.  Occasionally  they  may  have 
formed  upon  a  hematogenous  and  lymphogenous  base.  Such  ulcers  may 
also  perforate  into  the  abdominal  cavity  and  produce  the  symptoms  of 
perforative  peritonitis.  Kundrat,  Paulicki,  and  Struppler  have  reported 
typical  cases  of  this  kind. 

Syphilitic  ulcer  has  no  special  anatomical  characteristics.  In  the  ma- 
jority of  cases  that  have  been  accurately  observed  no  opinion  is  expressed 
as  to  whether  we  are  dealing  with  a  primary  lesion  or  with  a  decomposed 
gumma.  The  syphilitic  nature  of  the  ulceration  has  been  recognized  (Lux- 
enburg  and  Zawadzki)  only  by  the  presence  of  an  endarteritis  of  the 
gastric  vessels.  Engel  believes  that  10  per  cent.,  and  Lang  that  even  20 
per  cent.,  of  all  ulcers  are  of  a  syphilitic  nature,  but  this  seems  a  gross 
exaggeration.  The  syphilitic  nature  of  the  ulcer  is  favored  by  the  fact 
that  typical  symptoms  occur  simultaneously  with  the  secondary  symptoms 
of  syphilis,  and  are  cured  by  antisyphilitic  treatment  (Cullevrier,  Schwim- 
mer,  Leudet,  Murchison,  Hayem,  Gaillard,  Cesaris  Demel). 

The  fact  that  a  carcinomatous  neoplasm  may  develop  upon  the  floor 
of  an  ulcer,  preferably  one  situated  near  the  pylorus,  requires  especial 
mention.  This  was  emphasized  by  the  Vienna  School,  and  proven  beyond 
doubt  by  Hauser.  In  my  opinion  this  fact  is  not  affected  by  the  imsuc- 
cessful  attempt  of  P.  Hirschfeld  to  prove  by  statistics  that  cancer  of  the 
stomach  occurs  independently  of  the  presence  or  absence  of  gastric  ulcer. 
Everything  can  be  proven  by  statistics,  but  these  do  not  militate  against 
the  force  of  direct  observation,  and  the  latter  will  convince  all  who  have 
had  considerable  practical  experience  (instead  of  having  seen  but  a  few 
cases)  that,  in  many  instances  of  gastric  ulcer,  particularly  those  seated 
at  the  pylorus,  there  is  a  gradual  but  uninterrupted  transition  of  the  ulcer 
into  cancer.  Borrmann,  in  his  excellent  monograph  upon  gastric  cancer, 
in  which  he  differs  from  Hauser,  does  not  deny  this  change,  as  Hirschfeld 
erroneously  assumed.  In  their  ideas  of  the  propagation  of  the  neoplasm 
into  the  tissue,  these  investigators  are  wide  asunder.  Clinically,  however, 
these  are  the  cases  in  which  hydrochloric  acid  production  and  the  peptic 
function  of  the  stomach  continue  for  a  long  time,  although  they  gradually 
decrease  toward  the  norm — cases  which,  upon  the  basis  of  chemism,  have 
been  diagnosticated  as  benign  tumor  of  the  pylorus,  while  operation  or 
autopsy  shows  a  more  or  less  carcinomatously  degenerated  old  ulcer. 

It  is  always  difficult  to  quote  statistics  in  regard  to  the  frequency  with 
which  definite  diseases  occur  and  their  peculiarities;  rather,  to  utilize  the 
so-called  statistics  for  nosological  and  diagnostic  purposes.  We  deal  with 
different  classes  of  patients  and  different  conditions,  which  to  a  great 
extent  depend  upon  unavoidable  circumstances.  If,  however,  in  the  con- 
crete case  we  attempt  to  base  our  opinion  upon  statistics,  we  may  not  know 


168  GASTRIC   ULCER  AND  GASTRIC   HEMORRHAGE 

whether  tlie  case  is  typical  or  exceptional.  It  is  true  that  certain  circum- 
stances, that  is  experiences,  are  so  positive  and  invariable  that  they  require 
no  statistical  proof.  Among  these  is  the  well  known  fact  that  women 
suffer  more  frequently  from  gastric  ulcer  than  men,  but  the  reports  of 
authors  differ  widely  as  to  the  exact  proportion.  Joslin  gives  the  ratio 
as  1:5,  Rheinwald  as  1 : 1.2.  Both  authors  base  their  figures  upon  com- 
paratively few  cases,  respectively  190  and  187,  while  in  3,114  cases  Murrell 
found  a  proportion  of  1 :  2.1  and  1 :  3.4.  All  authors  agree  that  the  age 
in  which  most  are  affected  is  the  third  decade,  i.  e.,  the  time  between  the 
twentieth  and  thirtieth  years  of  life.  Among  2,164  cases  Murrell  found 
393  between  the  twentieth  and  thirtieth,  and  265  between  the  thirtieth 
and  fortieth,  years  of  life.  Joslin  found  the  average  age  in  men  as  37,  in 
women  27.  In  Rheinwald's  cases  9  males  and  31  females  between  sixteen 
and  twenty  years  of  age,  and  19  males  and  22  females  between  twenty-one 
and  twenty-five  years  of  age,  were  attacked. 

It  is  well  known  that  the  proportion  in  cancer  of  the  stomach  is  just 
the  reverse,  i.  e.,  that  more  men  than  women  are  attacked,  and  that  in 
later  life  those  between  the  fiftieth  and  sixtieth  years  are  most  liable; 
therefore,  the  comparative  youth  of  the  patient  in  a  doubtful  diagnosis  of 
ulcer  would  be  of  some  weight  if  we  had  not  recently  learned  by  surpris- 
ingly numerous  experiences  that  youth  is  not  exempt  from  cancer.  The 
youngest  case  of  cancer  of  the  stomach  that  I  have  observed  occurred  at 
sixteen,  the  oldest  at  sixty-five  years  of  age.  It  is  true  that  in  the  former 
case  carcinoma  had  developed  from  an  ulcer. 

SYMPTOMS 

The  symptoms  of  gastric  ulcer  which  authors  have  described  as  belong- 
ing to  the  so-called  normal  type  need  not  be  dwelt  upon;  only  the  most 
prominent  will  be  referred  to." 

Our  discussion  will  be  chiefly  devoted  to  the  manifold  deviations  which 
often  make  the  so-called  classical  clinical  picture  appear  quite  differently 
from  that  described  in  the  text-books. 

The  symptom-complex  of  ulcus  ventriculi  may  be  divided  into  the 
following  groups : 

1.  Cases  in  which  the  irritative  symptoms  which  result  from  hemor- 
rhagic erosion  or  the  corrosion  of  larger  or  smaller  areas  of  the  mucous 
mcnil)rane  predominate,  and  there  are  no  complications. 

2.  Cases  in  which  the  previously  mentioned  irritative  symptoms  and 
hemorrhage  simultaneously  appear. 

3.  Cases  with  symptoms  of  irritation  and  perforation, 

4.  Cases  which  run  a  latent  course  up  to  the  time  of  death  from  hem- 
orrhage or  perforation. 

5.  Cases  which  present  the  sequelae  of  ulcer. 


SYMPTOMS  169 

When  we  remember  merely  the  fact  that  in  these  groups  the  symptoms 
may  be  variously  combined,  an  ever-changing  clinical  picture  is  presented. 

As  is  well  known,  we  usually  diagnosticate  gastric  ulcer  when  the 
classical  triad  of  symptoms  is  present:  Hematemesis  which  can  be  defi- 
nitely traced  to  the  stomach;  typical,  and  usually  sharply  localized,  pain 
occurring  at  regular  intervals  after  the  ingestion  of  food;  and  the  increase 
of  free  hydrochloric  acid  in  the  gastric  contents. 

From  this  it  is  evident  that  gastric  ulcer  can  only  be  diagnosticated 
with  certainty  in  advanced  stages,  and  can  only  then  be  recognized  if  the 
previously  mentioned  symptoms  occur  in  combination.  This,  however,  in 
my  experience  is  hy  no  means  invariably  the  case,  and  I  might  even  say 
that  such  cases  are  exceptional. 

As  the  nerves  exposed  in  the  ulcerated  surface  are  irritated  by  the  in- 
gesta  and  thus  the  pain  is  produced,  and  the  muscular  contractions  which 
arise  in  consequence  of  the  irritation  may  also  cause  painful  sensations, 
gastralgia  soon  forms  an  important  feature  of  the  clinical  picture. 

Early  in  the  affection  the  pain  becomes  localized  in  a  definite  area, 
usually  the  seat  of  the  ulcer,  and  mostly  in  the  pit  of  the  stomach.  The 
boring,  sharply  defined  pain  which  frequently  extends  antero-posteriorly 
is  characteristic.  It  usually  increases  upon  pressure,  and  its  intensity 
may  be  determined  by  the  so-called  algesimeter  which  is  employed  by 
nerve  specialists,  without  the  diagnosis  becoming  any  clearer  or  any  points 
of  support  being  gained  as  to  the  localization  (Boas).  Women  cannot 
lace,  and  men  cannot  wear  a  firm  belt;  only  exceptionally  is  the  pain 
ameliorated  by  pressure.  It  is  obvious  that  the  pain  is  most  intense  when 
the  raw,  ulcerated  surface  is  exposed  to  great  mechanical  irritation.  First, 
and  most  frequently,  that  after  eating,  either  because  the  ingested  food 
directly  irritates  or  by  its  weight  distends  the  gastric  wall,  that  is,  causes 
contraction  and  spasm,  especially  if  the  ulcer  is  located  at  the  pylorus. 
This  is  relieved  as  soon  as  the  stomach  rids  itself  of  its  contents;  as, 
however,  small  or  coarse  particles  of  food  are  occasionally  caught  in  the 
grooves  of  the  ulcer  and  may  remain  there,  it  is  not  remarkable  that  the 
organ  to  a  certain  extent  reacts  to  these  irritative  bodies,  and  repeatedly 
makes  an  effort  to  expel  them.  Thus  spasmodic  contractions,  pyloro- 
spasms,  which  may  last  for  days  or  may  recur  at  short  intervals,  arise  and 
greatly  weaken  the  patient  by  their  duration  and  the  suffering  they  cause. 

These  are  generated  in  highly  developed  processes  of  stenosis  of  the 
pylorus  or  of  great  atony  of  the  muscles  of  the  stomach  by  the  retention 
of  acid  products  of  secretion,  with  the  starches  which  are  feebly  or  not 
at  all  digested.  Distention  of  the  stomach  from  gas  and  irritation  of  the 
nerves  by  the  continuous  ulcerative  process  produce  gastralgia,  which 
must  be  looked  upon  rather  as  a  reflex  effect  when  cold  and  psychical 
stimulation  produce  gastralgic  attacks,  or  the  pains  increase  in  severity 
before  the  menstrual  period,  and  lessen  when  it  appears. 


170  GASTRIC   ULCER  AND   GASTRIC   HEMORRHAGE 

These,  however,  are  not  the  only  causes.  In  patients  with  peptic  ulcer 
I  have  repeatedly  seen  severe  gastralgia  after  a  cold  drink  or  a  spoonful  of 
hot  soup,  a  swallow  of  too  hot  tea  or  any  similar  thing;  in  these  instances 
the  previously  mentioned  factors  were  out  of  the  question,  but  a  thermic 
irritation  was  the  cause.  In  my  experience  too  hot  ingesta  is  a  cause 
much  more  rarely  than  cold,  perhaps  for  the  reason  that  with  the  former, 
the  mouth  and  pharynx  to  a  certain  extent  act  as  gourds,  the  gastric  mu- 
cous membrane  is  more  tolerant  to  high  temperatures  than  to  low  ones, 
and  also  because  less  is  consumed  of  the  former  than  of  the  latter. 

Gastralgia  accounts  for  the  fact  that  these  spasmodic  pains  usually 
come  on  suddenly  and  with  great  intensity,  and  that  they  disappear  almost 
as  r;i])idly  as  they  occur,  and  the  patient  quickly  returns  to  nearly  a 
normal  condition,  while  a  gradual  increase  to  a  paroxysmal  height  is  rarely 
heard  of. 

The  occasional  occurrence  of  cutaneous  hyperesthesia  and  anesthesia,  as 
was  observed  by  Traube,  is  peculiar,  and  is  attributable  to  central  irradia- 
tion. Attacks  of  angina  pectoris,  of  intercostal  neuralgia,  of  neuralgia 
of  the  left  brachial  plexus,  of  sensations  of  pain  in  the  right  shoulder 
(Brinton)  and  in  the  arms  and  legs  (Miiller)  appear.  Pressure  points  are 
noted  upon  the  back,  and  along  the  vertebral  column,  corresponding  to  the 
posterior  roots  of  the  lower  thoracic  and  upper  lumbar  intercostal  nerve.>, 
or  a  spontaneous  pain,  or  one  after  pressure,  appears  in  the  spinous 
processes. 

In  opposition  to  some  recent  investigators,  particularly  Pariser,  I  main- 
tain that  these  pain  and  pressure  points  upon  the  posterior  walls  of  the 
thorax  are  hy  no  means  invariable.  On  the  contrary,  in  my  patients  they 
W'Cre  often  absent,  and,  like  the  author  mentioned  above,  I  should  be  un- 
willing to  base  a  diagnosis,  or  the  permanency  of  the  cure  of  an  ulcer, 
upon  their  presence  or  absence.  As  the  demonstration  of  this  phenomenon 
is  very  simple,  errors  can  hardly  result  from  the  method. 

At  this  point  tetany  must  be  mentioned,  which,  however,  is  but  slightly 
connected  with  gastric  ulcer,  being  not  an  immediate  but  only  a  remote 
sequel.  This  peculiar  symptom-complex  is  often  attributed  to  a  deficiency 
of  water  in  the  organism,  and  is  characterized  by  the  hyperirritability  of 
certain  peripheral  nerves,  above  all,  the  facial  nerve  and  those  wMch  inner- 
vate the  extensors  of  the  extremities ;  among  other  conditions  it  occurs  in 
gastrectasis  following  ulcer  of  the  pylorus,  and  gives  rise  to  stenosis. 

Gastric  dilatation  which,  in  its  course,  leads  to  stasis  of  the  gastric  con- 
tents and  a  deficiency  of  water  in  the  organism,  may,  however,  be  due  to 
various  causes.  Hence,  tetany  does  not  clinically  belong  to  the  picture 
of  LMstrie  ulcer,  but  is  only  a  complication  which  occurs  in  a  slight  number 
of  cases.  At  this  point  I  cannot  refrain  from  expressing  my  belief  that 
dfficiciK  V  of  water  in  the  organism,  brought  forth  so  prominently  l)y 
Kussuiiuirs  adherents,  is  the  causative  factor  in  only  a  small  number  of 


SYMPTOMS  171 

cases.  Other  authors,  as  well  as  I,  have  observed  cases  of  tetany  in  which 
there  were  no  signs  of  gastrectasis  and  its  consequences,  but  the  cause 
was  to  be  sought  for  in  the  increased  reflex  irritability  due  to  abnormal 
decomposition  of  the  ingesta  and  the  formation  of  toxins  thereby. 

In  nearly  three-fourths  of  all  cases  of  gastric  disease,  there  is  an  "  epi- 
gastric pressure  point"  i.  e.,  an  area  in  the  scrobiculus  cordis  sensitive  to 
pressure,  and  this  is  also  present  in  most  patients  suffering  from  ulcer.  That 
this  has  nothing  in  common  with  the  localization  of  the  ulcer  is  a  well  known 
fact  and  experience.  To  be  distinctly  differentiated  from  it  is  a  point 
lower  down  and  to  the  left  which  upon  pressure  also  very  frequently,  but 
not  so  often  as  the  first  mentioned  one,  is  sensitive  to  pressure,  and  in  its 
position  corresponds  to  the  solar  plexus.  In  fact  in  most  persons,  with 
and  without  ulcer,  a  decided  sensitiveness  to  pressure  may  be  observed  in 
this  area,  provided  the  pressure  is  exerted  obliquely  toward  the  median 
line,  and  thereb}^  the  solar  plexus  is  forced  toward  the  bony  vertebral 
column.  That  in  thin  persons  with  rigid  abdominal  walls  a  distinct  epi- 
gastric pulsation  is  felt  in  this  area  hardly  requires  mention. 

Only  rarely  is  the  accompanying  gastric  catarrh  so  prominent  that 
actual  anorexia,  a  pappy  taste,  eructations,  a  disagreeable  odor  to  the 
breath,  and  a  coated  tongue  are  observed.  On  the  contrary,  the  latter 
organ  is  usually  of  fair  appearance,  smooth,  moist,  and  distinctly  red,  so 
that  the  findings  just  mentioned  in  patients  with  severe,  colicky,  gastric 
disturbance  should  at  once  awaken  our  suspicions  of  ulcer.  What  of  the 
chemical  processes  going  on  in  the  stomach? 

Here  we  are  forced  to  touch  upon  the  question  so  often  discussed 
whether  it  is  permissible,  with  a  certain  or  suspected  ulcer,  to  introduce 
the  sound  or  the  stomach-tul)e  for  diagnostic  or  therapeutic  purposes. 
Absolutely  yes !  In  many  hundreds  of  patients  with  ulcer  I  have  intro- 
duced the  stomach-tube,  or  have  had  it  introduced,  thousands  of  times, 
and  have  never  seen  deleterious  effects. 

This  is  maintained  by  all  authors  of  great  experience.  Of  course,  this 
manipulation  is  not  to  be  undertaken  immediately  after  a  profuse  hemor- 
rhage. But  we  shall  see  later  on  that  during  decided  bleeding  it  is  very 
beneficial  to  wash  out  the  stomach  with  ice-water. 

That  in  a  majority  of  the  cases  the  chemism  is  not  decreased  is  evident 
from  the  fair  appetite  of  patients  with  ulcer.  Yet  the  early  view  that 
an  increased  production  of  Iwdrochloric  acid  is  a  necessary  or,  at  least, 
an  almost  invariable  accompaniment  of  gastric  ulcer  can  no  longer  be 
maintained,  being  contrary  to  the  comprehensive  observations  of  the  last 
few  years.  In  my  cases  I  found  hyperacidity  in  only  34.1  per  cent.,  normal 
acidity  in  56.8  per  cent,  and  subacidity  in  9  per  cent. ;  T  must  admit  that 
these  results  surprised  me  greatly.  It  must  be  remarked,  however,  that 
in  the  last  mentioned  group  there  were  five  cases  in  which  the  acidity  on 
repeated  investigations  was  found  to  be  either  14  per  cent,  or  24  per  cent.. 


172  GASTRIC  ULCER   AND  GASTRIC   HEMORRHAGE 

while  the  presence  of  a  typical  gastric  ulcer  without  carcinomatous  degen- 
eration was  made  certain  by  an  operation  and  the  subsequent  microscopic 
investigation  of  a  resected  portion  of  the  tissue.  It  is  true  that  in  the 
other  cases  of  this  category  we  were  dealing  with  persons  in  whom  a  more 
or  less  advanced  degeneration  was  either  assumed  or  was  determined  posi- 
tively by  operation. 

Rheinwald  tested  the  chemistry  of  the  stomach  in  66  cases,  and  found 
hydrochloric  acid  in  84.5  per  cent.,  hyperchlorhydria  in  65.5  per  cent.,  an 
absence  of  hydrochloric  acid  in  7  per  cent.,  lactic  acid  5  times.  The  fre- 
quency of  non-increased,  and  even  subacid,  values  has  also  been  noted  by 
other  authors. 

In  38  cases  of  ulcer  Schneider  found  hyperacidity  in  only  18  to  19 
per  cent.  The  reason  he  assigns  for  this  is  that  simultaneously  complica- 
tions of  various  kinds  arose,  such  as  ectatic  conditions,  chronic  peritonitis, 
more  or  less  severe  anemia,  etc. 

Kohler,  wlio  observed  the  cases  in  Gerhard t's  Clinic  from  1890  to  1895, 
found  among  165  tests  for  hydrochloric  acid  65  per  cent,  of  positive,  and 
34.7  per  cent,  of  negative  results.  It  is  true  the  extreme  proportion 
of  lactic  acid,  namely,  33.3  per  cent.,  forces  us  to  conclude  that  in 
many  of  his  cases  there  was  already  well  advanced  carcinomatous  de- 
generation. 

According  to  these  experiences,  the  opinion  that  all  gastric  ulcers  during 
the  time  of  their  existence  cause  a  typical  increase  of  acidity,  must  at  all 
events  he  rejected  as  incorrect. 

On  the  contrary,  here — as  in  many  other  points  in  the  diagnosis  of 
gastric  disease — we  must  be  very  cautious  in  utilizing  the  chemical 
findings.  Increased  acidity  favors  ulcer,  its  decrease  does  not  positively 
exclude  it. 

In  fact,  upon  repeated  examinations  the  values  for  acidity  show  de- 
cided variations.  In  35  cases,  in  which  I  was  not  content  with  a  single 
test  but  made  repeated  examinations,  sometimes  six  or  seven,  the  values 
in  some  respects  differed  widely  from  each  other.  Thus,  in  a  woman,  aged 
25,  who  several  times  suffered  from  hematemesis,  and  in  whom  the  gastric 
contents  after  a  test  breakfast  frequently  showed  small  quantities  of  blood, 
tlie  values  for  acidity  varied  between  28  and  44;  in  a  patient  aged  26 
])etween  36  and  T8 ;  in  a  man  with  repeated  hematemesis,  and  who  per- 
islied  from  perforation,  between  38  and  54;  in  another  patient,  in  whom 
resection  was  performed  for  ulcer  at  the  pylorus,  between  29  and  71,  etc. 
Treatment,  and  particularly  the  diet,  influences  these  variations,  but  they 
are  especially  important  because  these  are  usually  the  cases  in  which  we 
resort  to  the  stomach-tube  to  obtain  a  positive  finding,  if  possible.  Kohler 
also  states  that  in  some  cases  of  undoubted  ulcer  of  the  stomach  a  number 
of  tests  are  apt  to  be  negative  until  free  hydrochloric  acid  is  produced  in 
large  quantity,  and  sometimes  no  hydrochloric  acid  can  be  found  with 


SYMPTOMS  173 

any  tests.  Riegel's  statement  that  hyperacidity  is  a  constant  sign  in  ulcer 
of  the  stomach  must,  therefore,  he  accepted  with  limitations. 

Gluczinsky  has  called  attention  to  the  fact  that  chemism  changes  when 
a  correct  diet  is  instituted,  that  is  to  say,  changes  with  the  food.  For 
example,  in  the  first  week  on  a  mixed  diet  an  acidity  value  of  30  (hydro- 
chloric acid)  was  found  after  a  test  breakfast,  in  the  second  week  upon 
a  milk  diet  8,  in  the  third  week  upon  mixed  diet  25,  and  in  the  fourth 
week  upon  a  milk  diet  5.  In  the  cases  which  I  cited  it  is  unnecessary 
to  consider  this  circumstance ;  for,  during  the  entire  time  the  patients  were 
under  observation,  they  were  kept  upon  the  same  bland  diet. 

In  a  certain  group  of  cases,  however,  an  increase  in  the  excretion  of 
hydrochloric  acid  is  unquestionably  present,  and  these  are  the  cases  desig- 
nated as  gastrosuccorrhea  or  hypersecretion  (parasecretion,  Ewald).  For- 
merly relegated  by  many  authors  to  the  true  neuroses,  they  are  now  re- 
garded as  the  consequences  of  ulcer  running  a  latent  course.  Soupault 
operated  upon  28  cases  of  typical  gastrosuccorrhea,  and  in  each  instance 
found  an  ulcer  of  the  pylorus.  In  48  cases  of  gastrosuccorrhea  Mathieu 
and  Laboulais  found  hematemesis  or  melena  six  times,  and  eleven  times 
very  severe  pains  were  referred  to  spasm  of  the  pylorus.  Gluczinsky  at- 
tributes all  cases  of  gastrosuccorrhea  to  ulcer  with  stenosis  of  the  pylorus. 
This,  in  my  opinion,  is  to  act  without  discrimination.  The  outpouring 
of  gastric  juice  is  occasionally  irregular  and  unsteady.  It  is  unreasonable 
to  assume  in  each  case  a  newly  formed  ulcer,  but  in  all  of  these  instances 
we  must  consider  nervous  irritation  as  a  cause,  as  well  as  the  fact  that 
these  cases  cannot  be  strictly  separated  into  "  retention  secretion "  and 
"  hypersecretion,"  nor  do  they"  belong  exclusively  to  one  or  the  other  cate- 
gory. Every  one  of  extensive  experience  knows  that  transitions  occur, 
and  that  the  same  case  may  at  certain  times  show  the  characteristics  of 
a  pure  neurosis,  and  at  other  times  may  present  the  picture  of  deranged 
stasis.  Therefore,  explicit  descriptions  to  show  that  either  the  one  or  the 
other  condition  was  alone  decisive  and  causative  appear  to  me  to  be  quite 
superfluous.  Yet  this  is  now  a  secondary  question.  I  desire  only  to  show 
that  certain  cases  of  ulcer  positively  present  increased  secretion  of  hydro- 
chloric acid,  and,  disregarding  the  limitations  mentioned  above,  the  latter, 
i.  e.,  hyperchlorhydria,  is  unquestionably  of  great  diagnostic  value. 

I  go  a  step  further,  and  maintain  that  in  all  cases  in  which  the  course 
points  with  more  or  less  likelihood  to  gastric  ulcer,  the  chemism  of  the 
stomach,  however,  showing  insufficiency  of  hydrochloric  acid  secretion  and 
of  peptic  digestion,  the  view  of  a  carcinomatous  transition  of  the  ulcer 
is  well  founded.  This  is  particularly  true  in  young  persons.  In  this 
respect  I  have  recently  seen  a  most  tjrpical  case:  A  woman,  aged  26,  had  a 
large,  freely  movable  tumor  situated  upon  the  greater  curvature  and  toward 
the  pylorus,  the  raucous  gastric  contents  showing  undigested  remains  of 
a  roll  but  without  free  hydrochloric  acid.     Operation  revealed  two  flat 


174  GASTRIC   ULCER  AND  GASTRIC   HEMORRHAGE 

ulcers  the  size  of  a  twenty-five  cent  piece,  one  close  to  the  pylorus,  the  other 
toward  the  fundus,  in  the  surroundings  of  which  the  submucosa,  the 
muscularis  and  serosa  were  markedly  thickened.  The  floor  of  the  ulcers 
was  almost  smooth,  of  a  light  flesh  color,  the  margin  was  slightly  raised, 
l)ut  not  undermining  the  neighboring,  greatly  swollen  mucous  membrane. 
^Microscopical  investigation  showed  a  carcinomatous  neoplsism  extending 
into  the  muscularis,  which  only  in  quite  isolated  areas  had  left  some 
glandular  tissue.  In  this  case  the  history  revealed  no  former  symptoms 
of  ulcer,  but  the  age  of  the  patient  was  against  a  primary  carcinoma.  In 
other  similar  cases,  however,  typical  signs  of  an  old  ulcer  could  be  gleaned 
from  the  history. 

The  hemorrhages  are  either  from  small  vessels  and  slight  in  amount, 
and  then  are  only  accidentally  observed  in  the  form  of  fine  hemorrhagic 
streaks  when  freshly  admixed  with  the  vomited  material,  or  they  are  seen 
as  reddish-brown,  granular  masses  after  the  gastric  juice  has  for  some  time 
acted  upon  the  accumulated  blood.  Upon  superficial  examination  small 
hemorrhages  of  this  kind  may  be  entirely  overlooked,  for  the  blood  is  not 
vomited  at  all,  but  passes  into  the  intestine,  and  is  there  so  decomposed 
that  the  appearance  of  the  feces  is  not  decidedly  altered.  Slight  admix- 
ture of  blood  to  the  gastric  contents  does  not  give  it  a  characteristic  appear- 
ance, but  often  only  a  dirty  gray  color,  which  does  not  at  once  awaken 
the  suspicion  of  hemorrhage.  On  the  other  hand,  it  need  hardly  be  stated 
that  cocoa,  chocolate,  strawberry  wine,  bilberry  wine,  and  the  like  may 
lead  to  errors  upon  superficial  examination.  In  such  cases,  as  Schmauss 
has  shown,  we  must  occasionally  make  microscopic,  spectroscopic,  or  chem- 
ical examinations  in  order  to  detect  the  pre^nce  of  the  smallest  quantities 
of  hemoglobin  or  of  blood  in  the  gastric  contents  or  in  the  feces,  and  to 
recognize  them  as  the  cause  of  so-called  essential  anemia. 

Occult  Hemorrhage. — In  latent  gastric  ulcer  Eossel,  and  subsequently 
Boas  and  I,  repeatedly  made  the  diagnosis  of  ulcer  from  the  proof  of 
"  occult "  blood  in  the  feces,  naturally,  when  other  sources  of  hemorrhage 
were  excluded,  and  the  food  administered  prior  to  the  examination  did  not 
contain  large  amounts  of  blood. 

The  chemical  examination  of  the  feces  for  blood  is  best  made  either 
with  the  resin  of  guaiac  or  with  aloin.  In  either  case  a  quantity  of  feces 
about  the  size  of  a  hazelnut  is  rubbed  up  with  water  (or  a  corresponding 
quantity  of  fluid  feces  is  taken),  and,  after  the  addition  of  some  glacial 
acetic  acid,  is  shaken  up  in  a  test-tube  with  ether  (the  previous  removal 
of  fat  from  the  feces  by  shaking  with  ether  is  proper,  but  is  by  no  means 
always  necessary).  The  hemoglobin  which  may  be  present  is  changed 
into  honiatin  (methemoglobin)  by  the  acetic  acid,  and  taken  up  by  the 
etlier.  To  the  clear,  over-lying  ether  which  is  poured  off  resin  of  guaiac 
which  has  been  dissolved  in  alcohol  is  added  (or  the  dry  powder  which  is 
readily  soluble  in  ether),  and  finally  about  a  cubic   centimeter  of  the 


SYMPTOMS  175 

resin  of  turpentine  or  Hiihnerfeld's  reagent.^  When  larger  quantities 
of  blood  are  present,  a  blue  color  at  once  appears ;  when  smaller  quantities, 
this  change  takes  place  after  a  few  minutes.  The  test  is  made  in  the  same 
way  with  aloin,  of  which  a  freshly  prepared  alcoholic  solution  should  be 
used.  In  a  few  minutes  the  ethereal  mixture  changes  to  a  beautiful,  cherry- 
red  color,  and  the  hemoglobin  forms  a  uniform  layer  of  precipitate  at 
the  bottom  of  the  test-tube.  According  to  Boas,  the  test  may  be  made  in 
the  same  way  as  for  the  reaction  of  indican;  the  addition  of  a  few  drops 
of  chloroform  will  make  the  reaction  more  distinct,  but  in  my  opinion  this 
is  superfluous.  No  matter  how  the  reaction  for  blood  is  produced,  in 
those  cases  which  present  no  other  characteristic  sign  of  gastric  ulcer  the 
difficulty  will  be  to  prove  that  the  blood  found  is  actually  from  the  stomach 
and  not  from  other  portions  of  the  digestive  tract.  It  is  self-evident  that 
no  blood  or  hemoglobin  should  be  given  with  the  food. 

The  microscopic  proof  of  small  quantities  of  blood  in  the  feces  is  al- 
ways very  difficult,  because  the  blood-corpuscles  in  their  migration  through 
the  intestine  are  usually  so  distorted  that  they  lose  their  characteristics. 
In  profuse  hemorrhages  there  is  no  danger  of  this,  but  in  lesser  ones, 
especially  when  mercurial  preparations  or  those  containing  sulphur  have 
been  administered,  it  must  be  considered. 

Copious  hemorrhages  presuppose  the  erosion  of  a  large  vessel,  and  they 
act  upon  the  stomach  like  an  emetic,  so  that  this  organ  rids  itself  of  its 
contents.  Many  patients  have  distinct  premonitory  symptoms,  flashes  of 
heat,  epigastric  pulsation,  a  sense  of  fulness  in  the  gastric  region,  great, 
and  apparently  groundless,  internal  disquietude  which  to  a  great  degree 
produces  depression  and  anxiety.  In  other  patients  the  only  preceding 
symptoms  are  an  unusual  feeling  of  illness  and  complete  loss  of  appetite. 
The  time  which  the  blood  remains  in  the  stomach  varies  greatly,  and  this 
also  changes  the  appearance  of  the  vomited  material.  Sometimes  the  coagu- 
lated blood  is  light  red  and  lumpy,  at  other  times  it  forms  dark  red  masses, 
and  sometimes,  in  a  minority  of  cases,  the  vomited  material  resembles 
coffee-grounds.  Large  quantities  of  blood  in  the  vomited  material  may 
even  be  noted  with  the  naked  eye,  certainly  by  the  aid  of  the  microscope, 
perhaps  by  the  spectroscope,  or  by  the  various  chemical  tests  for  blood. 
As  mentioned  above,  a  portion  of  the  blood  finds  its  way  into  the  intestines. 
If  a  profuse  hemorrhage  has  occurred,  or  if  the  ulcer  is  in  the  duodenum, 
the  evacuations  have  a  tarry  appearance,  and  consist  of  very  offensive 
masses  in  which  the  presence  of  blood  may  be  detected. 

In  most  cases  the  hemorrhages  occur  suddenly  without  an  assignable 
cause.  Occasionally  they  are  preceded  by  circumstances  either  of  a  psychic 
or  a  physical  nature  which  accelerate  the  cardiac  action,  such  as  joy, 
fright,  unusual  exertion,  external  trauma   (blow,  fall,  pressure,  etc.),  or 

1  Acid,  acetic,  Aq.  destill.  aa.  2.0,  01.  Terebinth.,  Spirit,  dilut.  aa.  100.0. 
13 


176  GASTRIC   ULCER   AND   GASTRIC   HEMORRHAGE 

strain  upon  evacuation.  Improper  food,  for  example,  hard  tendinous  meat, 
fibrous  vegetables,  such  as  beans  or  asparagus,  may  cause  hemorrhage  by 
direct  mechanical  lesion.  One  of  my  patients,  who  up  to  that  time  had 
never  vomited  blood,  had  a  severe  hemorrhage  after  taking,  on  the  advice 
of  Cohnheim,  200  grams  of  oil  by  the  mouth  to  relieve  pyloric  spasm. 
Nausea,  retching,  and  hematemesis  were  the  consequences  of  this  form  of 
medication  which  is  greatly  praised  by  its  author. 

The  frequency  of  hematemesis  is  reckoned  at  50  per  cent.,  but  this  is 
too  high  rather  than  too  low.  Brinton  gave  29  per  cent.,  Witte  in  Copen- 
hagen found  it  100  times  in  339  cases  (=  29.4  per  cent.),  Gerhardt  saw  it 
in  47  per  cent,  of  his  cases,  so  that  we  may  safely  assume  that  more  than 
half  of  the  patients  do  not  suffer  from  hematemesis.  Among  556  cases 
V.  Leube  found  it  in  46  per  cent.  I  observed  it  in  54.5  per  cent.  In  187 
cases  Joslin  found  no  less  than  81  per  cent,  showing  gastric  hemorrhages, 
from  which  we  may  see  how  unreliable  and  how  dependent  upon  accidental 
conditions  these  so-called  statistics  are. 

In  an  interesting  compilation  based  upon  the  records  of  Guy's  Hospital 
from  1870  to  1890,  W.  Charles  Hood  reports  that  in  the  majority  of  cases 
of  gastric  hemorrhage  in  the  course  of  ulcer  occurring  in  patients  under 
30  years  of  age  women  are  chiefly  affected,  and  that  during  this  period  of 
life  fatal  hemorrhage  is  extremely  rare.  Of  66  cases  of  this  kind  29  were 
under  thirty,  among  these  only  2  men.  On  the  other  hand  there  were 
11  men  among  21  cases  between  thirty  and  forty  years  of  age.  All  recov- 
ered. Seven  other  cases  in  which  death  occurred  immediately  after  the 
hemorrhage  were  all  over  30  years  of  age,  among  them  4  women,  respect- 
ively 33,  35,  50  and  53  years  of  age.  Although  we  can  hardly  assume 
that  the  prognosis  of  gastric  hemorrhage  changes  particularly  with  the 
critical  age  of  thirty  in  women,  nevertheless  this  report  indicates  that 
gastric  hemorrhages  in  younger  women  present  a  less  unfavorable  prog- 
nosis, since  a  conspicuous  improvement,  the  cessation  of  the  distressing 
symptoms  and  regeneration  of  the  blood,  is  often  observed  after  such  an 
event.  In  one  of  my  cases  the  number  of  erythrocytes  within  three  weeks 
after  the  hemorrhage  increased  from  1,900,000  to  3,040,000,  and  the 
amount  of  hemoglobin  from  31  per  cent,  to  51  per  cent.  Similar  observa- 
tions have  be^n  repeatedly  made. 

The  hemorrhagic  masses  from  a  bleeding  peptic  ulcer  are  free  from 
specific  elements,  and  the  blood-corpuscles  preponderate  to  such  an  extent 
tliat  the  cellular  elements  of  the  gastric  mucous  membrane  are  either  scant 
or  do  not  appear  at  all. 

When  a  copious  hemorrhage  has  once  occurred  the  danger  of  a  repeti- 
tion is  always  present  and  hangs,  like  the  sword  of  Damocles,  over  the 
patient's  head  in  a  two-fold  manner.  In  the  first  place,  at  brief  intervals 
in  the  course  of  a  day,  or  even  several  times  a  day,  or,  perhaps,  at  l)rief 
intervals  during  a  week,  hemorrhages  repeatedly  occur.     We  must  then 


SYMPTOMS  177 

assume  that  we  are  dealing  with  relapses  from  the  same  vessel  which  was 
first  eroded.  Secondly,  after  longer  intervals,  months  or  even  years,  hem- 
atemesis  may  be  renewed,  and  then,  in  consequence  of  the  tendency  of 
the  individual  to  hemorrhages  of  this  kind,  repetitions  are  likely.  Occa- 
sionally it  appears  as  though  the  thrombus  formed  is  not  adherent,  and 
that  it  readily  sloughs  off  when  the  cardiac  action  becomes  stronger,  as 
under  normal  conditions.  Twice  I  saw  a  hemorrhage  occur  after  a  long 
interval  when  the  patient,  from  a  mistaken  idea  that  it  would  be  beneficial, 
took  strong  alcoholic  liquors,  although  only  in  small  quantity. 

Slight  hemorrhages,  aside  from  their  psychical  effect,  have  no  influence 
upon  the  condition  of  the  patient;  copious  hemorrhages,  particula  ly  when 
in  rapid  succession,  lead  to  extreme  anemia  and  its  consequences.  Wax- 
like  pallor  of  the  skin,  a  small  frequent  pulse,  slight  fever,  tinnitus  aurium 
and  vertigo,  loss  of  consciousness,  transitory  mild  delirium,  and  total 
anorexia  follow.  Subsultus  tendinum  and  spasms  in  the  extremity  like 
those  of  cholera  have  been  observed.  Nevertheless,  the  patients  recover 
with  comparative  rapidity,  and  under  suitable  treatment  the  lost  strength 
is  regained.  Edema  of  the  extremities,  which  is  observed  particularly  in 
the  evening  if  the  patient  has  been  upon  his  feet  during  the  day,  and 
amaurosis  which  sometimes  occurs  immediately,  perhaps  some  time  after 
the  hemorrhage  (but  which,  according  to  Fries,  occurs  in  65.5  per  cent, 
of  all  hemorrhages  in  the  intestinal  tract),  show  an  internal  relation  to 
hematemesis  which  as  yet  has  not  been  clearly  demonstrated.  As  has  al- 
ready been  stated,  cases  of  gastric  hemorrhage  with  fatal  outcome,  particu- 
larly in  youth,  are  comparatively  rare. 

Here  also  the  reports  of  authors  differ  widely,  and  the  results  vary 
between  8  per  cent.  (Rodman)  to  0.8  per  cent.  (Bramwell).  My  own 
statistics,  based  upon  360  cases  observed  in  the  hospital,  give  1.3  per  cent. 

Usually  death  is  due  to  the  rupture  of  the  ulcer  and  corrosion  of  the 
splenic  or  pancreatic  artery,  the  portal  vein,  or  the  left  heart,  as  will  sobn 
be  described.  A  case  of  chronic  gastric  ulcer  with  fatal  hemorrhage  from 
an  eroded  left  renal  vein  has  lately  been  reported  by  A.  Markel. 

A  small  aneurysm  of  the  coronary  artery  was  the  cause  of  death  in  a 
case  described  by  Powell.  The  ulcer  was  situated  in  the  lesser  curvature 
close  to  the  cardia ;  in  its  center  was  an  aneurysm  about  the  size  of  a  pea 
which  had  ruptured,  and  by  profuse  hemorrhage  had  caused  death  in  a 
few  moments.  A  similar  case  was  described  by  Sachs.  Here  a  small  artery 
of  the  submucosa  was  implicated. 

The  hemorrhages  which  take  place  by  the  perforation  of  an  aortic 
aneurysm  into  the  stomach  or  into  the  esophagus  are  of  a  more  indirect 
nature.  Gastric  hemorrhages  have  also  been  observed  (Naunyn)  in  chole- 
lithiasis. Minkowski  reported  a  remarkable  case  at  the  Congress  of  In- 
ternal Medicine  in  1902.  It  was  that  of  a  small  aneurysm  at  the  arch 
of  the  aorta  which  had   ruptured  through   the   walls   of  the   esophagus. 


178  GASTRIC   ULCER  AND  GASTRIC  HEMORRHAGE 

Thence  the  blood  found  its  way  to  the  cardia  and  to  the  floor  of  an 
ulcer  in  the  stomach. 

Any  of  these  hemorrhages  may  occur  without  preceding  symptoms  of 
an  ulcer  of  the  stomach.  Fatal  hemorrhages  are  usually  preceded  by 
indistinct  signs  of  a  severe  disease ;  in  other  cases,  however,  the  hemorrhage 
may  occur  suddenly  like  lightning  from  a  clear  sky,  attacking  a  person 
apparently  in  the  best  of  health,  and  bringing  about  a  fatal  termination. 

At  this  point  we  must  call  attention  to  other  forms  of  "  gastric  hem- 
orrhages," which,  because  less  familiar,  may  tend  to  grave  diagnostic 
errors. 

First,  are  the  hemorrhages  from  varicose  veins  of  the  esophagus.  Here 
the  condition  is  such  that  occlusion  of  the  hepatic  circulation  takes  place, 
and  the  blood  in  the  portal  vein  attempts  to  force  its  way  through  the 
venous  plexus  formed  by  the  combination  of  the  gastric  veins  with  the 
esophageal  veins.  The  blood  then  takes  a  retrogressive  course,  and,  as  the 
esophageal  veins  cannot  withstand  the  force  of  such  large  amounts  of  blood, 
they  become  enormously  dilated.  The  least  resistant  areas  dilate  and  form 
varices,  which,  with  the  great  pressure  of  the  blood,  readily  rupture  and 
cause  profuse  hemorrhage.  The  blood  at  first  flows  into  the  stomach  and 
is  vomited  as  a  "  gastric  hemorrhage."  Only  a  thorough  investigation  and 
the  consideration  of  the  just  mentioned  possibility  will  furnish  a  clue  to 
the  true  situation.  Frequently  this  is  revealed  only  at  the  autopsy.  I 
have  seen  a  great  number  of  cases  of  this  kind  in  which  grave  errors  were 
made.  Only  recently  a  gentleman  from  the  provinces  was  sent  to  me  with 
the  diagnosis  "  hematemesis  from  an  ulcer  of  the  stomach";  examination 
revealed  a  decided  enlargement  of  the  spleen  and  a  hard,  enlarged  liver. 
In  the  gastric  contents  there  was  a  marked  decrease  of  free  HCl ;  no  en- 
larged glands.  The  patient  had  twice  suffered  from  a  decided  gastric 
lieinorrliage  which  had  appeared  without  prodromes.  Typical  symptoms 
of  ulcer  were  never  present.  Under  these  circumstances  a  diagnosis  was 
made  of  hepatic  cirrhosis  with  hemorrhage  from  the  esophagus,  and  this 
was  soon  confirmed  by  the  development  of  marked  ascites. 

In  this  group  we  must  include  the  hemorrhages  from  varices  of  the 
gastric  mucous  membrane  (Sachs,  Letulle,  A.  Cohn),  which  often  recur 
in  close  succession,  and  "  are  combined  with  venous  stasis  phenomena  of 
the  abdominal  organs,  often  with  hepatic  cirrhosis,  and  almost  invariably 
with  decided  enlargement  of  the  spleen." 

In  regard  to  the  splenic  tumor  in  these  cases,  it  must  be  borne  in  mind 
tliat,  under  some  circumstances,  as  has  been  previously  stated,  thrombosis 
of  the  splenic  vein  from  a  corroding  ulcer  of  the  stomach  may  cause  acute 
ciilargenient  of  the  spleen.  If  the  thrombus  be  simultaneously  affected, 
and  if.  in  consequence,  a  septic  fever  develops,  the  diagnostic  perplexity 
is  less  great. 

Another  form  of  gastric  hemorrhage  not  originating  from  ulcer  is  the 


SYMPTOMS  179 

so-called  "parenchymatous  gastric  hemorrhage."  There  is  also  a  group 
of  hemorrhages  which  are  not  limited  to  the  stomach,  but  attack  the 
entire  intestinal  tract,  and  occur  as  the  consequence  of  venous  stasis  in 
diseases  of  the  heart,  the  liver,  and  the  lungs,  particularly  in  thrombosis 
of  the  portal  veins,  and  in  infectious  diseases,  such  as  enteric  fever,  yellow 
fever,  cholera,  etc.  As  a  rule,  they  do  not  lead  to  typical  hematemesis,  and 
scarcely  ever  simulate  gastric  ulcer.  The  condition  is  quite  different  when 
the  bleeding  appears  suddenly,  as  a  single  or  repeated  attack  of  hemorrhagic 
vomiting,  and  the  most  minute  investigation  fails  to  reveal  the  source 
of  the  henjorrhage.  As  many  cases  of  gastric  ulcer  run  a  latent  course 
prior  to  the  appearance  of  severe  hematemesis  or  melena,  we  will  not  err 
in  such  cases,  after  excluding  the  previously  mentioned  causes  of  hemor- 
rhage— here,  in  my  experience,  hepatic  cirrhosis  taker  precedence — if  we 
assume  a  gastric  ulcer,  and  in  the  further  course  this  view  is  confirmed  by 
the  fact  that,  soon  or  late,  the  classical  picture  of  gastric  ulcer  develops. 
Now  and  then,  however,  the  course  is  exactly  the  opposite  of  this.  The 
hemorrhage  soon  ceases ;  for  a  few  days  or  weeks,  although  great  debility 
remains,  the  patient  feels  perfectly  well,  and  shows  no  gastric  symptoms. 
On  the  other  hand,  repeated  hemorrhages  may  lead  to  collapse  and  death. 
At  the  autopsy,  except  for  the  occasional  but  by  no  means  invariable 
superficial  erosions  of  the  mucosa,  no  pathological  changes  are  found  which 
are  either  directly  or  indirectly  related  to  the  hemorrhages.  There  are 
quite  a  number  of  such  cases  in  literature — I  have  seen  five  such,  some  of 
which  were  published  by  Eeichard — in  which  the  most  careful  microscopic 
examination  did  not  show  the  origin  of  the  bleeding.  In  a  case  of  Ham- 
peln's,  a  few  erosions  of  the  mucosa  were  found  near  the  pylorus  and  the 
lesser  curvature,  but,  upon  injecting  the  gastric  artery,  no  fluid  passed 
through  the  eroded  areas  of  the  mucosa.  In  one  of  my  cases  the  hemor- 
rhage was  due  to  extreme  irritation  of  the  gastric  mucous  membrane,  the 
drinking  of  a  hot  infusion  of  red  wine,  chamomile,  thuja,  and  various 
spices.  Under  some  circumstances  nothing  remains  but  the  assumption 
of  a  special  permeability  of  the  vessels  which  are  unable  to  resist  the 
local  hyperemia.  A  case  described  by  Hirschfeld  occurred  in  an  old, 
cachectic  woman  in  whom  no  change  except  a  very  marked  arteriosclerosis 
of  the  vascular  system  could  be  found.  Minkowski  reports  a  case  of 
amyloid  degeneration  of  the  heart  and  gastrointestinal  vessels  without  a 
similar  change  in  the  large  glandular  organs  (liver,  spleen,  kidneys)  leading 
to  parenchymatous  gastric  hemorrhage. 

Menstrual  gastric  hemorrhages,  and  those  occurring  vicariously  in  place 
of  menstruation  which  sometimes  may  appear  intermediately  between  two 
periods,  usually  belong  to  the  group  of  so-called  occult  hemorrhages. 
Actual  hematemesis  is  not  observed.  On  the  contrary,  tlie  blood  is  dis- 
covered accidentally,  or  is  found  while  evacuating  the  gastric  contents 
(Kuttner).     Therefore,  this  condition  may  very  readily  be  overlooked; 


180  GASTRIC  ULCER  AND  GASTRIC  HEMORRHAGE 

nevertheless,  it  exists,  and  v.  Schrotter,  Sr.,  only  placed  his  tempera- 
mental ignorance  on  record  when  he  chose  to  designate  my  report  at  the 
Congress  of  Internal  Medicine  (1903)  as  a  canard  ("  Raubergeschichten  ")  ! 
Whether  simple  stenosis  of  the  pylorus  may  be  the  cause  of  the  hemorrhage, 
as  was  assumed  by  Lambotte  and  subsequently  by  Moser  (retention  of  gas- 
tric contents,  venous  hyperemia  of  the  mucous  membrane,  and  muscular 
contractions)  appears  to  me  very  doubtful  when  we  contrast  this  with  the 
numerous  cases  of  pyloric  stenosis  without  hemorrhage.  The  cases  re- 
ported by  Lambotte  certainly  do  not  permit  us  to  exclude  the  possibility 
of  ulcer.  At  this  point,  too,  the  occurrence  of  profuse  initial  hematemesis 
in  gastric  carcinoma  must  be  mentioned  (E.  Mey).  In  such  cases  the 
assumption  is  obvious  that  an  ulcer  originally  existed  which  must  have 
undergone  carcinomatous  degeneration.  In  the  4  autopsy  reports  commu- 
nicated by  Mey,  the  nodular  character  of  the  neoplasm  favors  a  primary 
carcinoma,  for,  in  the  transition  of  an  ulcer  into  carcinoma  an  infiltration 
of  the  tissue  is  much  more  likely  to  occur.  At  all  events,  in  such  cases 
the  possibility  of  this  must  be  considered. 

The  circumstances  are  different  when  hemorrhages  occur  as  complica- 
tions of  severe  purulent  processes  or  marked  circulatory  disturbance  in  the 
intestinal  vessels.  Surgeons,  for  example,  v.  Eiselsberg,  have  for  a  long 
time  called  attention  to  the  fact  that  after  abdominal  operations,  particu- 
larly for  strangulated  hernia,  gastric  hemorrhages  may  occur.  These  are 
attributed  to  displaced  thrombi  from  the  point  of  operation.  But  I  ex- 
plain the  condition  in  the  following  case  differently: 

A  man,  aged  47,  was  suddenly  attacked  with  severe  pain  in  the  umbilical  region ; 
there  was  absolute  constipation.  After  twenty-four  hours  an  operation  was  per- 
formed, at  which  a  diagnosis  of  internal  incarceration  was.piade.  Prior  to  the  opera- 
tion the  stomach  was  washed  out,  and  large  quantities  of  a  dark,  brownish-red  fluid 
were  evacuated;  this  proved  to  be  almost  pure  blood.  At  the  operation  a  portion 
of  the  small  intestine  amounting  in  length  to  1  meter  and  30  cm.  was  found  to  be 
constricted  by  a  band  reaching  from  the  sigmoid  flexure  to  the  root  of  the  mesentery. 
The  constricted  intestine  was  enormously  distended,  and  dark  bluish-red  in  color. 
The  circulation  was  not  reestablished  in  the  constricted  portion  of  the  intestine, 
hence  it  was  resected.  The  patient  lived  only  twenty  hours  after  the  severe  opera- 
tion. The  autopsy  revealed  a  greatly  distended  stomach ;  the  leaflets  of  the  dia- 
phragm were  forced  up  to  the  fourth  rib.  "  In  the  stomach  countless  erosions  of 
tho  mucous  membrane  of  the  size  of  a  pin's  head  were  found.  Some  of  these  were 
round,  others  angular  or  elongated;  in  isolated  cases,  they  extended  to  the  sub- 
nuK'osa  :  at  other  points  they  were  more  shallow.  Some  contained  greyish-red  blood, 
particularly  about  the  borders  and  at  the  base;  other  erosions  contained  no  blood. 
A  true  vascular  lesion  was  nowhere  to  be  found.  The  peritoneum  near  the  gastric 
region  showed  no  abnormalities."  (From  the  autopsy  report  of  Dr.  Oestreich.)  But 
little  muco-lieniorrhagic  contents  were  found  in  the  intestine;  the  vessels  were  mark- 
edly injoctod.  The  abdominal  cavity  contained  about  200  c.c.  of  a  hemorrhagico- 
serous  fluid.  In  this  case  we  probably  find  the  cause  and  anatomical  foundation 
for  the  hemorrhage  in  the  altered  circulation  of  the  abdominal  cavity,  and  in  the 
erosions  of  the  mucous  membrane  which  were  apparently  of  an  earlier  date. 


SYMPTOMS  181 

Severe  hemorrhages  into  the  stomach  and  the  intestine  occurring  in 
the  course  of  septic  processes  which  affect  the  abdominal  organs  without 
an  apparent  anatomical  lesion,  and  which  cannot  be  attributed  to  the 
formation  of  thrombus,  have  until  recently  been  observed  only  in  isolated 
cares.  Dieulafoy  mentions  them  in  perityphlitis,  and  regards  them  as  the 
result  of  toxin  infection  of  the  gastric  mucous  membrane,  the  latter,  in 
his  cases,  showing  no  ulceration  in  the  region  of  the  pylorus.  Guyon 
has  reported  a  case  of  sepsis  in  the  urinary  passages  without  any  injury 
to  the  urinary  organs.  Such  cases  may  present  insurmountable  difficulty 
in  the  diagnosis,  as  will  be  noted  from  a  case  which  I  recently  observed. 

A  man,  aged  37,  who  had  been  ill  for  four  days,  was  awakened  during  the  night 
with  pain  which  soon  spread  over  the  entire  abdomen.  He  stated  that  he  had  pre- 
viously suffered  from  gastric  difficulty,  and  that  upon  the  second  day  of  the  disease 
a  chill  with  rise  in  temperature  to  103.2°  F.  had  taken  place;  except  for  this  there 
was  no  fever  during  the  entire  course  of  the  disease.  I  found  the  patient  with  all 
the  signs  of  diffuse  peritonitis, — slight  dulness  in  the  right  and  left  inguinal  regions. 
The  pains  varied,  being  both  spontaneous  and  upon  pressure,  and  were  said  to  have 
first  appeared  in  the  pit  of  the  stomach.  During  the  night  the  patient  vomited 
large  quantities  of  a  blackish-brown  mass  containing  blood.  The  vomiting  recurred 
in  the  course  of  the  day  and  also  during  the  lavage  with  ice-water  which  was  later 
undertaken,  the  water  each  time  evacuated  containing  blood.  The  slight  quantity 
of  feces  discharged  from  the  large  intestine  after  enemata  showed  no  blood.  Con- 
sequently, I  diagnosticated  a  perforating  gastric  ulcer,  and  rejected  the  possibility 
of  a  perforative  perityphlitis  on  account  of  the  hemorrhagic  gastric  contents  and 
the  original  seat  of  the  pain  in  the  scrobiculus  cordis.  The  surgeon  called  in  con- 
sultation was  of  the  same  opinion,  but,  on  account  of  the  advanced  peritonitis,  re- 
fused to  operate.  The  man  succumbed  on  the  third  day  of  my  observation,  and  upon 
the  sixth  of  the  disease.  The  autopsy  revealed  general  peritonitis  starting  from  a 
perforating  gangrenous  appendix.  The  gastric  mucous  membrane  was  entirely  in- 
tact. But  the  intestinal  mucous  membrane  in  some  areas  showed  a  bright  red 
injection,  a  velvety  swelling,  and  hemorrhagic  contents  were  still  present  in  the 
intestine  itself. 

Composition  of  the  Blood. — Most  authors — I  mention  Laache,  Leich- 
tenstern,  Reinert,  Osterspey  (Ewald),  and  also  recently  Rencki  and  Dol- 
matow — have  found  the  composition  of  the  blood  (and  this  quite  inde- 
pendent!}'' of  a  possible  hematemesis)  so  changed  that  a  decided  alteration 
in  the  number  of  red  blood-corpuscles,  and  in  the  hemoglobin,  and,  occa- 
sionally, an  increase  of  the  leukocytes,  was  present.  But  these  changes 
are  due  to  secondary  conditions,  chlorosis,  anemia,  etc.,  and  are  not  typical 
of  ulcer.  For  well  known  reasons,  the  composition  of  the  blood  immedi- 
ately after  a  licmorrhage  will  invariably  be  found  changed,  i.  e.,  the  red  cells 
and  tlio  liciiioglolnn  are  decreased,  and  the  leukocytes  slightly  increased. 

Vomiting. — The  next  symptom  of  importance  is  vomiting. 

Vomiting  usually  occurs  after  eating.  It  is  caused  by  an  irritation 
of  the  walls  of  the  stomach,  particularly  of  the  exposed  ulcer  surface,  from 
the  food,  that  is,  the  hyperacid  gastric  contents.     This  is  partly  due  to 


182  GASTRIC   ULCER   AND   GASTRIC   HEMORRHAGE 

the  fact  that  the  strong  acid  causes  a  spasmodic  contraction  and  closure 
of  the  pylorus,  and  thus  not  only  pains  but  an  increased  and  even  anti- 
peristaltic action  of  the  stomach  is  produced.  The  food  is  often  but  little 
changed,  and  is  vomited  admixed  with  mucus  as  is  the  case  in  the  so-called 
vomitus  matutinus  of  alcoholics.  Fungi  of  fermentation  and  other  foreign 
cellular  elements,  with  the  exception  of  occasional  admixtures  of  blood, 
are  either  rare  or  absent  (sarcinae).  At  other  times  the  vomitus  is  a  thin 
fluid,  of  slightly  greenish  color,  and  very  acid,  which  upon  standing  forms 
a  pappy  precipitate  consisting  of  starch  granules,  cellular  detritus,  but  only 
a  few  markedly  digested  remains  of  meat.  Periods  occur  in  which  there 
is  an  increase  of  the  vomiting,  and  the  stomach  absolutely  rejects  food. 

It  is  quite  apparent  even  from  the  external  appearance  of  the  vomitus, 
particularly  if  it  is  ejected  a  considerable  time  after  the  ingestion  of  food, 
that  the  gastric  contents  are  decidedly  acid.  Upon  standing  two  layers 
form :  The  upper  is  a  thin  fluid,  clear,  not  foaming,  and  containing  a 
finely  granular  precipitate  consisting  of  slightly  altered  remains  of  starch, 
plant  cells,  and  the  like,  in  which,  however,  there  are  no,  or  very  few, 
muscle  fibers,  that  is,  remains  of  meat.  The  test  with  Congo  paper  gives 
a  strong  reaction  for  free  hydrochloric  acid.  As  a  rule  spontaneous  vomit- 
ing is  not  frequent.  It  is  most  prone  to  occur  when  the  ulcer  is  situated 
at  the  pylorus. 

Perigastritis. — When  the  ulcer  has  extended  to  the  serosa,  and  before 
complete  rupture  takes  place,  an  inflammation  of  the  external  layer  of  the 
serosa  with  the  formation  of  a  plastic  exudate  and  perigastritis  occasion- 
ally occurs.  This  may  be  limited  to  a  definite  area,  or  may  extend  into 
adjacent  parts,  or  may  change  to  hard,  indurated  masses  of  exudate  which 
upon  examination  resemble  tumors.  Associated  with  this  are  local  irri- 
tative phenomena,  retching,  and  even  mild  fever.  Distortion  of  the  stom- 
ach may  take  place  and,  under  some  circumstances,  it  may  be  very  difiicult 
or  even  impossible  to  recognize  the  true  nature  of  these  conditions.  From 
their  character,  they  are  insusceptible  to  internal  treatment,  and  form  a 
permanent  source  of  perplexity.  (See  also  p.  185  in  the  description  of 
cicatrization.) 

Perforation. — A  severe  complication  of  the  disease  and,  perhaps,  of  the 
clinical  picture  is  produced  by  the  rupture  of  the  ulcer  and  the  implication 
of  nrighboring  organs.  When  the  peptic  process  reaches  the  external  layer 
of  tlie  gastric  wall  and  attacks  one  of  the  neighboring  organs,  this  is 
occasionally  manifested  by  a  localized  sensation  of  pain  in  the  region  of 
the  organ  attacked.  As  a  rule,  however,  it  runs  its  course  without  any 
external  sign,  so  that  only  when  we  test  the  disturbance  of  function  of  the 
organ  in  question  can  we  recognize  that  it  has  been  implicated  in  the 
process.  As  previously  mentioned,  there  may  be  hemorrhages  from  the 
larger  vascular  trunks. 

The  various  conditions  which  arise  for  consideration  may  be  readily 


SYMPTOMS  183 

reviewed  if  we  remember  the  topography  of  the  organs  surrounding  the 
stomach.  A  most  interesting  complication  is  a  rupture  through  the  dia- 
phragm and  pericardium  into  the  left  heart  followed  by  pneumopericar- 
ditis,  also  into  the  mediastinum  with  emphysema  of  the  external  skin  and 
the  accumulation  of  combustible  gas.  West  describes  a  preparation  in 
which  an  ulcer  had  attacked  the  portal  vein  and  led  to  a  fatal  pylephlebitis. 
Cases  are  described  as  pyopneumothorax  subphrenicus  in  which  an  encap- 
sulated abscess  containing  air  had  formed  below  the  diaphragm.  Osier 
has  described  a  very  unusual  case  in  which  rupture  into  the  left  heart 
occurred;  nevertheless^  the  patient  lived  two  days,  for  the  perforation 
closed  during  every  systole  and  opened  during  the  diastole.  Thus  the 
patient  gradually  bled  to  death.  Rupture  into  the  pleural  cavity  may  be 
diagnosticated  when  it  leads  to  pneumothorax  and  empyema  or  to  a  direct 
communication  with  the  lungs,  and,  as  has  happened,  particles  of  food 
may  actually  be  coughed  up.  In  a  case  reported  by  Miiller  nematodes 
were  found  in  the  pleural  cavity. 

Eupture  into  the  colon  and  subsequent  lientery  are  rare.  When,  in  a 
favorable  case,  the  ulcer  ruptures  into  the  abdominal  cavity,  the  preceding 
adhesive  inflammation  between  the  stomach  and  the  neighboring  intestinal 
wall  and  the  omentum  forms  a  cavity  which  is  a  sac  within  a  sac,  and 
prevents  the  propulsion  of  the  stomach  contents  into  the  abdominal  cavity. 
After  this  peritoneal  irritative  phenomena  appear,  with  circumscribed  pain, 
distention  of  the  upper  abdominal  region,  and  fever,  perhaps  also  severe 
vomiting.  If  the  adhesions  are  very  extensive,  there  may  be  complete 
stoppage  of  intestinal  activit}^  which,  with  permanent  obstruction  and  in- 
creasing marasmus,  leads  to  death,  as  in  a  case  reported  by  Budd. 

Perforation  into  the  free  peritoneal  cavity  is  by  far  the  most  frequent 
complication,  and  happens  either  after  preceding  adhesion  and  abscess 
formation  or  without  these.  It  may  appear  slowly  and  gradually  or,  on 
the  contrary,  the  exit  of  the  stomach  contents  may  be  slow.  Adhesive 
abscesses  then  form  which  may  later  become  encapsulated,  or  may  rupture 
and  produce  general  peritonitis.  Usually  perforation  occurs  suddenly 
without  prodromes  or,  at  least,  without  symptoms  which  point  to  such 
an  accident.  Without  any  cause  or  after  a  preceding  trauma,  such  as 
an  accidental  blow,  or  pressure  against  the  edge  of  a  table  or  when  leaning 
over  a  window-sill,  in  riding,  after  they  have  eaten  heartily,  or  after  or 
during  vomiting,  the  patients  suddenly  feel  severe  pains  in  the  abdomen 
which  cause  a  feeling  of  collapse  and,  in  a  brief  time,  the  picture  of 
perforative  peritonitis  develops:  Distention  of  the  abdomen,  obliteration 
of  liver  dulness,  on  even  the  slightest  touch  excruciating  pain  which  may 
have  a  colicky  or  paroxysmal  character,  vomiting,  singultus,  facies  hippo- 
cratica,  small  pulse,  and  with  these  symptoms  the  patient  succumbs. 

Spontaneous  pain  is  usually  referred  to  the  gastric  region ;  the  ileo-cecal 
region  is  mentioned,  that  is,  is  sensitive  to  pressure,  only  in  duodenal 


184  GASTRIC   ULCER  AND  GASTRIC   HEMORRHAGE 

ulcers.  According  to  the  exhaustive  compilation  of  Brunner,  in  about  90 
per  cent,  of  all  cases  of  perforation  the  history  discloses  the  sjonptoms  of 
a  preceding  ulcer,  which,  upon  the  average,  had  been  first  noticed  about  3| 
years  before.  These  may,  however,  be  absent,  and  I  remember  a  case  in 
which  a  young  girl,  previously  always  healthy,  collapsed  at  night  while 
dancing,  succumbing  -to  a  perforating  ulcer. 

Such  perforation  may  also  be  caused  by  spasmodic  contractions  of  the 
stomach  either  from  vomiting  after  medication,  or  from  introducing  the 
finger  into  the  pharynx,  as  is  done  by  many  patients  to  produce  eructation 
and  vomiting,  or  it  may  occur  after  introducing  the  stomach-tube,  Faber 
describes  a  case  of  perforation  after  vomiting  induced  by  the  patient. 
The  normal  act  of  defecation  is  said  by  Bouillaud  to  have  also  been  a 
cause. 

The  youngest  female  patient  was  nine  years  old,  the  oldest  seventy-one. 
The  youngest  male  was  seventeen,  the  oldest  seventy-two  (Brunner). 

The  seat  of  perforation  in  the  gastric  wall  is  usually  the  greater  or 
lesser  curvature,  very  rarely  the  pylorus  or  the  cardia.  The  lesion  is  cir- 
cular, with  smooth,  non-elevated  borders,  and  surrounded  by  a  more  or 
less  extensive  zone  of  smooth,  cicatricial  tissue,  which  is  usually  friable 
so  that  at  operation  the  suture  will  not  hold  but  tears  through,  and  the 
healing  of  the  wound  is  exceedingly  difficult. 

Cases  of  such  perforation  that  have  recovered  without  operation  are 
among  the  greatest  rarities,  Brunner  collected  from  literature  the  records 
of  17,  all  of  whom  were  treated  with  opium,  ice,  and  rectal  alimentation. 
Almost  invariably  the  perforation  occurred  a  few  hours  after  eating,  while 
the  stomach  was  empty. 

In  these  cases  there  is  a  justifiable  doubt  as  to  the  correctness  of  the 
diagnosis.  In  a  case  described  by  Harland,  as  the  author  himself  reports, 
an  ulcer  with  a  simultaneously  existing  gastrectasis  simulated  perforation. 
In  this  category  I  must  also  include  the  case  reported  by  Spicker  of  the 
spontaneous  cure  of  perforative  peritonitis  in  ulcer  of  the  stomach,  which 
was  probably  nothing  but  an  acute  gastric  dilatation. 

It  is  certain  that  the  symptoms  mentioned  above  may  be  absent,  yet 
perforation  may  have  occurred.  I  have  seen  two  cases  in  which  there 
was  at  first  no  marked  distention  of  the  abdomen,  no  shock  or  collapse, 
the  pulse  was  regular,  the  temperature  normal.  It  was  obvious,  however, 
tliat  perforation  had  occurred.  In  both  instances  the  stomach  contained 
neitlior  food  nor  gas,  the  patient  for  three  days  previously  having  re- 
frained almost  entirely  from  food,  and,  therefore,  the  rupture  of  the  ulcer 
was  accompanied  only  by  the  signs  of  intense  shock — loss  of  consciousness, 
Clieync-Stokes  respiration,  absence  of  pulse,  cold  skin,  etc. — while  the 
abdomen  was  neither  greatly  distended  nor  very  painful. 

The  "  disappearance  "  of  liver  dulness,  in  particular,  is  a  very  uncer- 
tain sign,  as  this  may  also  be  produced  by  the  distended  transverse  colon 


SYMPTOMS  185 

that  extends  high  above  the  liver,  or — in  very  rare  cases — by  a  dilated 
stomach  adherent  to  the  liver. 

Musser  and  Wharton  calculate  that  perforation  occurs  in  about  7  to  18 
per  cent,  of  all  cases.  If  this  includes  the  most  marked  cases  only,  even 
this  low  figure  is,  in  my  opinion,  much  too  high.  I  have  not  observed 
more  than  1.3  per  cent,  of  perforations.  Greenough  and  Joslin  saw  perfora- 
tion in  3.2  per  cent,  of  all  cases.  Those  serious  accidents  in  which  several 
isolated  ulcers  in  different  areas  of  the  stomach  simultaneously  rupture, 
usually  in  the  anterior  and  posterior  walls  (Lovell-Keays  and  others),  are 
very  rare. 

Occasionally  a  gastrocutaneous  fistula  forms  with  an  opening  into  the 
epigastric  or  left  hypochondriac  region  or  between  the  ribs.  This  is  a 
very  rare  occurrence;  nevertheless,  Murchison  collected  12  reports  of  such 
cases.  Sudden  perforation  has  repeatedly  awakened  a  suspicion  of  poison- 
ing and  led  to  unjust  criminal  trials. 

The  nature  of  the  cicatrization  is  of  great  importance.  It  is  obvious 
that  cicatricial  distortion  may  lead  to  the  severest  disturbance  of  the  gastric 
functions,  one  of  which,  dilatation  of  the  organ  with  cicatricial  pyloric 
stenosis,  has  already  been  described;  this  produces  a  limited  pathologic 
picture.  In  other  cases,  cicatricial  contraction  causes  torsion  of  the  nerves 
of  the  gastric  wall  or  deformity  of  the  organs,  or  the  function  of  large 
portions  of  the  muscularis  is  lost,  or  adhesions  with  neighboring  organs 
form  and  lead  to  gastralgia  or  to  functional  disturbances  which  appear 
under  the  guise  of  "  dyspepsia  "  of  different  kinds,  the  original  cause  of 
which  is  usually  difficult  to  recognize  and  from  which  recovery  without 
operation  is,  as  a  rule,  impossible.  In  the  course  of  years  I  have  learned 
to  dread  this  cicatrization  even  more  than  the  primary  ulcer.  Not  rarely 
such  patients  are  erroneously  considered  as  "  nervous  dyspeptics."  If  the 
cicatrix  is  circular  and  at  about  the  middle  of  the  stomach,  the  various 
forms  of  hour-glass  stomach  or  large  sac-like  dilatations  of  the  same  are 
produced.  In  washing  out  the  stomach  the  curious  symptom  then  appears 
that  the  stomach  apparently  cannot  be  evacuated.  After  some  time  the 
water  injected  for  washing  returns  clear,  suddenly,  however,  again  becom- 
ing turbid  and  admixed  with  gastric  contents,  and  this  phenomenon  may 
be  repeated  several  times.  This  indicates  either  the  condition  just  de- 
scribed or  an  insufficiency  of  the  pylorus,  the  contents  of  the  duodenum 
being  regurgitated  into  the  stomach. 

Hemorrhagic  Erosions. — Einhorn  has  lately  devoted  much  attention 
clinically  to  the  previously  mentioned  "  hemorrhagic  erosions,"  which  have 
long  been  known  anatomically,  and  frequently  described.  They  do  not 
present  the  classical  picture  of  ulcer  of  the  stomach  but  dyspeptic  symp- 
toms, even  decided  pain,  which  increases  soon  after  taking  food,  and  con- 
tinues from  one  to  two  hours;  emaciation  and  weakness  appear.  The 
chemism  is  not  specially  characteristic.     Yet  almost  always  in  the  water 


186  GASTRIC   ULCER   AND  GASTRIC   HEMORRHAGE 

used  for  lavage — and  authors  lay  particular  stress  upon  this  constancy — 
small  reddish-white  fiocculi  are  present  which,  upon  minute  examination, 
prove  to  be  desquamated  portions  of  the  mucous  membrane.  They  show 
well  retained  glands  with  small  cell  infiltration  and  an  accumulation  of 
red  blood-corpuscles  between  them. 

These  reports  have  been  several  times  discussed  (Pariser,  Hemmeter, 
Platter,  Ewald  and  others).  That  no  positive  diagnostic  value  can  be  at- 
tached to  these  mucous  membrane  particles  which  appear  in  the  water 
after  lavage,  i.  e.,  that  they  do  not  reveal  histologic  changes  characteristic 
of  a  definite  pathologic  type,  Leuk  proved  in  my  wards  after  thorough 
and  careful  investigation.  His  conclusions  have  been  confirmed  by  Cohn- 
hcim,  Lubarsch,  Hari  and  others. 

Eisner  examined  35  cases  in  which  inflammatory  symptoms  attributable 
to  the  stomach  with  a  decrease  or  cessation  of  the  gastric  juice  secretion 
were  determined  only  12  times,  i.  e.,  in  35  per  cent.,  and  found  exfoliations 
of  the  mucous  membrane  either  transitorily  or  permanently  in  the  water 
used  for  lavage.  Only  four  of  these  complained  of  difficulties  such  as 
Einhorn  described.  I  have,  however,  elsewhere  expressed  my  opinion 
( Transactions  of  the  Twentieth  Congress  for  Internal  Medicine,  Wies- 
baden, 1902)  that  a  well  characterized  pathologic  picture  of  hemorrhagic 
erosions  does  not  exist,  and  that  every  author  who  has  attempted  to  por- 
tray this  has  presented  a  type  differing  from  that  of  his  predecessors. 
Not  only  the  differential  diagnosis  of  true  ulcer,  but  also  that  between 
neuroses  with  hypersensitiveness  of  the  gastric  mucous  membrane  and  spas- 
modic conditions  of  the  pylorus,  occasions  perplexity.  A  positive  diagnosis 
in  such  cases  cannot  be  made  from  the  course  and  the  results  of  treatment ; 
the  methods  of  treatment  which,  under  various  authors,  have  resulted  in 
a  cure  of  "  erosions,"  for  example,  lavage  of  the  stomach  with  a  one  per 
cent,  silver  nitrate  solution,  will  also  cure  an  underlying  gastric  catarrh 
or  the  ulcer,  which,  as  some  observations  invariably  prove,  may  develop 
from  such  erosions.  Henschen,  in  his  autopsy  reports,  mentions  erosions 
in  3  cases  of  tuberculosis,  in  2  cases  of  nephritis  (which  I  can  corroborate, 
Ewald),  twice  in  mental  diseases,  once  in  pneumonia  and  only  once  in 
gastritis,  and  these  circumstances  raise  the  question  whether  the  erosions 
are  not  rather  the  consequence  of  a  general  affection  than  the  expression 
of  a  local  disease.  In  any  case,  the  diagnosis  "  erosion "  is  very  con- 
venient, and  will  therefore  probably  maintain  its  position. 

Fissures  of  the  Mucous  Membrane. — Here  a  change  in  the  mucous 
membrane  which  is  said  to  have  its  seat  at  the  pylorus  must  be  mentioned: 
Fissures  of  the  mucous  membrane  which  produce  pyloric  spasm,  just  as 
anal  fissures  give  rise  to  rectal  spasm.  In  his  report  upon  the  curative 
effect  of  large  doses  of  olive  oil  in  gastric  disease  (see  under  Treatment) 
Cohnheim  discusses  these  fissures  extensively  without  positively  demon- 
strating their  existence.     He  considers  a  fissure  to  be  present  from  the 


SYMPTOMS  187 

fact  of  the  rapid  recovery,  i.  e.,  the  cessation  of  pains,  and  maintains  that 
the  patients'  symptoms  could  not  be  relieved  in  such  a  few  days  if  they 
were  due  to  well  developed  ulcer.  In  my  opinion  this  argument  does  not 
warrant  a  positive  diagnosis.  For  he  has  neither  seen  these  hypothetical 
fissures  himself,  nor  does  he  construct  from  them  a  characteristic  symp- 
tom-complex, nor,  finally — and  this  is  certainly  remarkable — are  there  any 
reports  or  proofs  to  justify  this  in  the  literature  cited  by  him.  In  the 
many  hundreds  of  autopsies  in  which  I  have  examined  the  stomach  with 
the  closest  attention,  I  have  never  seen  such  a  fissure.  Now,  I  will  nftt 
deny  that  an  ulcer  may  occasionally  bear  a  certain  resemblance  to  a  fissure 
— a  fissure  is  really  nothing  more  than  an  ulcerated  lesion  of  the  mucous 
membrane — although,  as  the  name  implies,  it  must  have  more  of  a  lacer- 
ated appearance  than  the  ulcer  which  develops  evenly — but  it  remains  to 
be  proven  that  these  fissures  are  so  frequent  as  Cohnheim  believes,  that 
among  24  cases  (I  exclude  the  6  cases  of  undoubted  carcinomatous  ulcer) 
he  made  this  diagnosis  four  times,  therefore  in  16.6  per  cent,  of  the  cases. 

Syphilis  and  Ulcer. — In  1838  Andral  propounded  the  question.  Why 
do  not  syphilitic  manifestations  appear  upon  the  mucous  membrane  of 
the  stomach  as  well  as  upon  the  mucous  membrane  of  the  mouth?  Since 
then  this  question  has  been  much  discussed,  and  more  or  less  positive 
cases  have  been  reported  by  Goldstein,  Hiller,  Virchow,  Leudet,  Lan- 
cereaux,  Fauvel,  Klebs,  and  Cornil.  The  simultaneous  occurrence  of 
gumma  and  ulcer  of  the  stomach  has  been  reported  in  only  two  cases. 
In  others  (Frerichs,  Drozda,  Murchison,  Chvostek)  cicatrices  were  found 
in  the  stomach  and  simultaneously  general  syphilis.  Among  100  cases 
of  ulcer,  Engel  found  a  preceding  syphilis  in  10  per  cent.,  Lang  in  20 
per  cent.  Julien,  in  his  great  "  Traite  des  maladies  veneriennes,"  quite 
properly,  is  very  conservative.  In  diseases  so  frequent  as  the  two  in 
question  it  must  always  be  doubtful  whether  cause  and  effect  or  mere 
coincidence  is  before  us,  particularly  as  confusion  with  ulcerating  gum- 
mata  can  by  no  means  be  always  excluded.  Only  the  result  of  specific 
treatment  is  decisive.  Several  such  cases  have  been  reported,  for  example, 
by  Hiller  and  Gaillard,  but  the  latter,  w^ho  has  written  the  most  recent 
monograph  upon  this  subject,  admits  that  we  have  no  certain  proof.  Spe- 
cific symptoms  are  certainly  not  peculiar  to  syphilitic  ulcers.  Neverthe- 
less, with  coexisting  syphilis  and  the  signs  of  gastric  ulcer  it  is  advisable 
to  institute  specific  treatment. 

Tuberculosis  and  Ulcer. — Tuberculous  ulcerations  of  the  intestinal 
canal  occur  frequently,  as  is  well  knowm,  but  they  are  not  often  combined 
with  ulceration  of  the  stomach,  perhaps  for  the  reason  that  the  dissolving 
gastric  juice  prevents  the  propagation  of  bacilli,  whether  introduced  with 
swallowed  sputum  or  with  the  blood.  Typical  symptoms  are  not  peculiar 
to  tuberculous  ulcers  of  the  stomach.  Sudden  death  from  hematemesis 
in  consequence  of  eroded  vessels  has  also  been  observed. 


188 


GASTRIC  ULCER  AND  GASTRIC   HEMORRHAGE 


DIAGNOSIS 

The  diagnosis  of  chronic  ulcer  of  the  stomach  is  easy,  and,  when  all 
of  the  classical  symptoms  are  present,  can  scarcely  occasion  perplexity. 
When  this  is  not  the  case  it  is  exceedingly  difficult  or  even  impossible. 
Important  diagnostic  factors  have  already  been  indicated;  we  may,  there- 
fore, be  brief.  Two  other  diseases  of  the  stomach,  gastralgia,  or  gastro- 
dynia  (as  the  expression  of  a  functional  nervous  disturbance),  and  car- 
cinoma resemble  the  symptom-picture  of  ulcer  when  ulcer  deviates  from 
its  typical  course.  It  seems  advisable  to  tabulate  their  important  points 
of  difference  as  follows: 


Nervous  Gastralgia. 

Ulcee. 

Cancee. 

Tongue    varies,    often    pale, 
and  fissured  at  the  borders 
or  upon  the  surface. 

Tongue  dry,  red,  with  white 
streaks     in     the    center, 
or  smooth  and  moist,  or 
slightly  coated. 

Tongue  pale,  furry,  in  rare 
cases  very  red,  dry. 

Frequent  eructation  of  odor- 
less gas. 

Eructations  either  rare  or 
acid  eructations  with  py- 
rosis. 

Frequent  fetid  eructations. 

Taste  unaltered.     Dryness  of 
mouth  frequent,  sometimes 
salivation. 

Taste  unaltered. 

Pappy,  insipid  taste. 

Appetite     irregular,     capri- 
cious. 

Appetite  good  in  the  inter- 
vals.    Thirst. 

Appetite  decreased  or  ano- 
rexia. Early  repugnance 
to  meat. 

Varying    sensations    in    the 
stomach,  sometimes   heat, 
sometimes  cold. 

Burning    sensation    in    the 
stomach.     Circumscribed 
boring  pain,  often  radiat- 
ing posteriorly. 

Sensation  of  weight;  draw- 
ing pains  of  varying  char- 
acter, perhaps  pain  in  the 
shoulder. 

Spasmodic,  burning  pain,  in- 
dependent  of   food,  often 
ameliorated   by  the  latter 
or  by   pressure    upon   the 
stomach.     Pressure  points 
over   the    intestinal  plex- 
uses. 

Pains  gnawing,  rare  upon 
an  empty  stomach,  usual- 
ly appearing  after  eating 
or   upon   motion   and   on 
assuming  positions  which 
dilate  the    stomach ;    in- 
creased    upon     pressure. 
Pressure      points      upon 
back. 

Continuous  dull  sensations 
of  pain,  periodically  in- 
creasing to  paroxysms,  of- 
ten produced  by  pressure 
or  increased  by  it. 

The    chemism    of    digestion 
not  especially  altered. 

Digestion    of   starches   fre- 
quently slow ;  that  of  meat 
normal,  or   even   acceler- 
ate ^ :  usually  hyperchlor- 
hydria. 

Digestion  insufficient;  usu- 
ally absence  of  free  HCl; 
formation  of  organic  prod- 
ucts of  decomposition. 

DIAGNOSIS 


189 


Nervous  Gastralgia. 

Ulcer. 

Cancer. 

Epigastric  pulsation. 

Epigastric  pulsation  only 
with  marked  emaciation. 

Vomiting    irregular,    some- 
times  mucus   only,  some- 
times more  or  less  digested 
'gastric  contents,  rarely  ad- 
mixed with  bile. 

Vomiting,  as  a  rule,  imme- 
diately  or    shortly    after 
eating,  and  frequently  the 
first  symptom  of  the  dis- 
ease ;  very  rarely  without 
taking  food,  voraitus  hy- 
peracidas. 

Severe  and  frequent  vomit- 
ing, often  periodical,  occa- 
sionally also  before  the 
ingestion  of  food ;  mucoid ; 
when  acid,  due  to  organic 
acids ;  only  occurring  dur- 
ing the  course  of  other 
dyspeptic  symptoms;  vom- 
itus  shows  but  slight  di- 
gestion ;  sometimes  cancer 
cells  present. 

No  hematemesis,   except  as 
accompaniment     of    very 
rare  complications. 

Vomiting  of  light  red  blood 
or  coffee-ground   masses; 
usually  repeated  in  a  brief 
space   of  time,   occasion- 
ally very  profuse,  followed 
by  extreme   anemia   and 
collapse.       Compensation 
with   comparative  rapid- 
ity.   Blood  in  the  feces. 
Occult  hemorrhages. 

Decomposed  blood  more  fre- 
quent than  fresh ;  quan- 
tity usually  slight,  but, 
having  once  appeared,  re- 
curring' frequently  at  short 
intervals. 

Almost  invariably  stubborn 
constipation;  normal  evac- 
uations  very  rare;    occa- 
sionally fluid  mucoid  de- 
jecta, the  so-called  pseudo- 
diarrhea.     Mucous    colic, 
that     is,     colitis     mucosa 
membranacea. 

Bowel  discharges  vary,  not 
infrequently   diarrhea    in 
consequence  of  intestinal 
irritation.     Lientery  after 
perforation  into  the  colon. 

Almost  invariably  bowels 
stubbornly  constipated. 
Lientery  after  perforation 
of  the  colon. 

No  fever. 

Mild  fever  only  with  adhe- 
sive   inflammation    after 
rupture  of  the   ulcer,   or 
following  profuse  hemor- 
rhages. 

Fever  rare,  and  only  toward 
the  termination  of  life. 
Initial  fever  quite  rare. 

Skin     pale,     rarely     ruddy. 
Skin    of    normal    turges- 
cence. 

Skin  usually  of  ruddy  ap- 
pearance, anemic  only  af- 
ter profuse  hemorrhages. 
Frequently     the     visible 
mucous   membranes,  and 
even  the  cheeks,  slightly 
cyanotic.     Patients  some- 
times   present    the    chlo- 
rotic  type. 

Skin  sallow,  yellowish,  dry, 
and  flaccid.  Marked  ca- 
chexia. 

Often    conjoined   with   hys- 
terical symptoms.     Occurs 
at  all  ages,  more  frequently 
in  women  than  in  men. 

Most    frequent     in    middle 
life;  rare  in  children.  Ac- 
companied by  a    varying 
psychical   condition,    fre- 
quently great  depression. 

Most  frequent  between  the 
fortieth  and  sixieth  years. 
Psychical  condition  that 
of  depression ;  melan- 
cholia, but,  strange  to  say, 
less  profound  than  in  se- 
vere cases  of  ulcer. 

190 


GASTRIC   ULCER   AND  GASTRIC   HEMORRHAGE 


Nervous  Gastralgia. 

Ulcer. 

Cance«. 

No     tumor     on      palpation, 
unless,  as  rare  exceptions, 
when  foreign  bodies,  hair, 
etc.,  have  been  swallowed. 
Chernism    varies;    absence 
of  lactic  acid. 

When  the  ulcer  is  situated 
at  the  pylorus  with  con- 
secutive hypertrophy,  an 
ovoid,   smooth    tumor  at 
the  right  of  the  median 
line  mav  be  palpated.    Oc- 
casionally  in    old    ulcers 
with  a  hard  base  and  cal- 
lous borders   a    palpable 
tumor  with  circumscribed 
encapsulation,  perforation 
or  adhesions  with  the  head 
of  the  pancreas,  the  left 
lobe  of  the  liver,  the  spleen 
or  omentum,  and  does  not 
move  with  the  expiratory 
excursion.     HCl   present, 
and  usually  increased. 

Tumor  of  varying  size  and 
shape,  nodular  or  smooth, 
distinctly  palpable:  as  a 
rule,  passively  moved,  oc- 
casionally also  in  respira- 
tion. In  the  majority  of 
cases  no  HCl ;  absence  o( 
pepsin  digestion ;  lactic 
acid.  Lab-ferment  some- 
times absent  (cancer  of  the 
pylorus),  sometimes  pres- 
ent (cancer  of  the  fundus). 
Secondary  glandular  en- 
largement.   Metastases. 

No  symptom  of  perforation. 

Perforation   into  neighbor- 
ing organs  with  character- 
istic symptoms,  frequently 
after  apparent  brief  dura- 
tion of  the  disease  even 
occurring    without    pro- 
dromes. 

Perforation ;  implication  of 
neighboring  organs  only 
after  prolonged  existence 
of  the  disease. 

Nevertheless,  distinct  as  these  three  clinical  pictures  may  appear  to 
be  upon  paper,  in  practice  the  most  prominent  symptoms  are  often  so 
ill-developed  or  so  merged  into  one  another  that  a  precise  diagnosis  is 
impossible,  as,  for  instance,  in  the  onset  of  the  ulcerative  process.  So 
long  as  the  symptoms  indicate  only  general  digestive  disturbances,  so 
long  as  there  are  no  typical  gastralgic  attacks,  and  especially  so  long 
as  there  is  no  trace  of  hematemesis,  we  have  no  clue  by  which  to  dis- 
tinguish this  condition  -from  the  great  category  of  dyspepsias.  An  im- 
portant aid  in  the  recognition,  which  makes  an  early  diagnosis  possible, 
is  the  proof  of  hyperchlorhydria,  although  we  should  not  forget  that  rare 
exceptions  to  this  occur,  and  that  chemically  slight  hemorrhages  into  the 
gastric  and  intestinal  contents  cannot  be  macroscopically  recognized. 

The  diagnosis  is  most  positive  when  we  find  the  symptoms  of  typical 
gastralgia,  vomiting  of  blood,  blood  in  the  feces,  absence  of  tumor  and 
cachexia.  In  such  cases  it  is  unnecessary  to  examine  the  patient  with 
the  stomach-tube;  for  this  may  be  a  serious  procedure,  and  it  had  better 
be  avoided.  On  the  other  hand,  in  indefinite  cases  the  investigation  of 
the  chernism  is  absolutely  necessary,  but  all  precautions  must  be  ob- 
served. The  proof  of  hyperchlorhydria  or  of  gastrosuccorrhea  with  a 
large  amount  of  hydrochloric  acid  is  then  decisive,  and  indicates,  par- 
ticularly the  latter  occurrence,  that  the  seat  of  the  ulcer  is  at  the  pylorus, 


DIAGNOSIS  191 

and  there  is  consequent  stenosis.  I  have  seen  patients  with  undoubted 
ulcer  of  the  stomach  with  extreme  loss  of  strength,  and,  on  the  other 
hand,  cases  of  gastric  cancer  with  unimpaired  strength,  appetite,  and  the 
general  habitus.  Occasionally,  as  Leube  also  states,  the  diagnosis  can  be 
made  solely  by  the  efficacy  or  fruitlessness  of  a  specific  treatment  for  ulcer. 
Extreme  difficulty  in  the  differentiation  may  be  caused  by  the  above  de- 
scribed tumor-like  cicatrization,  which  draws  the  neighboring  organs 
toward  the  base  of  an  ulcer  to  which  they  are  adherent,  or  which  forms 
above  a  perforated  ulcer.  In  the  latter  case  the  head  of  the  pancreas,  the 
left  lobe  of  the  liver,  or,  more  rarely,  the  spleen,  may  be  involved.  In 
the  gastrocolic  ligament  there  is  a  lymph-gland,  or  a  band  of  closely  situ- 
ated glands,  which  under  some  circumstances  enlarge  and  become  sensitive 
to  pressure;  they  may  be  palpated  as  small  tumors  the  size  of  a  hazelnut 
at  the  lower  boundary  of  the  stomach,  and  have  repeatedly  caused  me  the 
greatest  perplexity  in  diagnosis.  In  all  of  these  cases  the  persistent  size 
of  the  tumor,  the  maintenance  of  strength,  and  the  presence  of  hydrochloric 
acid,  favor  ulcer  in  opposition  to  cancer,  just  as  a  course  lasting  more 
than  three  years  and  the  absence  of  a  typical  cancerous  cachexia  favor 
the  first  named  affection.  Since  we  know  that  hyperacidity  exists  in 
numerous  cases  of  ulcer,  it  is  obvious  that  those  distinct  tumors  of  the 
stomach,  particularly  those  situated  about  the  pylorus,  which  in  spite  of 
tA'pical  signs  of  malignant  cachexia  run  their  course  with  profuse  excre- 
tion of  hydrochloric  acid,  may  be  referred  to  the  fact  that  cancer  has 
developed  upon  the  foundation  of  a  gastric  ulcer.  I  have  repeatedly 
observed  such  cases.  In  several  instances  in  which  a  tumor  of  the  pylorus 
while  under  observation  and  within  a  year  developed  to  the  size  of  a  walnut, 
the  acidity  amounted  to  104  and  101.  Gastroenterostomy  was  performed, 
and  at  this  time  the  tumor  was  inspected  and  subsequently  removed;  it 
proved  to  be  an  unquestioned  carcinoma. 

A  test  of  the  chemism,  as  advised  by  Gluczinsky,  is  valuable  for  the 
early  recognition  of  beginning  carcinomatous  degeneration  of  an  ulcer 
and  may  be  carried  out  upon  one  and  the  same  day,  first  upon  an  empty 
stomach,  secondly,  after  a  test  breakfast,  and,  finally,  after  a  midday  meal. 
In  a  florid  ulcer  all  tests  give  normal  values;  decrease  or  absence  of  one 
or  more  favors  a  beginning  carcinoma.  In  17  cases  in  my  wards  Dr. 
Sigel  has  put  Gluczinsky's  results  to  the  test,  and,  although  not  in  every 
case,  in  the  main  he  confirmed  them. 

Diagnosis  of  Perforation. — The  diagnosis  of  perforation  of  an  ulcer 
is  based  upon  the  above  described  symptoms,  and  only  those  features  will 
be  discussed  which  may  lead  to  error.  Here  we  must  consider  perforation 
of  a  gastric  carcinoma  (a  relatively  rare  occurrence),  of  the  gall-bladder, 
that  is,  by  a  gall-stone,  of  the  appendix,  of  an  intestinal  ulcer,  and  acute 
diffuse  peritonitis  caused  by  rupture  of  the  spleen,  of  a  pyosalpinx,  or  of 
an  ovarian  tumor.  The  greatest  differentio-diagnostic  perplexity  may 
14 


192  GASTRIC  ULCER  AND  GASTRIC  HEMORRHAGE 

arise  from  the  rupture  of  a  gastric  cancer,  which,  however,  as  has  already 
been  mentioned,  is  extraordinarily  rare  because  the  neoplasm  is  prone  to 
attach  itself  by  inflammatory  adhesions  to  the  surrounding  organs.  The 
other  possibilities  enumerated  may  be  excluded  by  a  careful  examination 
and  the  history.  But  there  are  other  diseases  which,  without  producing  per- 
foration and  peritonitis,  may  simulate  these  conditions.  Here  are  to  be 
mentioned :  Gall-stone  and  renal  colics,  torsion  of  pedicles,  torsion  of  the 
ureters  in  -movable  kidney,  severe  gastralgia,  poisoning,  embolism  and 
thrombosis  of  the  mesenteric  arteries,  and,  finally,  even  pleurisy  and 
pneumonia,  the  latter  affection  occasionally,  i.  e.,  in  a  few  cases,  being 
complicated  by  a  similar  symptom-complex.  I  can  only  call  attention  to 
these  occurrences;  the  diagnosis  will  be  in  part  described  in  the  follow- 
ing pages. 

Unfortunately,  we  have  no  means  of  recognizing  a  threatening  perfora- 
tion because  there  is  nothing  to  indicate  whether,  in  a  given  case,  we 
are  dealing  with  a  superficial  or  deeply  invading  ulcer.  Symptoms  per- 
sisting for  a  long  time  may,  perhaps,  be  utilized  in  the  latter  sense,  but 
the  uncertainty  of  such  a  conclusion  is  obvious,  and  the  great  majority 
of  cases  of  ulcer  run  their  course  for  years  without  perforation. 

The  diagnosis  may  be  very  obscure  when  we  are  deciding  between 
cholelithiasis,  renal  colic,  and  gastralgia  occurring  in  the  course  of  ulcer 
of  the  pylorus  or  ulcer  of  the  duodenum;  of  course,  not  in  typical  cases 
of  either  disease.  Eecurring  pain  in  the  right  hypochondrium  independent 
of  the  ingestion  of  food,  slight  fever,  jaundice,  enlargement  of  the  liver, 
pain  over  the  liver,  a  palpable  gall-bladder  perhaps  containing  stones, 
drawing  pains  along  the  ureter,  hematuria,  the  passage  of  gall-stones  or 
renal  stones  are  just  as  typical  of  gall-stone  colic  or  renal  colic  as  the 
total  complex  of  the  symptoms  previously  described  is  of  ulcer.  But  in 
many  cases  the  symptoms  are  so  indefinite  that  confusion  can  scarcely  be 
prevented.  If  in  gall-stone  colic  jaundice  is  frequently  absent  or  very 
feebly  developed,  there  are,  on  the  other  hand,  not  seldom  cases  of  gas- 
tralgia which  run  their  course  with  mild  jaundice,  either  because  bile  is 
forced  into  the  blood-vessels  from  spasmodic  contraction  of  the  abdominal 
organs  or  because  a  rapid,  transitory,  sympathetic  spasm  of  the  hepatic 
duct  occurs,  and  with  this  biliary  stasis.  The  patients  with  gall-stone 
colic  are  apt  to  locate  their  pain  in  the  median  line,  particularly  women, 
in  whom  the  topography  of  the  liver  has  been  changed  from  lacing.  Fink 
even  makes  the  very  remarkable  statement  that  among  403  cases  of  gall- 
stone colic  which  he  observed  in  Carlsbad,  in  380  =  94.3  per  cent.,  gastric 
spasm  occurred  alone  without  pain  in  the  hepatic  region !  If  the  pylorus 
is  displaced  somewhat  to  the  right,  or  if  the  ulcer  is  situated  in  the  hori- 
zontal axis  of  the  duodenum,  there  can  be  no  question  of  a  local  difference. 
Hence,  it  may  for  a  long  time,  or  perhaps  always,  be  a  mooted  question 
whether  cholelithiasis  or  gastralgia  is  present.    But  here  hyperchlorhydria 


DIAGNOSIS  193 

of  the  gastric  juice,  if  present,  gives  us  a  valuable  clue.  Acidity  over  80, 
i.  e.,  0.3  per  cent.  HCl,  may  be  utilized  in  this  way. 

A  tuberculous  ulcer  is  recognizable  by  its  reaction  to  tuberculin,  ac- 
cording to  Petruschky's  method.  I  should  like  to  remark  in  this  connec- 
tion that  we  must  never  be  content  in  such  cases  with  one  test  if  this  be 
negative,  but  several  injections,  in  increasing  doses,  must  be  given.  Re- 
peatedly I  had  no  reaction  with  1  and  2  mgm.,  but  obtained  a  typical 
one  after  employing  3  and  5  mgm. 

Position  of  the  Tumor. — Only  an  unusually  favorable  combination  of 
circumstances  will  enable  us  to  recognize  the  position  of  an  ulcer  at  the 
pylorus  or  in  the  duodenum,  perhaps  even  in  the  greater  curvature.  On 
the  other  hand,  by  exclusion  we  may  decide  that  the  ulcer  is  situated 
elsewhere.  An  ulcer  at  the  pylorus  is  characterized  by  sharp,  localized 
pain  a  little  to  the  right  of  the  median  line.  Fleiner  attaches  great  weight 
to  the  symptom  of  pyloric  spasm.  But  the  significant  factor  of  pain 
cannot  here  be  reckoned  upon,  and  the  assumption  that  ulcer  situated  in 
the  cardia  of  the  stomach  is  accompanied  by  sensations  of  pain  immedi- 
ately after  eating  while  those  at  the  pylorus  produce  pain  only  later  has, 
I  find,  neither  been  sufficiently  proven  clinically,  nor  is  it  justified  by  the 
actual  conditions.  An  attempt  has  been  made  to  locate  the  seat  of  the 
ulcer  from  the  position  which  some  patients  assume  to  alleviate  their  pain. 
If  the  pain  is  less  in  the  left  lateral  position,  the  ulcer  is  said  to  be  situ- 
ated at  the  lesser  curvature,  or  vice  versa.  This  also  is  a  very  doubtful 
and  uncertain  symptom,  inasmuch  as  it  does  not  accord  with  the  experi- 
ence of  the  majority  of  patients.  According  to  Gerhardt :  "  Sensitiveness 
to  pressure  and  tumor  favor  the  seat  of  the  ulcer  upon* the  anterior  wall, 
pain  in  the  back  and  hemorrhage  its  seat  upon  the  posterior  wall.  The 
seat  of  the  pain  and  its  increase  in  the  latter  position  often  permit  the 
differentiation  of  ulcer  of  the  fundus  or  of  the  pyloric  region.  When 
an  ulcer  at  the  fundus  is  adherent  to  the  spleen  it  may  by  producing 
splenitis  give  rise  to  chills,  as  I  (Gerhardt)  have  seen  in  three  cases." 
That  gastrectasis  indicates  the  seat  of  an  ulcer  at  the  pylorus  or  in  the 
duodenum  and  contraction  at  the  cardia,  requires  no  special  emphasis. 
When  we  reflect  how  vague  is  the  symptom  of  pressure  sensitiveness,  how 
rare  is  the  appearance  of  tumor  due  to  ulcer  in  proportion  to  the  total 
number  of  cases,  how  very  difficult  is  it  in  these  cases  to  determine  the 
constriction  of  the  stomach  intra  vitam  since  we  do  not  inflate  the  organ 
or  introduce  the  stomach-tube,  and,  lastly,  when  we  remember  that  often 
several  distinct  ulcers  are  situated  in  different  areas,  no  great  weight  will 
be  attached  to  this  symptom. 

But,  in  my  experience,  the  most  reliable  of  the  symptoms  which  have 
been  mentioned  is  the  pain,  often  spasmodic,  in  the  region  of  the  pylorus, 
therefore,  in  the  right  mammary  line,  localized  below  the  border  of  the 
liver.     As,  however,  the  pylorus  is  occasionally  very  movable,  and  may 


194  GASTRIC  ULCER  AND  GASTRIC  HEMORRHAGE 

frequently  be  found  even  at  the  left  of  the  median  line,  it  is  clear  that 
pain  in  the  latter  region  cannot  always  be  referred  to  the  greater  curva- 
ture or  even  to  the  fundus,  v.  Leube  very  correctly  remarks :  "  We  must 
beware  of  such  diagnoses.  They  are  at  least  uncertain,  as  well  as  all 
diagnoses  based  upon  the  subjective  symptom,  pain,  even  when  some  spe- 
cial condition  is  pointed  out  by  this;  for  instance,  when  pain  is  developed 
only  on  displacing  the  gastric  contents  from  a  particular  position,  there- 
fore only  appearing  when  the  patient  assumes  the  right  lateral  position." 
Xor  must  we  forget  the  well  known  fact,  to  which  Schiitz  has  recently 
again  called  attention,  that  there  are  inflammatory  conditions  in  the  trans- 
verse colon  associated  with  pain  which  may  readily  but  erroneously  be 
referred  to  the  stomach. 

It  would  materially  aid  us  in  the  comprehension  of  this  condition  if 
we  possessed  a  really  good  gastroscope,  but,  at  present,  this  does  not  appear 
to  be  the  case.  It  need  hardly  be  stated  that  the  same  consideration  which 
deters  us  from  introducing  a  stomach-tube  or  a  soft  sound  in  ulcer  is 
more  strongly  deterrent  in  the  case  of  a  rigid  metal  tube. 

It  is  true  that  a  stenotic  gastric  ulcer  at  the  pylorus  with  consecutive 
gastric  dilatation,  and,  vice  versa,  the  same  condition  at  the  cardia  with 
resultant  contraction  of  the  stomach,  are  readily  recognized,  the  latter, 
perhaps,  requiring  the  aid  of  the  esophagoscope ;  but,  even  with  this,  we 
get  little  further  knowledge,  and  to  the  cases  mentioned  by  Gerhardt  I 
may  oppose  another  where  the  perforation  of  a  broken-down  carcinoma 
of  the  smaller  curvature  manifested  itself  by  chills  and  intense  pain,  espe- 
cially upon  the  left  side.  We  are  in  an  extremely  difficult  position  when 
several  ulcers  are  simultaneously  present,  and  this  condition  is  not  rare. 
Exact  I'nowledge  of  the  location  is,  therefore,  for  many  and  perhaps  for 
most  cases,  very  desirable,  and  the  more  important  because  accurate  loca- 
tion of  the  seat  of  the  ulcer  is  of  the  utmost  significance  in  the  treatment, 
and  particularly  for  operative  intervention  when  hemorrhage  occurs.  How 
difficult  this  determination  is  may  be  understood  from  the  fact  that 
Schloffer  was  unable  to  find  it  in  2  of  5  cases  even  at  the  operation. 

But  even  if  we  were  so  fortunate  as  almost  to  grasp  the  ulcer  with 
our  hands,  i.  e.,  to  detect  tumor  at  the  pylorus,  and  although  other  factors, 
particularly  the  chemism  of  the  stomach,  the  age  of  the  patient,  his 
geueral  condition  and  strength,  were  of  such  a  nature  as  to  exclude  car- 
cinoma, an  absolute  diagnosis  could  not  be  made.  Hence  the  following  con- 
ditions come  into  view,  and  these  we  must  discuss  for  a  few  moments: 

I.  Pylorospasm. 

II.  Muscular  hypertrophy,  that  is,  cicatricial  thickening  of  the  pyloric 
region. 

III.  Carcinomatous  neoplasm. 

Of  the  first  it  must  be  remarked  that  although  its  most  frequent  cause 
is  an  ulcer  at  or  in  the  immediate  vicinity  of  the  pylorus,  cases  have  been 


DIAGNOSIS  195 

undoubtedly  observed  in  which  pylorospasm  occurs  without  any  alteration 
in  the  mucous  membrane  that  can  be  detected.  Here  the  observations  of 
surgeons  are  of  great  weight.  Both  Schloffer  and  Alberti  have  reported 
such  cases. 

The  case  of  the  first  author  was  that  of  a  woman,  aged  44,  in  whom 
the  gastric  contents  showed  no  hydrochloric  acid,  but  lactic  acid.  At  the 
operation  an  oval,  slightly  diagonal,  extraordinarily  hard,  circumscribed 
resistance  of  about  2  cm.  in  length  and  1  cm.  in  breadth,  which  prolonged 
investigation  showed  to  be  nowise  altered,  was  found  at  the  greatly  nar- 
rowed pylorus,  and  on  its  posterior  wall.  The  area  in  question  was  re- 
sected, and,  most  astonishing  to  relate,  absolutely  no  pathological  changes 
were  found.  Histological  examination  merely  showed  a  slight  hypertrophy 
of  the  musculature  in  this  area,  and  Schloffer  assumes  the  case  to  be  one 
of  circumscribed  spasm  of  the  musculature  of  the  pylorus  in  its  pos- 
terior wall. 

The  case  of  Alberti  is  interesting  from  the  fact  that  at  the  laparotomy 
a  pyloric  tumor  was  found  which  was  of  uniform  hardness,  sharply  de- 
marcated toward  the  duodenum,  but  toward  the  stomach  and  particularly 
at  its  posterior  wall  it  showed  merely  a  coarse  and  firm  wedge-shaped 
swelling  amounting  to  about  4  cm.  in  length.  Alberti  looked  upon  it  as 
a  neoplasm,  and  concluded  to  perform  pylorectomy,  the  more  so  since 
no  adhesions  or  metastases  were  apparent.  When,  however,  the  lesser  and 
greater  omentum  were  detached,  all  signs  of  tumor  suddenly  disappeared, 
and  the  stomach,  that  is,  the  pylorus,  became  soft  and  perfectly  normal. 
Pyloroplasty  after  Heinecke-Mikulicz  was  performed,  and  the  pylorus  was 
found  to  be  narrowed  but  no  firm  cicatrix  could  be  detected.  The  attacks 
of  intense  pain  were  arrested,  and  the  patient,  in  spite  of  the  continuance 
of  symptoms  of  stenosis  of  the  pylorus  for  five  years,  showed  very  slight 
dilatation  of  the  stomach. 

This  case  appears  to  leave  no  room  for  doubt.  Here  marked  reaction 
for  hydrochloric  acid  was  always  present.  On  the  other  hand,  in  the 
light  of  our  experience  in  the  Augusta  Hospital,  the  case  of  Schloffer  may 
be  regarded  as  questionable. 

We  have  observed  two  such  cases  in  which  resection  was  apparently 
performed  on  account  of  a  benign  pyloric  tumor,  and  the  most  minute 
histologic  examination  of  the  resected  tissue  not  only  by  us  but  also  by 
our  pathologists  showed  no  change  characteristic  of  carcinoma.  The  first 
case  was  that  of  a  woman,  aged  47,  who  had  been  suffering  for  several 
months  from  a  gastric  affection,  and  complaining  of  vomiting  and  eructa- 
tion; examination  showed  a  moderate  gastric  dilatation  and  a  pyloric 
tumor  causing  stenosis.  Free  HCl  was  repeatedly  found  to  amount  to 
0.5-0.6  per  cent.,  albumin  digestion  to  about  75  per  cent.  Lactic  acid  and 
blood  were  never  present.  The  gastric  tumor  was  resected  and  gastro- 
enterostomy performed.     In  20  sections  from  the  resected  tissue  nothing 


196  GASTRIC   ULCER  AND   GASTRIC   HEMORRHAGE 

characteristic  of  cancer  could  be  found.  For  five  years  the  woman  re- 
mained in  good  condition,  then  ascites  developed  combined  with  abdominal 
symptoms  which  pointed  to  a  tumor  of  the  abdomen.  An  indistinct  re- 
sistance could  be  palpated  both  by  the  vagina  and  by  th^  rectum. 

Operation  performed  in  the  summer  of  1901  revealed  extrauterine 
pregnancy  and,  simultaneously,  a  neoplasm  of  both  ovaries  which,  at  the 
histologic  examination — the  patient  died  soon  after  the  operation — proved 
to  be  an  adenocarcinoma.  There  can  be  no  doubt  that  this  was  a  metas- 
tasis from  the  stomach. 

The  other  case  occurred  in  a  man,  aged  37,  who,  six  weeks  prior  to 
Christmas  of  1897,  was  suddenly  attacked  by  diarrhea  which  continued 
until  the  time  of  his  admission  upon  the  9th  of  March,  1898.  Fourteen 
days  previously  he  began  to  vomit  brownish  masses,  bnit  had  never  suf- 
fered from  pain  in  the  stomach;  he  felt  quite  strong,  and  had  a  good 
appetite.  After  inflation  of  the  stomach  a  tumor  the  size  of  a  small 
apple  was  found  in  the  epigastric  region  upon  the  right  below  the  border 
of  the  liver.  The  stomach  was  slightly  enlarged;  no  glandular  enlarge- 
ment. Acidity  was  58  upon  the  empty  stomach  and  lactic  acid  25.  In 
the  test  breakfast,  acidity  was  54,  lactic  acid  16  (0.058  per  cent).  Pepsin 
digestion  was  barely  10  per  cent.  Laparotomy  upon  the  14th  of  May 
disclosed  a  tumor  of  the  greater  curvature  extending  to  the  pylorus,  and 
in  its  middle  a  deep  ulcer.  About  two-thirds  of  the  stomach  was  resected, 
and  on  the  remainder  of  the  stomach  gastroenterostomy  antecol.  anter. 
was  performed.     The  patient  was  discharged  cured  upon  the  7th  of  April. 

Although  the  diagnosis  of  carcinomatous  ulcer  was  made  from  the 
macroscopic  appearances,  histologic  examination  did  not  reveal  a  charac- 
teristic picture.  The  man  has  just  been  readmitted  to  my  ward  with  a 
large,  undoubtedly  malignant  tumor  of  the  greater  curvature. 

We  see,  therefore,  that  in  the  differentiation  of  these  so-called  spastic 
tumors  and  muscular  hypertrophies  of  the  pylorus  we  must  be  very  cau- 
tious. It  is  not  surprising  that,  in  spite  of  resection  of  an  apparently 
healthy  organ,  metastases  should  develop.  Years  ago  I  stated  that  typical, 
cancerous  nests  might  be  found  in  the  submucosa  and  muscularis  far 
beyond  the  macroscopic,  visible  portions  of  a  malignant  tumor. 

Tumors  due  to  muscular  hypertrophy  are  generally  differentiated  from 
spasm  by  their  consistence.  The  same  cause  which  generates  them  always 
produces  stenosis  of  the  pylorus,  whether  they  originate  from  the  cicatrix 
of  an  ulcer  causing  stricture,  or  from  reflex  contraction,  from  the  irrita- 
tion of  a  fresh  ulcer  by  the  ingesta,  or,  finally,  from  a  malignant  neoplasm. 
I  must  also  mention  that  occasionally  a  gall-stone  is  incarcerated  in  the 
pylorus  (Naunyn,  Eisner)  or  tumors  from  hair  or  trichobezoar  may  be 
present.  In  how  far  dilatations  of  the  stomach  occur  in  connection  with 
these  conditions,  and  how  far  they  may  be  attributed  to  it,  depends  upon  ' 
(lie  duration  of  the  affection,  upon  the  permeability  of  the  stenosis,  and 


DIAGNOSIS  197 

upon  the  degree  of  the  compensatory  muscular  hypertrophy  of  the  stomach. 
Here,  however,  there  are  marked  gradations  in  the  condition.  We  meet 
with  convincing  proof  of  the  fact  that  ulcer  of  the  pylorus  frequently 
merges  into  carcinoma  of  the  pylorus  and  here,  as  in  other  areas,  persistent 
mechanical  irritation  from  the  chyle  which  presses  through  the  pylorus 
performs  an  active  part.  These  are  the  cases  in  which  hydrochloric  acid 
secretion  and  the  peptic  function  of  the  stomach  are  long  retained,  al- 
though they  finally  decrease  from  the  norm.  With  these  also  belong  some 
of  the  cases  which  I  first  mentioned,  cases  in  which,  on  account  of  the 
chemism  of  the  stomach,  the  diagnosis  of  a  benign  tumor  of  the  pylorus 
was  made,  while  operation  or  autopsy  revealed  that  we  were  dealing  with 
a  more  or  less  carcinomatously  degenerated  old  ulcer.  It  always  appears 
to  me  that  the  general  condition  of  such  patients  suffers  but  little  provided 
high-graded  pyloric  stenosis  does  not  occur,  and  this  is  another  factor 
which  may  lead  to  diagnostic  errors. 

In  conclusion  we  must  consider  the  last  of  the  three  groups  mentioned, 
namely,  carcinomatous  tumors  situated  at  the  pylorus  or  in  other  portions 
of  the  wall  of  the  stomach.  Here,  of  course,  we  are  only  dealing  with 
those  cases  in  which  the  age,  the  patient's  strength,  the  chemism,  the 
gastric  contents,  and  the  objective  condition  raise  doubts  as  to  whether 
we  have  before  us  a  carcinoma,  the  old  cicatrix  of  an  ulcer,  or  an  epi- 
gastric process. 

In  my  opinion,  during  the  short  or  long  course  of  the  disease  a  cer- 
tain grouping  of  the  symptoms  may  sometimes  entirely  preclude  our 
making  a  diagnosis  at  the  time,  because  neither  the  individual  symptoms 
nor  their  totality  are  sufficiently  clear  to  lead  in  any  direction  to  a  de- 
cision. This  is  particularly  true  of  two  symptoms  to  which  we  otherwise, 
quite  justly,  attach  great  significance:  The  pain  and  the  emaciation. 

Here  I  entirely  leave  out  of  consideration  those  cases  in  which  gas- 
tralgia  occurs  at  the  initial  stage  of  pulmonary  phthisis  in  young,  chlorotic 
and  anemic  persons  or  where  these  attacks  occur  in  the  so-called  preataxic 
stage  of  tabes  dorsalis  (locomotor  ataxia),  because  these  may  be  easily 
differentiated  by  a  minute  examination  which,  in  women,  should  include 
also  the  genitalia. 

A  number  of  years  ago  Aufrecht  called  attention  to  cases  of  sevete 
gastralgia  without  anatomical  findings  which  even  showed  a  family  rela- 
tionship. I  have  never  seen  cases  of  this  kind,  and  must  say  that  Aufrecht's 
brief  report  does  not  appear  to  me  convincing :  "  At  the  autopsy  nothing 
was  found  in  the  stomach,  the  biliary  passages,  or  the  duodenum  to  make 
clear  the  cause  of  the  disease." 

In  old  gasftric  ulcers  the  typical  pain  beginning  at  a  definite  time  after 
the  ingestion  of  food  is  either  absent,  or  it  is  so  irregular  that  it  does 
not  differ  from  cardialgia  due  to  other  causes;  therefore,  it  does  not 
differ  from  the  pain  produced  by  perigastric  adhesions  and  carcinoma, 


198  GASTRIC   ULCER  AND  GASTRIC   HEMORRHAGE 

either  typically,  or  by  its  seat,  or  by  the  frequency  of  its  appearance.  Here 
we  must  also  consider  the  typical  pains  due  to  a  hernia  of  the  linea  alba. 
In  general  these  may  be  readily  demonstrated,  but  it  is  necessary  to  bear 
them  in  mind,  for,  in  my  experience,  they  lie  somewhat  beyond  the  pale 
of  the  experience  of  most  practitioners.  By  proving  that  the  condition 
was  hernia,  and  by  a  slight  operation,  I  have  succeeded  in  promptly 
curing  many  a  case  diagnosticated  as  gastric  ulcer. 

If,  however,  there  are  no  well  developed  attacks  of  pain,  and  we  are 
dealing  only  with  more  or  less  decided  discomfort,  a  sense  of  pressure, 
and  fulness  after  eating,  we  know  that  these  may  exist  for  a  long  time 
and,  even  until  death,  be  the  only  symptoms  in  patients  with  cancer. 

It  is  true  that  in  ulcer  emaciation  is  usually  much  less  marked  than  in 
cancer,  and  that  the  color  of  the  skin  characteristic  of  malignant  cachexia 
is  usually  absent.  Where,  however,  an  ulcer  forms  in  debilitated,  nervous, 
hysterical  persons  or,  vice  versa,  in  the  robust  who,  from  a  fear  of  pain, 
limit  for  a  long  time  the  amount  of  their  food,  rapid  and  striking  losses 
of  weight  occasionally  occur  and  lead  us  to  consider  seriously  the  exist- 
ence of  carcinoma. 

But  the  condition  of  the  peripheral  lymph-glands  should  give  us  relia- 
ble information  on  this  point ! 

Long  ago,  in  1886,  Dietrich  proved,  after  a  careful  examination  of 
normal  persons,  that  is,  those  not  suffering  from  malignant  disease,  the 
great  frequency  of  slight  glandular  enlargement — thus,  for  example,  the 
inguinal  glands  in  93  per  cent,  and  the  axillary  glands  in  64.9  per  cent, 
were  swollen  to  the  size  of  a  bean.  But  decided  tumefaction  must  be 
present  for  this  to.be  of  any  importance.  Tarchetti  lays  special  stress 
upon  enlargement  of  the  supraclavicular  glands  which  he  met  with  in 
18.4  per  cent,  of  cases  of  cancer.  But  in  my  experience  statistics  of  glandu- 
lar enlargements  are  not  very  reliable.  In  125  cases  of  positive  ulcer  of 
which  I  have  notes  regarding  this,  sixty  times  the  inguinal  glands  were 
enlarged  to  the  size  of  a  bean,  and  twenty-four  times  the  glands  of  the 
axillary  cavity  to  the  size  of  a  pea.  Nevertheless,  I  must  admit  that  the 
condition  of  the  lymph-glands,  particularly  the  enlargement  of  the  left- 
sided  supraclavicular  glands,  is  of  some  significance.  Still  greater  weight 
must  be  attached  to  the  state  of  the  tongue,  which  in  ulcer — especially  in 
recent  ulcer — is  red,  moist,  glistening,  while  in  cancer  it  has  a  white 
coating  and  is  usually  dry,  in  nervous  disturbances  it  is  deeply  fissured, 
particularly  upon  the  sides,  so  that  the  tongue  resembles  a  freshly  ploughed 
field,  or,  to  use  a  more  striking  comparison,  a  glacier  with  its  clefts.  And 
this,  fortunately,  again  brings  us  to  the  symptom  per  tot ' discrimina  rerum 
to  which  the  ancients,  without  any  knowledge  of  our  modern  methods, 
attached  so  high  a  diagnostic  value !  • 

Duodenal  Ulcer. — What  is  true  of  the  seat  of  ulcer  of  the  stomach  is 
also  true  of  the  seat  of  ulcer  of  the  duodenum:  in  at  least  90  per  cent. 


PROGNOSIS  199 

of  the  cases  it  is  impossible  to  decide  positively  whether  we  are  dealing 
with  ulcer  of  the  duodenum  or  ulcer  of  the  stomach.  Leo  adds  an  addi- 
tional symptom  in  the  diagnosis  of  duodenal  ulcer.  Upon  lavage  there  is 
a  profuse  subacid  fluid.  The  gastric  contents  show  large  amounts  of 
organic  acid,  and  there  is  a  constant  green  discoloration  from  the  admix- 
ture of  bile  and  pancreatic  juice.  As  a  rule  there  is  no  vomiting.  Factors 
which  favor  ulcer  of  the  pylorus  are  also  operative  for  ulcer  of  the  duo- 
denum, all  the  more  so  as  the  ulcer  sometimes  directly  attacks  the  duode- 
num from  the  pylorus.  A  duodenal  ulcer  is  likely  when  the  pains  only  set 
in  some  time  after  the  ingestion  of  food;  their  seat,  as  well  as  a  passive 
sensitiveness  to  pressure,  is  decidedly  to  the  right  of  the  parasternal  line, 
and  profuse  hemorrhagic  dejecta  and  hematemesis  may  appear.  Jaundice 
and  peritonitis  have  been  repeatedly  observed.  The  fact  that  ulcer  of  the 
duodenum  frequently  occurs  in  old  persons  after  extensive  cutaneous  burns 
may  in  a  given  case  be  of  value  in  the  diagnosis.  A  point  of  support,  but 
no  more  than  this,  is  the  rare  occurrence  of  duodenal  ulcer,  for,  according 
to  Willigk,  to  225  cases  of  gastric  ulcer  there  are  only  6  ulcers  of  the  duo- 
denum, according  to  Trier  only  28  to  261.  Moynihan  has  recently  empha- 
sized the  seriousness  of  this  condition.  In  the  last  seventeen  3'ears  he  has 
operated  upon  114  cases.  In  107  of  these  the  ulcer  was  near  the  pylorus. 
There  were  91  recoveries.  Gastralgia  is  said  to  be  not  so  frequent  as  Budd 
believes,  because  the  duodenum  is  exposed  to  less  distention  and  less  change 
of  position  than  the  stomach.  Jaundice,  which  is  very  rare  in  ulcer  of  the 
duodenum,  can  be  little  utilized  in  the  diagnosis  from  the  circumstance 
that,  in  the  main,  intestinal  hemorrhage  is  more  frequent  and  hematemesis 
rarer,  but  gastric  ulcer  also  leads  to  hemorrhage  from  the  intestines,  and 
ulcer  of  the  duodenum  may  be  accompanied  by  hematemesis. 

PROGNOSIS 

Until  recently,  and  quite  properly,  a  doubtful  prognosis  was  given  in 
gastric  ulcer  when  it  was  differentiated  by  the  signs  which  have  been 
mentioned.  Since  we  have  become  able  to  make  an  early  diagnosis,  and 
to  separate  it  from  the  forms  of  dyspepsia,  since  the  principles  of  treat- 
ment have  been  clearly  established,  and  we  are  in  a  position  to  use  them 
at  the  onset  of  the  process,  the  prognosis  in  at  least  the  early  stage  of 
ulcer  has  decidedly  improved.  If  the  patient  is  subjected  to  rational 
treatment  at  the  proper  time,  i.  e.,  if  a  rest  cure  is  instituted,  well  founded 
hopes  of  recovery  may  be  entertained,  and  even  in  classical  ulcer  recovery 
or  decided  improvement  may  be  looked  for.  Unfortunately,  during  the 
first  stages,  which  subjectively  do  not  occasion  great  difficulty,  very  few 
patients  are  inclined,  or  are  in  a  position,  to  submit  to  such  treatment. 
If,  however,  we  succeed  in  curing  the  ulcer  by  permanently  changing  the 
abnormal  composition  of  the  blood  or  the  secretion  of  the  gastric  juice, 
the  fear  of  relapse  is  also  removed,  which,  otherwise,  always  threatens 


200  GASTRIC   ULCER  AND  GASTRIC   HEMORRHAGE 

and  only  too  frequently  occurs.  Invariably,  however,  and  particularly  in 
the  healing  of  extensive  ulcers,  there  is  danger  of  a  permanent  damage  to 
the  health  from  the  consequences  of  cicatricial  tissue  formation,  and  this 
cannot  be  lost  sight  of.  In  such  cases  the  prognosis  must  be  made  with 
great  caution.  That  it  is  not  bad  is,  nevertheless,  evident  from  the  well 
known  fact  that  cicatrices  from  gastric  ulcers  are  found  about  twice  as 
frequently  as  open  ulcers.  In  hemorrhage,  provided  it  is  not  immediately 
fatal,  the  prognosis  is,  as  a  rule,  favorable,  and  it  is  better  the  younger 
the  individuals  in  question.  By  suitable  treatment  we  usually  succeed  in 
mastering  the  hemorrhage,  and  even  extreme  anemias  are  improved  in  a 
relatively  short  time.  At  the  Surgical  Congress  in  Berlin  (1897),  v. 
Leube  gave  the  following  statistics  of  his  cases:  Of  424  hospital  patients 
314,  =  74  per  cent.,  were  cured  after  a  treatment  of  four  weeks,  93,  =  33 
per  cent.,  were  improved,  10,  =  2.4  per  cent.,  died,  7,  =  1.6  per  cent., 
were  unimproved.  Therefore,  in  only  4  per  cent,  was  careful  treatment 
Avithout  result.  This  coincides  with  my  reports  of  233  hospital  patients, 
in  which  I  had  76  per  cent,  of  recoveries. 

But  it  cannot  be  denied  that  in  these  statistics  the  factors,  which  have 
often  l)ecn  mentioned,  of  unlike  circumstances  and  insufficiently  long  ob- 
servation play  a  part.  The  surgeon  reaches  other  results  than  the  physi- 
cian, and  thus  it  comes  to  pass  that  v.  Mikulicz  gives  a  mortality  of  from 
20  to  30  per  cent.,  while  Leube  has  only  4.1  per  cent.  It  is  obvious  that 
the  brief  period  of  observation  in  the  hospital  can  only  be  regarded  as 
corresponding  to  the  "  healing "  of  the  ulcer ;  it  does  not  strictly  apply 
to  the  period  after  the  patient's  discharge  from  the  hospital,  and  tells 
us  nothing  of  the  mortality.  The  latter  depends  upon  accidental  con- 
ditions, and  can  only  be  arrived  at  with  some  degree  of  certainty  from 
the  reports  of  many  autopsies.  But  the  "  statistics  of  cures "  are  also 
open  to  doubt  from  the  fact  that  groups  denominated  as  ulcer  include 
many  cases  in  which  true  ulcer  was  not  present,  as  is  evident  from  the 
nature  of  these  cases.  For  this  reason  I  have  refused  to  utilize  my  statis- 
tics in  this  way.  J.  Schulz  has  decidedly  cleared  the  situation.  He 
analyzed  291  cases,  184  from  the  Breslau  Clinic,  and  107  from  the  Eppen- 
dorf  Hospital,  all  of  which  were  recognized  as  ulcer  by  the  appearance 
of  hemorrhage.  Of  course  under  these  circumstances  a  diagnostic  error 
was  not  absolutely  excluded,  but,  nevertheless,  it  was  scarcely  possible. 
Questions  were  sent  to  all  of  these  patients  from  which  deductions  were 
to  be  made  regarding  the  results  of  treatment.  One  hundred  and  fifty- 
seven  answers  were  received,  and  the  accurate  investigation  of  these  justi- 
fi(  (1  tlie  conclusion  that  internal  treatment  of  ulcer  of  the  stomach  accord- 
ing: <o  tli(^  method  instituted  by  v.  Ziemssen  and  Leube  gives  a  perma- 
nently good  result  in  64  per  cent.  In  18  per  cent,  relapses  occurred,  but, 
nevortlieloss,  most  of  these  patients  were  finally  cured.  It  might  be  as- 
suiikm]   that  under  renewed  proper  treatment  the  others  would  decidedly 


TREATMENT  201 

improve.  In  18  per  cent,  the  treatment  was  without  result,  and  of  these 
7.6  per  cent.  died.  If,  therefore,  we  count  those  who  were  not  benefited 
among  the  unsuccessful  cases,  64  per  cent,  were  cured,  in  13  per  cent,  there 
was  temporarily  either  no  result  or  a  relapse,  and  in  23  per  cent,  absolute 
failure. 

TREATMENT 

Whenever  possible,  gastric  ulcer  should  be  treated  by  the  rest  cure  in- 
augurated by  V.  Ziemssen  and  v,  Leube,  in  which  all  irritation  of  the 
stomach  is  to  be  prevented,  just  as  a  fractured  bone  is  immobilized  by  a 
plaster  dressing,  naturally  with  the  difference  that  in  the  latter  case  this 
rest  is  absolute  while  in  the  former  it  is  only  approximate.  Rest  in  bed 
and  nutrition  by  the  rectum  or  by  food  which  burdens  the  stomach  as 
little  as  possible  are  the  foundations  of  this  treatment  which,  in  England, 
was  long  practised  by  Wilson  Fox  and  Balthazar  Forster.  As  adjuvant, 
anodyne  remedies,  and  at  the  same  time  calculated  to  lessen  irritation, 
moist  heat  in  the  form  of  hot  compresses  and  the  drinking  of  hot  Carlsbad 
water  or  a  solution  of  Carlsbad  salt  which  neutralizes  acid,  are  recom- 
mended. V.  Leube  administers  the  Carlsbad  water  lukewarm;  the  com- 
presses, however,  should  be  as  hot  as  they  can  be  borne;  according  to  his 
latest  reports,  he  no  longer  uses  nutritive  enemata.  To  the  latter,  how- 
ever, I  attach  the  greatest  importance,  while  I  have  discarded  the  hot 
compresses,  chiefly  because  they  leave  an  ugly  pigmentation  upon  the  abdo- 
men. It  is  astonishing  how  well  the  majority  of  patients  will  bear  exclu- 
sive rectal  alimentation  for  three,  four  or  more  days,  the  nutritive  property 
of  which,  according  to  all  recent  investigations  (Eichhorst,  Ewald,  Huber, 
Eost  and  others),  and  in  spite  of  several  attempts  to  depreciate  its  practical 
value  (Plantenga,  v.  Mering),  admits  of  no  question,  particularly  if  small 
quantities  of  a  5  per  cent,  solution  of  cocain  upon  pellets  of  ice  be  given 
by  the  mouth. 

Whether  nutritive  enemata,  as  Zierko  maintains,  actually  diminish  the 
acidity  of  the  gastric  juice,  has  not  yet  been  positively  determined. 

Acting  upon  Kussmaul's  advice,  I  have  for  some  time  administered 
large  doses  of  bismuth  in  suspension  (about  15  to  20  grams  in  200  of 
water  daily,  divided  into  three  doses,  well  shaken,  and  given  before  meals) 
which,  according  to  the  experimental  reports  of  Matthes,  forms  a  protec- 
tive coat  over  the  exposed,  ulcerated  surface. 

This  treatment,  according  to  universal  experience,  gives  excellent  re- 
sults where  the  ulcers  do  not  invade  too  deeply,  or  where  the  condition 
resembles  that  of  a  florid  ulcer,  while,  in  truth,  other  affections — peri- 
gastric adhesions,  neuroses,  cholelithiasis,  renal  stones  and  the  like — are 
the  causative  agents.  Bourget  has  lately  declared  that  rectal  alimentation 
is  rather  harmful  than  beneficial  (why?);  on  the  other  hand,  he  admin- 
isters rice  soups  and  milk  and  rice,  and,  therapeutically,  washes  the  stomach 

J  :L-Ll£Gi£   OF    c  v-:TI£lM-, 


202  GASTRIC   ULCER  AND  GASTRIC   HEMORRHAGE 

with  a  2  per  cent,  solution  of  iron  chlorid,  to  which  ^  per  cent,  of  potassium 
chlorate  is  added;  so  far,  I  have  had  no  occasion  to  test  his  method. 

Leube  attaches  weight  to  the  fact  that  Carlsbad  salt  has  a  neutralizing, 
and,  on  account  of  the  sodium  chlorid  it  contains,  also  a  stimulating 
effect;  but  the  latter  might  rather  be  looked  upon  as  deleterious,  since 
we  know  that  in  many  cases  the  acidity  is  greatly  increased,  and  there- 
fore a  depressant  rather  than  a  stimulant  is  indicated.  As  to  the  neutral- 
ization, or  decrease,  of  the  aciditj^,  I  do  not  attach  much  importance  to 
tliis  if  it  is  observed  but  a  single  time  in  an  empty  stomach,  provided 
there  is  not  always  a  secretion  in  the  stomach  when  it  should  be  empty. 
On  the  contrary,  the  diminution  of  the  hypersecretion  and  the  laxative 
effect  of  the  neutral  salts,  as  well  as  the  soothing  influence  of  large  quan- 
tities of  warm  water,  appear  to  me  to  be  of  the  utmost  importance.  If 
the  water  of  simple  alkaline  springs  has  been  found  to  be  less  effective 
than  that  of  the  saline  alkaline  springs,  it  is  only  because  we  have  for- 
gotten to  produce  the  desired  laxative  effect  by  other  means. 

Where  there  is  no  laxative  effect  from  Carlsbad  water,  as  is  frequently 
the  case,  it  must  be  brought  about  by  the  addition  of  Glauber  salt  or, 
still  better,  by  vegetable  laxatives,  preferably  rhubarb  or  senna.  It  is 
unnecessary  to  adhere  rigidly  to  a  formula,  the  principle  alone  is  impor- 
tant. Whether  the  pains  are  relieved  by  warm  fomentations  or,  in  case 
these  are  ineffectual,  by  small  doses  or  subcutaneous  injections  of  mor-. 
phin,  whether  the  patient  is  given  a  solution  of  Sprudel  salt  or  the  natural 
spring  water  from  Carlsbad,  or,  for  example,  Ems,  Vichy,  or  the  Neue- 
nahr  Spring,  and  the  absent  neutral  salt  be  supplied  by  the  addition  of 
other  aperients,  is  immaterial.  Of  the  Carlsbad  spring  water  300  to  500 
c.c.  should  be  given.  But  which  spring?  This  is  unessential  since  there 
are  no  important  differences  in  the  chemical  combination,  and  the  differ- 
ences in  temperature  of  the  individual  Carlsbad  springs  are  of  little  con- 
sequence because  these  waters  can  only  be  taken  as  hot  as  the  patient  can 
bear  them;  therefore  are  all  taken  quite  hot.  Fifteen  grams  (about  one 
tablespoonful)  of  the  salts  should  be  taken  daily,  small  quantities  dis- 
solved in  half  a  liter  of  water  at  intervals,  with  corresponding  pauses 
between.  For  the  first  three  days  absolutely  no  food  is  to  be  adminis- 
tered by  mouth,  but  a  nutritive  enema  is  given  three  times  daily;  subse- 
quently, besides  the  enemata,  milk,  or  milk  in  flour  soup,  in  tablespoonful 
doses,  or  bland  pigeon  or  chicken  broth.  The  milk,  on  account  of  its 
fin(>  floccular  coagulation,  has  some  pegnin  added.  If  this  diet  is  well 
horno.  it  is  added  to  in  a  manner  soon  to  be  described;  otherwise,  absolute 
rectal  nutrition  is  again  instituted.  If  no  pain  follows  the  careful  admin- 
istration of  milk,  we  may  permit  somewhat  larger  quantities  (up  to  a 
tlat  ])latoful.  i.e.,  about  180  c.c),  leguminous  flour  soup,  then  legumes, 
later  j'appy  food  made  of  chestnuts,  sago,  tapioca,  Kufeke's  flour,  hygiama 
and   others,  and  later  small  quantities  of  meat.     Among  nutritive   sub- 


TREATMENT  203 

stances  cow's  milk  takes  the  first  place;  it  was  first  advised  for  this  pur- 
pose by  Cruveilhier.  It  is  suitable  because  it  contains  all  of  the  nutritive 
elements  in  solution,  that  is,  finely  divided,  is  free  from  irritating  sub- 
stances, because  the  acid  is  neutralized,  and  because  the  coagula  which 
forms  from  the  action  of  the  gastric  juice  remains  soft.  The  patient, 
however,  must  drink  it  very  slowly  and  lukewarm.  To  prevent  the  floccu- 
lent  coagulation  of  the  milk,  and  the  irritation  of  the  ulcerative  surfaces 
due  to  this,  I  now  add  pegnin  (lab-ferment),  which  produces  a  very  fine 
flocculent  coagulation,  v.  Mering  advises  lab  cheese  for  patients  who 
cannot  take  milk.  Besides  pigeon  or  veal  soups,  the  yolk  of  an  egg,  and 
beaten-up  egg  albumin,  pulverized  meat  or  leguminous  soups  may,  per- 
haps, be  given.  We  must  limit  ourselves  to  these  foods  until  the  severe 
symptoms  have  disappeared.  In  the  third  week  a  food  richer  than  this, 
both  quantitatively  and  qualitatively,  is  permissible,  and  we  should  then 
carefully  try  food  of  somewhat  greater  consistence,  such  as  scraped  raw 
ham,  raw  or  very  soft  boiled  eggs,  scraped  venison  or  the  breast  of  fowl, 
rolls  or  zvneback  softened  in  cocoa,  but  milk  is  always  preferable,  and 
we  should  always  be  ready  to  return  to  a  simpler  diet  as  soon  as  symptoms, 
or  even  pains,  appear. 

Even  small  portions  of  coarse  bread,  legumes,  fruit,  cabbage,  salad, 
pickles,  mushrooms,  high  spices,  fatty  foods  or  those  prepared  with  vine- 
gar, liver,  fatty  acids,  confectionery,  alcohol  and  coffee  are  to  be  strictly 
prohibited. 

In  regard  to  the  diet  in  liyperclilorliydria,  the  article  by  Strauss,  "  The 
Diagnostic  and  Therapeutic  Significance  of  Secretory  Disturbances  of  the 
Stomach"  (see  this  volume),  which  embodies  the  latest  views  on  this 
subject,  should  be  consulted. 

It  is  absolutely  necessary  that  the  patient  take  but  little  food  at  a  time 
but  somewhat  more  frequent  meals,  that  he  eat  slowly,  avoiding  all  hot 
food;  after  recovery  he  should  never  overload  the  stomach,  but  must  re- 
frain from  foods  difficult  of  digestion  or  highly  spiced,  so  as  to  prevent 
any  lesion  of  the  cicatrized  area. 

Lenhartz  proposes  quite  a  different  dietetic  treatment.  Starting  from 
the  fact  that  hyperchlorhydria,  chlorosis  and  anemia  frequently  develop 
in  the  course  of  ulcer,  he  permits  his  patients  from  the  start  to  take 
concentrated  foods  rich  in  albumin.  The  patients,  even  when  hemorrhage 
has  occurred  immediately  before  treatment,  receive  doses  from  a  spoonful 
up  to  300  c.c.  of  iced  milk  in  which  as  many  as  3  eggs  have  been  beaten; 
from  the  third  day  sugar  is  allowed,  and  from  the  sixth  day  scraped 
meat,  then  milk,  rice,  and  fine  bread;  from  the  tenth  day  raw  ham  and 
butter.  Rest  in  bed,  applications  of  ice,  one  to  two  grams  of  bismuth 
daily  and,  perhaps,  iron  with  arsenic  are  ordered.  In  sixty  cases  treated 
in  this  way  the  results  are  said  to  have  been  very  good;  one  case  proved 
fatal,  seven  cases  of  relapsing  hematemesis  remained  in  the  hospital. 


204  GASTRIC   ULCER   AND   GASTRIC   HEMORRHAGE 

The  pains  ceased  almost  immediately  after  the  ingestion  of  food  rich 
in  albumin,  and  the  patients  recovered  more  rapidly  than  those  on  the 
preceding  diet.  Of  25  patients  who  were  subsequently  questioned,  18  (72 
per  cent.)  were  entirely  free  from  symptoms. 

The  editor  of  the  Fortschritte  der  Medicin  quite  properly  remarks  of 
these  reports  that  the  results  are  no  better  than  with  the  old,  reliable 
diet,  and  that  there  are  very  few  who  would  risk  the  employment  of  such 
food  in  the  stomach  of  a  patient  with  ulcer.  The  reason  given  by  Lenhartz- 
Wagner  in  favor  of  this  coarse  diet,  that  the  patients  recover  more  quickly, 
does  not  appear  to  me  to  be  justified.  Patients  with  ulcer  recover  very 
rapidly  when  the  pains  cease,  and  this  takes  place  the  more  quickly  when 
the  gastric  mucous  membrane  is  allowed  absolute  rest  instead  of  being 
stimulated  to  greater  activity. 

It  is  true  that  patients  on  this  diet  are  at  first  debilitated  and  lose 
weight,  but  even  here  we  must  individualize.  To  attempt  to  regulate  the 
diet  in  these  cases  according  to  calories  is  a  form  of  play  under  a  scientific 
cloak  which  to-day  is  much  in  vogue.  As  soon  as  the  patients  are  able 
to  eat  at  all  they  are  prone  to  eat  so  much,  even  without  calory  force,  that 
they  soon  recover  from  the  former  undernutrition.  Convalescence  is  rapid, 
gastralgia  ceases,  and  the  time  arrives  when  we  must  consider  the  second 
indication,  the  strengthening  of  the  constitution. 

For  this  purpose  iron  preparations^  either  alone  or  in  combination  with 
arsenic,  are  serviceable,  the  former  in  cases  of  pure  chlorosis  or  anemia, 
the  latter  when  we  are  combating  a  weakened  nervous  system,  and  it  is 
desirable  indirectly  to  influence  this  by  the  direct  stimulation  of  metab- 
olism. The  old  opposition  to  the  employment  of  iron  in  ulcer  of  the 
stomach  was  founded  on  the  experience  that  iron  is  frequently  badly  borne 
while  the  florid  process  is  present;  this,  however,  does  not  hold  good  when 
improvement  sets  in.  Which  iron  preparation  is  to  be  employed  depends 
largely  upon  personal  preference;  each  day  brings  forth  a  new  one,  and 
in  one  case  this,  in  another  that,  is  the  better  tolerated.  Of  late,  I  have 
frequently  employed  triferrin  which,  without  exception,  was  well  borne. 
I  formerly  used  arsenic  in  the  form  of  Fowler's  solution  with  tinctura 
ferri  chloridi.  After  Liebreich's  investigations  arsenious  acid  appeared 
to  be  more  serviceable  and  I  now  employ  this  in  pill  form,  1.5-2  mgm. 
of  arsenious  acid,  2  cgm.  of  ferri  sesquichlorat.  Considerably  smaller 
l)ut  decidedly  active  doses  of  iron  and  arsenic,  as  has  been  proven  by 
investigations  in  metabolism  conducted  by  Ewald  and  Dronke,  are  given 
in  the  waters  of  Levico  and  Eoncegno  and  the  Guber  Spring,  which  are 
excellently  borne.  The  remedy  should  be  given  in  increasing  doses  and 
after  meals.  This  regime  must  be  continued  for  months,  and  then  the 
administration  of  arsenic  must  be  interrupted  for  three  to  five  days  about 
every  three  weeks.  The  diet  may  gradually  become  more  liberal  but, 
nevertheless,  must  be  strictly  regulated  for  months,  and  patients  who  show 


TREATMENT  205 

a  tendency  to  exceed  their  allowance  must  be  given  a  written  diet  list 
indicating  the  amount  of  food  permitted. 

It  is  sometimes  impossible  to  carry  out  the  rest  cure  mentioned  above 
because  there  are  many  patients  who  are  unwilling,  or  not  in  a  position, 
to  undertake  it,  and  in  many  cases  it  is  necessary  to  fulfil  a  stringent 
indicatio  symptomatica. 

Under  these  circumstances  treatment  with  large  doses  of  bismuth  is 
recommended.  Kussmaul  (Fleiner)  advised  that  this  in  suspension  be 
introduced  in  large  doses  into  the  stomach  previously  washed  out,  and 
that  the  patient  then,  according  to  the  suspected  seat  of  the  ulcer,  assume 
for  some  minutes  such  a  position  as  will  enable  the  drug  to  sink  to  the 
lowest  area ;  therefore,  for  example,  in  ulcer  of  the  pylorus  the  right  lateral 
position.  Since,  as  a  rule,  I  avoid  lavage  in  ulcer,  and  because  I  know 
that  the  stomach  is  usually  empty  early  in  the  morning,  and  also  that 
by  a  previous  drinking  of  water  the  gastric  juice  present  may  be  diluted 
and  more  rapidly  propelled  into  the  intestine,  and  since,  moreover,  it  is 
scarcely  possible  so  to  cleanse  the  gastric  mucous  membrane  as  to  remove 
particles  which  may  possibly  be  adherent  to  the  ulcerated  surface,  and  this, 
at  all  events,  would  necessitate  the  use  of  many  liters  of  water,  therefore 
I  omit  the  washing  and  permit  the  patient  to  drink  the  bismuth  suspension 
upon  an  empty  stomach.  The  beneficial  results  I  have  obtained  prove  the 
reliability  of  this  modified  process.  Indeed,  the  patient's  tolerance  of  the 
drug  and  the  ensuing  freedom  from  pain  are  quite  remarkable,  although 
not  so  invariable  nor  so  prompt  as  would  appear  from  Fleiner's  report. 
This  is  quite  natural;  the  conditions  are  occasionally  much  more  compli- 
cated than  we  assume  and  the  method  presupposes  to  be  the  case. 

The  dose  is  large,  apparently  unlimited,  and  may  be  given  for  an 
indefinitely  long  period.  In  one  of  my  cases  the  patient  received  over 
800  grams  in  the  course  of  a  few  weeks  without  the  slightest  inconvenience, 
not  even  constipation  resulting.  In  this  case,  however,  considering  the 
size  of  the  dose,  the  result  was  not  very  satisfactory.  The  same  may 
probably  be  inferred  from  the  large  quantities  employed  by  Fleiner  (up 
to  1,000  grams).  In  place  of  bismuth,  Pariser  advises  equal  parts  of  the 
cheaper  white  chalk  and  talcum,  one  to  one  and  a  half  teaspoonfuls  in 
water  in  the  morning  upon  an  empty  stomach,  and  in  the  evening  three 
hours  after  the  full  evening  meal.  Under  this  treatment  the  feces  remain 
light  in  color,  and  small  hemorrhages  are  much  more  readily  recognizable 
than  in  the  dark  bismuth  feces.  In  place  of  bismuth  subnitrate,  bismuth 
subcarbonate  (Boas)  and  bismutose  have  been  advised. 

If  all  proceeds  as  we  anticipate,  and  a  protective  covering  of  bismuth 
forms  over  the  ulcer,  this  has  not  only  a  symptomatic  but  a  curative  effect. 
Under  this  protection  the  ulcer  has  time  to  heal,  and,  as  Matthes  has 
shown,  the  formation  of  granulation  tissue  at  the  base  of  the  ulcer  and 
the  proliferation  of  glandular  and  other  epithelia  take  place. 


206  GASTRIC   ULCER  AND   GASTRIC   HEMORRHAGE 

Under  thorough  treatment  which  is  long  enough  continued,  in  my  ex- 
perience for  at  least  four  weeks,  recent  ulcers  promptly  heal.  In  some 
cases  a  single  treatment  is  not  sufficient,  but  a  repetition  is  necessary. 
The  result  of  this  treatment,  however,  is  generally  so  uncertain  that  with 
an  unsuccessful  issue  we  may  at  once  assume  either  that  an  incorrect 
diagnosis  has  been  made  (particularly  the  pure  neuroses  lead  to  errors) 
or  that  we  have  old,  deeply  invading  ulcers  with  broken  down,  excavated 
borders,  that  malignant  degeneration  has  begun  or  induration  has  devel- 
oped. In  such  cases  other  curative  measures  are  indicated, — gastric  lavage, 
tonics,  and  stomachics,  small  doses  of  mild  narcotics,  aperients,  and  the 
like.  The  indications  for  the  employment  of  these  remedies  must  be 
obtained  by  testing  the  functional  activity  of  the  stomach. 

Of  additional  remedies  silver  nitrate  has  also  been  advised,  best  in 
solution,  and  in  decided  doses  (0.2  silver  nitrate  to  200.0  of  water,  a  table- 
spoonful  every  two  hours).  With  this  remedy  I  have  sometimes  seen 
decided  amelioration  of  the  symptoms,  and  even  a  complete  cure;  in  other 
instances,  after  a  little  time  the  remedy  had  to  be  stopped  because  in- 
creased disturbance  of  the  stomach,  nausea,  anorexia,  coated  tongue,  and 
derangement  of  the  intestinal  activity,  diarrhea  or  constipation,  appeared. 
In  one  of  my  cases,  every  time  a  spoonful  of  the  silver  solution  was  taken 
watery  dejecta  accompanied  by  severe  abdominal  pain  followed. 

In  my  opinion  the  dietetic  principles  •  enunciated  above  are  also  im- 
portant in  the  treatment  of  ambulatory  cases,  and  the  diet  should,  at  least, 
be  followed  as  far  as  possible.  As  the  patients  digest  meat  better  than 
starches  and  vegetables,  they  instinctively  eat  less  of  the  latter,  and  event- 
ually, therefore,  suifer  from  a  monotonous  meat  nutrition,  i.  e.,  they  ema- 
ciate, and  become  nervous  and  irritable.  This  must  Jse  counteracted  as 
much  as  possible,  and  larger  quantities  of  fat  in  the  nourishment  are 
not  contraindicated  because,  as  I  showed  some  years  ago,  fat  has  the  effect 
of  decreasing  acidity.  I  endeavor  to  modify  the  hyperacid  gastric  juice 
by  repeated  small  doses  of  alkali  combined  with  rhubarb  and  cane  sugar 
or  milk  sugar.  Rhubarb  has  a  mild  action  upon  the  intestines,  the  sugar 
has  a  decided  anodyne  effect,  and  for  this  purpose  has  been  repeatedly 
advised.     I  use  a  powder  of  about  the  following  composition: 

^  Magnes.  ust.,     1 

Natr.  carbon.,    I   aa 5.0 

Kalii  carbonic,  I 

Pulv.  rad.  Ehei 10.0 

Sacch.  lactis 25.0 

M.  D.     S. :  Every  hour  enough  to  cover  the  tip  of  a  knife. 

Tills  is  to  l)e  taken  dry;  I  have  seen  good  results  from  its  use.  Patients 
who  know  by  experience  the  beneficial  effects  of  alkalies,  particularly  of 


TREATMENT  .  207 

soda,  are  usually  afraid  of  taking  too  much.  In  this  respect  their  minds 
may  be  easy.  I  have  never  yet  observed  a  deleterious  effect  from  the  too 
long-continued  use  of  an  alkali,  particularly  of  sodium  bicarbonate. 

For  the  catarrh  which  accompanies  ulcer,  Ord  advises  potassium  iodid 
with  the  addition  of  sodium  bicarbonate  in  about  the  following  formula:, 

^  Kalii  iodat 3.0 

Natrii  bicarbonic 5.0 

Acid,  hydrocyan.  dil.  (m.  2  per  cent,  acid)  gutt.  tres 

Inf.  rad.  Gentian 3.0 :  150.0 

M.  D.     S. :  A  tablespoonful  three  times  a  day. 

It  is  well  to  remember  the  advice  of  Pariser  that  women  who  have 
suffered  from  ulcer,  even  after  treatment  is  discontinued,  should  be  kept 
in  bed  during  the  next  two  or  three  menstrual  periods  and  on  almost  the 
same  diet  as  while  suffering  from  ulcer. 

For  the  severe  gastralgia,  morphin  internally  or  subcutaneously  ranks 
first.  Chloroform  solutions  (1-120,  a  tablespoonful  every  two  hours)  or 
chloroform  in  drops  (5  to  6  in  a  teaspoonful  of  water  or  on  a  pellet  of 
ice)  occasionally  produce  excellent  effect,  not  only  upon  the  momentary 
pain  but  upon  the  course  of  the  process  in  general.  For  a  long  time  I 
have  been  in  the  habit  of  administering  bismuth  in  suspension  with  a  one 
per  cent,  addition  of  chloroform,  or,  instead  of  using  distilled  water,  I 
employ  chloroform  water.  Tincture  of  iodin,  5  drops,  three  times  daily 
in  water,  occasionally  acts  as  an  anodyne.  Of  other  sedatives  I  have 
occasionally  employed  lupulin,  extract  of  cannabis  indica,  extract  of  hyos- 
cyamus,  and  extract  of  belladonna,  but  have  always  been  compelled  to 
return  to  morphin  or  codein.  Cannabis  indica,  in  particular,  which  is 
so  greatly  praised  and  was  advised  by  G.  See,  has  in  my  hands  repeatedly 
failed  to  show  any  anodyne  or  quieting  effect,  but,  on  the  contrary,  has 
produced  an  unpleasant  irritation.  Formerly  leeches  were  applied  at  the 
seat  of  the  affection,  and  also  blistering  plaster ;  it  was  painted  with  strong 
solutions  of  iodin,  and  even  the  actual  cautery  was  used.  We  are  content 
to-day  with  the  ice  bag,  or  the  application  of  ice-cold  or  warm  compresses, 
or  Leiter^s  coil  which,  where  the  circumstances  permit,  is  the  most  cleanly 
and  convenient  mode  of  employing  cold. 

Treatment  with  Oil. — Treatment  with  oil  (linseed  oil  or  olive  oil)  has 
been  praised  by  various  authors.  Cohnheim,  in  1889  and  later,  was  the 
first  to  report  surprisingly  good  results.  The  oil  is  to  be  given  in  grad- 
ually increasing  doses  from  a  tablespoonful  to  a  wineglassful  or  may  be 
poured  in  through  a  stomach-tube.  Ageron  advises  the  admixture  of  10 
grams  of  dermatol  with  200  of  the  finest  linseed  oil  or  poppy  seed  oil. 
Walko  adds  bismutose  or  bismuth.  The  oil  is  best  taken  while  the  patient 
is  in  the  recumbent  posture,  and  Ageron  has  the  patient  assume  the  dorsal 
15 


208  GASTRIC   ULCER  AND  GASTRIC   HEMORRHAGE 

decubitus,  raising  the  pelvis  after  taking  the  remedy  to  relieve  the  greater 
curvature.  Aside  from  the  fact  that  the  stomach-tube  should  not  be  intro- 
duced in  cases  of  ulcer  without  very  clear  indications — which  I  think  do 
not  include  the  pouring  in  of  oil — I  have  previously  cited  a  case  in  whicli 
the  oil  caused  such  great  nausea  and  retching  that  it  was  the  immediate 
cause  of  a  severe  gastric  hemorrhage,  Cohnheim,  however,  in  about  30 
cases,  even  with  irreparable  organic  changes  at  the  pylorus  as  well  as  in 
functional  disturbances,  has  seen  no  unpleasant  secondary  effects  but  usu- 
ally a  very  favorable  influence  upon  the  pain,  the  spasm,  the  general 
nutritive  condition  and  the  degree  of  acidity  of  the  stomach.  Even  cases 
in  which  operative  interference  had  been  advised  by  others  were  cured 
by  this  treatment.  According  to  their  nature,  cases  of  the  first  category 
can  only  be  symptomatically  influenced,  while  permanent  results  have 
actually  been  attained  in  spastic  stenosis  of  the  pylorus,  in  ulcer,  in  fis- 
sures (?),  in  erosions  of  the  pylorus,  in  pyrosis  hydrochlorica  with  acid 
gastritis,  and  similar  conditions  when  a  pure  neurosis  formed  the  founda- 
tion of  the  difficulties,  and  provided  no  complicating  perigastric  processes 
existed.  Instead  of  oil,  an  emulsion  of  almond  milk  (about  a  tablespoonful 
of  sweet  almonds  ground  up  in  about  200  of  water)  also  has  a  quieting, 
but  not  a  nutritive,  effect.  The  oil  has  the  following  merits:  It  quiets 
spasm,  it  lessens  friction,  it  decreases  the  acid  secretion,  and  it  assists 
in  the  nutrition. 

Cohnheim,  in  his  last  publication  (1904),  remarks  that  it  is  strange 
that  his  reports  have  been  confirmed  only  by  Walko.  This  may  be  for 
two  reasons.  Either  the  process  has  been  generally  satisfactory,  and  only 
by  accident  others  have  failed  to  praise  it,  or  the  results  lauded  by  Cohn- 
heim have  not  been  attained  by  others,  and  judgment  has  been  suspended. 
The  latter  describes  my  own  position.  Ever  since  Cohnheim's  first  pub- 
lication I  have  repeatedly  employed  the  oil  treatment  in  my  private  prac- 
tice, in  the  Hospital,  and  in  the  Clinic,  and  I  have  observed  some  beneficial, 
and  also  some  very  ill,  effects.  The  oil  was  so  repugnant  to  many  of  the 
patients  that  it  was  impossible  for  them  to  take  it,  and  in  others  it  subse- 
quently caused  complete  loss  of  appetite,  eructations  and  vomiting,  no 
matter  whether  given  by  the  mouth  or  introduced  through  the  stomach- 
tube.  Fischl  in  a  study  of  19  cases  arrived  at  the  same  conclusion.  As 
the  poor  results  were  observed  chiefly  during  the  first  trial,  I  must  ac- 
knowledge that  no  extensive  test  was  made  by  me,  so  that  a  definite  state- 
ment regarding  the  method  is  at  this  time  impossible.  •  Cohnheim's  last 
publication  may  induce  me  methodically  to  test  the  oil  treatment  anew. 
But  at  present,  on  the  basis  of  my  previous  experience,  I  must  maintain 
that  in  this  treatment  we  possess  no  panacea  for  the  symptoms  in  question, 

Xeroform,  one  of  the  newer  remedies  (0.5  gram  four  times  daily)  has 
been  much  praised,  Jaworski  advises,  under  the  name  of  aq.  alcalina 
effervescens,  a  solution  of  sodium  bicarbonate  (8  or  5),  sodium  salicylate 


TREATMENT  209 

(2^  or  2),  and  sodium  biborate  (2  or  1)  in  a  liter  of  water,  one-third  to 
one-half  of  a  tumblerful  several  times  daily. 

For  the  vomiting  nothing  is  better  than  a  carefully  regulated  diet. 
Large  quantities  of  hot  water  may  be  taken  several  times  daily,  also 
pellets  of  ice  with  chloroform.  Tincture  of  iodin  (15  drops  in  150  of 
water)  has  been  advised  by  some  authors.  Special  care  is  necessary  if 
hematemesis  appear;  when  very  profuse  this  is  self-evident,  but  it  is  also 
enjoined  when  smaller  hemorrhages  take  place.  Under  all  circumstances, 
the  first  requirements  are  absolute  bodily  and  mental  rest  and  the  avoid- 
ance of  all  internal  and  external  irritation  of  the  stomach.  Even  in 
smaller  hemorrhages,  if  circumstances  permit,  the  patient  should  be  re- 
stricted to  this  regime  for  several  days,  and  the  fullest  precautions  should 
be  taken  because  these  small  hemorrhages  are  very  frequently  only  the 
precursors  of  more  profuse  ones.  Small  pellets  of  ice,  ice-cold  tea,  or 
ice-cold  solutions  of  peptone  in  spoonful  doses  may  be  given.  I  do  not 
give  milk  in  such  cases  unless  I  know  that  the  patient  takes  it  well,  but 
for  the  first  day  order  either  a  solution  of  grape  sugar  to  which  some  meat 
peptone  bouillon  is  added  and  given  ice-cold,  or  I  administer  cold,  gelat- 
inous soups  of  barley  or  oatmeal  gruel;  where  the  circumstances  permit, 
nutritive  enemata  are  cautiously  given.  The  fluid  extract  of  ergot,  2.5  to  5 
of  water  and  glycerin  in  equal  parts,  is  subcutaneously  injected  in  the 
gastric  region,  one  to  two  syringefuls  several  times  daily,  but  it  must  be 
remarked  that  ergotin  in  some  persons  gives  rise  to  very  unpleasant  symp- 
toms of  constriction  and  vertigo.  I  have  been  unable  to  convince  myself 
of  the  reliability  of  the  fluid  extracts  of  hydrastis  canadensis  and  hama- 
melis  virginica,  which  have  lately  been  much  used.  When  there  is  great 
irritability  of  the  stomach,  the  injections  of  ergot  should  be  combined 
with  injections  of  morphin.  This  will  usually  arrest  hemorrhage,  provided 
large  vessels  are  not  implicated.  Formerly  lead  acetate,  iron  chlorid,  and 
oil  of  turpentine  were  employed  internally  because  of  their  presumable  styp- 
tic influence,  but  these  are  no  longer  used  because  we  possess  a  more  rational 
and  active  remedy  in  ergot.  In  some  instances  in  which  hemorrhages 
recurred  for  several  days  and  the  above  measures  were  futile,  the  bleeding 
ceased  upon  lavage  of  the  stomach  with  ice  water.  After  preceding  cocain- 
ization  and  the  injection  of  a  small  quantity  of  morphin,  the  stomach-tube 
was  carefully  introduced,  and  the  stomach  wall  repeatedly  sprinkled  with 
ice  water,  large  amounts  of  hemorrhagic  gastric  contents  being  first  washed 
out,  whereupon  the  hemorrhage  immediately  ceased.  Before  proceeding 
to  operate  in  such  cases,  this  maneuver  should  always  be  first  tried.  It 
is  occasionally  astonishing  to  see  what  large  quantities  of  liemorrliagic 
fluid  are  evacuated  from  the  stomach.  As  some  blood  usually  passes  into 
the  intestine  and  is  there  decomposed,  and  perhaps  may  set  up  irritative 
phenomena,  it  is  advisable,  if  there  is  no  spontaneous  passage,  to  employ 
mild  evacuants,  preferably  rhubarb  with  sulphur,  or  enemata;  if  symptoms 


210  GASTRIC   ULCER   AND  GASTRIC   HEMORRHAGE 

of  collapse  appear,  injections  of  camphorated  oil  (1:6),  enemata  of  wine, 
or  wine  with  egg  or  peptone,  and  hot  applications  to  the  extremities. 
With  threatening  hemorrhage,  a  very  small  pulse,  anemic  murmurs  over 
the  heart,  or  cerebral  anemia,  normal  saline  infusions  are  indicated.  Sub- 
cutaneous infusions  are  best  given  by  employing  a  rather  large  Pravaz 
cannula.  If  the  salt  solution  (7.5:1,000)  warmed  to  the  temperature 
of  the  body  is  injected  simultaneously  through  two  needles,  and  the  fluid 
introduced  is  disseminated  by  gentle  friction,  one  liter  of  water  may  be 
introduced  in  a  very  short  time.  We  prefer  the  subclavicular  region  as 
the  point  in  which  the  needle  should  be  introduced.  In  favorable  cases  the 
blood  is  rapidly  regenerated.  In  a  patient,  aged  25,  who  had  received 
an  infusion,  the  blood  upon  the  next  day  showed  2,100,000  erythrocytes, 
two  weeks  later  3,560,000,  with  a  slight  increase  of  the  leukocytes. 

Adrenalin  or  suprarenal  extract  has  also  been  advised  for  gastric  hem- 
orrhage. Fen  wick  employs  1.3  grams  of  the  dry  glandular  substance  boiled 
in  230  of  water.  Internally  or  subcutaneously  it  is  more  rational  to  em- 
ploy adrenalin  hydrochlorid  in  solutions  of  1 :  1,000,  20  to  30  drops  in- 
ternally three  to  four  times  daily,  subcutaneously  0.5-1  c.c.  several  times 
daily.  There  are  quite  a  number  of  reports  (Roussel,  Renon  and  Louste, 
Mills,  Kirch,  Mamlock  and  others)  in  praise  of  its  action,  and  authors 
are  at  least  unanimous  on  the  point  that  no  unpleasant  sequelae  (glyco- 
suria, marked  increase  of  blood  pressure)  appear  even  after  its  use  for 
weeks. 

Up  to  the  present,  I  have  employed  the  remedy  internally  in  two 
cases,  and  it  failed  entirely.  I  must  also  say  the  same  of  gelatin,  of 
wliicli  I  gave  a  10  per  cent,  solution  up  to  100  c.c.  by  mouth  twice  daily 
(it  may  also  be  used  by  enemata).  C  Klemperer,  of  Berlin,  advises 
tlie  employment  of  escalin  (an  aluminum-glycerin  paste),  10  grams  to 
bo  given  daily  for  four  days  for  the  hemorrhage  of  gastric  ulcer.  This 
autlior,  as  well  as  others,  reports  excellent  results  from  this  method  of 
treatment. 

Perforative  peritonitis  necessitates  opium  in  large  doses  in  the  form  of 
a  suppository  or  as  an  enema,  and  the  use  of  cold  in  the  form  of  ice-cold 
compresses  about  the  abdomen.  If  we  suspect  that  the  stomach  is  full, 
we  must  first  try  to  empty  it  by  the  tube  after  either  giving  the  patient 
a  large  dose  of  morphin  or  by  applying  cocain  locally.  But  here  it  is 
necessary,  under  all  circumstances,  to  keep  the  patient  from  retching, 
which  may  perhaps  even  enlarge  the  perforative  opening.  By  this  treat- 
ment it  has  sometimes  been  possible  to  limit  the  peritonitis  locally,  and 
to  bring  about  adhesions.  Operative  measures  have  lately  been  advised 
for  such  cases,  and  several  successful  laparotomies  have  been  reported 
(see  below). 

Surgical  Measures. — For  the  florid  ulcer,  as  well  as  for  those  with 
recent    cicatrices,   surgical   aid   has   been    invoked.      Among   the    first    to 


TREATMENT  211 

favor  this  were  Eossoni  in  Eome,  Nissen  in  St.  Petersburg,  and  v.  Miku- 
licz in  Breslau.  At  the  Surgical  Congress  (1897)  the  last  author  enu- 
merated the  indications  as  follows:  "1.  When  the  life  of  the  patient  is 
directly  or  indirectly  threatened  by  hemorrhage,  perforation,  inanition. 
2.  When  continuous  treatment  produces  no,  or  but  a  temporary,  relief, 
and  the  sufferings  of  the  patient  make  his  life  miserable." 

These  indications  may  be  somewhat  more  accurately  defined,  and  opera- 
tive measures  resorted  to  under  the  following  circumstances: 

1.  In  stenoses  of  the  pylorus  and  hour-glass  stomach  due  to  cicatricial 
contraction,  or  when  continuous  internal  treatment  is  powerless  to  remove 
the  symptoms.  This  presupposes  the  consideration  that  all  internal  reme- 
dies have  been  thoroughly  and  exhaustively  employed.  At  the  Interna- 
tional Congress  at  Moscow  in  1899  I  gave  the  preference  to  this  method 
of  treatment  in  the  but  slightly  developed  field  of  gastric  surgery  rather 
than  to  operations  for  cancer,  and  ascribed  to  it  the  most  satisfactory 
and  the  most  lasting  results. 

2.  In  perigastric  adhesions  of  the  stomach  to  the  surrounding  organs. 
Here  those  adhesions  of  the  greater  curvature  and  at  the  pylorus  are  espe- 
cially to  be  considered  which  by  volvulus  and  torsion  of  the  organs  and 
the  neighboring  structures  produce  unbearable  pain,  all  anodynes  being 
ineffectual,  while  an  operation  at  once  removes  the  difficulties  which  may 
have  existed  for  years.  It  is  very  surprising  to  see  how  delicate  these  adhe- 
sions sometimes  are.  In  a  case  of  ours  recently  operated  upon  the  thin 
layers  of  the  greater  curvature  led  to  the  transverse  colon,  and  could  be 
almost  completely  detached  without  hemorrhage.  Notwithstanding  this, 
they  must  have  been  the  cause  of  pains  for  months,  since  the  patient  had 
no  symptoms  after  the  operation. 

3.  In  gastric  hemorrhage.  While  the  previously  mentioned  indications 
are  clear  and  beyond  question,  provided  the  diagnosis  is  positive,  in  hemate- 
mesis  it  is  extremely  difficult  to  say  whether  and  when  operative  measures 
are  indicated.  For  even  very  threatening  and  very  massive  hemorrhages 
are  apparently  promptly  arrested  by  proper  internal  treatment.  Throm- 
bosis appears  with  decreasing  cardiac  power,  and  it  is  astonishing  to  see 
how  rapidly  these  exsanguine  patients  recuperate,  v.  Leube  found  uncon- 
trollable hemorrhage  to  be  the  cause  of  death  in  1  per  cent,  of  his  case>. 
Personally  I  have  never  seen  a  patient  succumb  immediately  to  hemor- 
rhage. When  Brinton  claims  5  per  cent,  of  fatal  cases  in  ulcer  due  to 
hemorrhage,  only  the  subsequent  consequences,  but  not  immediate  death 
from  hemorrhage,  can  be  meant.  This  makes  the  decision  as  to  operation 
difficult,  as  the  results  of  surgery  are  by  no  means  brilliant. 

Often  it  is  impossible  to  find  the  bleeding  vessel  at  the  operation,  and 
there  are  cases  in  which  this  cannot  be  discovered  even  at  the  autopsy. 
Statistics  are  always  -very  unreliable,  for,  according  to  the  nature  of  the 
case,  the  successful  operations,  but  not  all  of  the  unsuccessful  ones,  are 


212  GASTRIC   ULCER   AND   GASTRIC   HEMORRHAGE 

published.  Kaupe,  the  most  recent  author,  collected  16  cases  up  to  1902 
in  which  operation  was  performed  because  of  acute  life-threatening  hemor- 
rhage, and  10  of  these  were  discharged  as  cured;  this  gives  a  mortality 
of  only  37  per  cent.,  which  figure  decidedly  differs  from  the  actual  facts. 
The  prospects  would,  perhaps,  be  more  favorable  if  it  could  be  proven, 
and  to  this  surgeons  have  recently  called  attention,  that  gastroenterostomy 
arrests  the  hemorrhage,  that  is,  prevents  its  recurrence,  without  reaching 
the  actual  source  of  the  bleeding.  Of  course  those  cases  only  can  be 
considered  in  which  operation  was  performed  during  the  hemorrhage, 
for,  under  other  circumstances,  we  can  never  be  sure  that  the  hemorrhage 
did  not  cease  spontaneously.  Petersen  and  Machol  actually  state :  "  We 
have  reached  the  positive  conclusion  that  gastroenterostomy  with  Murphy's 
button  might  save  many  a  patient  with  severe  gastric  hemorrhage  who 
would  be  lost  under  conservative  treatment  as  well  as  by  any  other  method 
of  operation."  The  decision  whether  Murphy's  button  is  actually  a  con- 
ditio sine  qua  non  for  the  successful  result  of  the  operation  I  must  leave 
to  the  surgeons.  But,  as  this  tcchnic  has  been  mentioned  in  the  words 
quoted,  I  cannot  refrain  from  raising  the  question  (although  from  prin- 
ciple I  do  not  interfere  in  the  technic  of  surgical  treatment,  and  do  not 
usually  ])crmit  myself  an  opinion)  whether,  for  example,  in  the  case  in 
question,  gastroenterostomy  antecolica  or  gastroenterostomy  retrocolica  is 
indicated. 

During  the  last  few  years,  i.  e.,  while  Murphy's  button  was  still  made 
use  of  by  our  German  surgeons,  I  witnessed  many  operations  with  and 
without  it,  and  I  am  convinced  that  its  advantage  of  a  more  simple,  and 
therefore  more  rapid,  technic  does  not  compensate  for  its  well  known  dis- 
advantages. We  are  never  sure  that  the  button  will  not  fail  back  into  the 
stomach,  and  in  pyloric  stenosis  its  fate  is  indefinite;  we  do  not  know 
whether  the  narrow  opening  will  functionate  sufficiently,  whether  the  but- 
ton has  actually  passed  or  has  remained  in  the  intestine  (its  passage  may 
have  been  overlooked  by  the  nurses),  and,  provided  everything  goes  well 
until  then,  it  may  even  happen  that  the  button  is  passed  some  weeks  later 
accompanied  by  very  alarming  symptoms  which  cause  the  greatest  anxiety 
to  the  patients  and  also  to  the  physician  not  sufficiently  familiar  with 
tliosc  conditions  (for  example,  after  the  patient  has  left  the  hospital).  All 
of  this  is  obviated  in  a  simple  suture  anastomosis  which,  in  skilful  hands, 
consumes  but  little  more  time  than  the  use  of  the  Murphy  button. 

4.  A  further  indication  for  operative  relief,  and  particularly  for  gas- 
troenterostomy, is  given  by  persistent  hyperacidity,  especially  if  combined 
with  dilatation  of  the  stomach  and  weakness  of  the  expelling  musculature; 
of  eoiirso,  only  in  those  cases  in  which  internal  remedies  have  proven 
inofToctnal  after  a  thorough  trial. 

This  occurs  in  connection  with  the  sequels  of  gastroanastomosis  which 
may  influence  the  function  of  the  stomach  in  various  ways.     We  might 


TREATMENT  213 

suppose,  a  priori,  that  when  anastomosis  is  produced  in  the  deepest  area 
of  the  stomach  a  perfectly  regular  propulsion  of  the  food  would  result. 
Some  authors,  for  example,  Rosenheim,  go  so  far  as  to  assume  the  formo 
Hon  of  a  new  sphincter.  The  latter,  however,  as  Petersen  correctly  re- 
marks, must  first  be  anatomically  proven,  and  this  has  never  yet  been 
done.  The  possibility  of  closure  of  the  anastomosis,  which  has  been  ob- 
served by  Rosenheim,  Carle  and  Fantino,  or,  more  correctly,  the  fact  that 
either  Avater  or  air  is  retained  in  the  stomach,  merely  proves  that  occa- 
sionally a  valve-Iike  closure  of  the  opening  occurs,  not,  however,  that  a 
sphincter  is  formed.  On  the  other  hand,  the  consensus  of  opinion  is,  and 
I  have  often  seen  convincing  proof  of  this,  that  the  propulsion  of  the 
gastric  contents  after  operation  is  more  rapid  than  before.  Certainly  if 
this  were  not  so  the  result  of  the  operation  would  be  most  unfortunate! 
Whether  this  is  due  to  an  increase  of  motility  or  to  a  freer  outflow  can 
hardly  be  decided.  The  absence  of  engorgement  of  the  duodenum  has 
been  regarded  as  indicating  an  increased  motility,  for,  according  to  Hirsch 
and  V.  Mering,  normally,  when  the  duodenum  is  full,  it  exerts  an  inhib- 
itive  reflex  upon  gastric  movement.  In  this  theory  the  fact  has  been  over- 
looked that  in  by  far  the  majority  of  cases  in  which  gastroenterostomy  is 
performed,  stenosis  of  the  pylorus  occurs  as  well  as  a  decrease  or  even 
a  suspension  of  the  propulsion  of  the  ingesta  from  the  stomach  into  the 
duodenum.  Whether  it  is  advisable  in  an  open  pylorus,  as  Kelling  pro- 
poses, to  close  the  passage  from  the  stomach  into  the  duodenum  by  the 
artificial  production  of  stenosis,  and  thus  prevent  the  conditions  which 
have  just  been  pointed  out,  can  only  be  learned  from  surgical  experience, 
reports  of  which  are  still  lacking. 

There  is  no  doubt  that,  in  many  cases,  improvement  in  the  chemism 
of  the  stomach  has  been  brought  about.  The  acidity  value,  more  accu- 
rately the  value  for  the  excretion  of  hydrochloric  acid,  decreases,  perhaps 
less  in  consequence  of  decreased  secretion  than  because  the  bile  which 
regurgitates  into  the  stomach,  possibly  also  the  pancreatic  juice,  neutralizes 
the  acid  gastric  contents.  But  that  such  a  decrease  of  acidity  does  not  take 
place  in  all  cases  may  be  adduced  from  my  own  experiences,  which,  un- 
fortunately, are  not  yet  published,  as  well  as  from  the  reports  of  numerous 
other  authors,  Dunin,  Odcrfeld,  Kausch,  Rosenheim,  Rencki,  Petersen  and 
others.  Nevertheless,  the  decrease  of  acidity  is  so  frequent  that  the  above 
indication  for  gastroenterostomy  in  hyperacidity  must  be  mentioned.  The 
regurgitation  of  bile  and  pancreatic  juice  into  the  stomach — which,  under 
the  present  method  of  performing  enterostomy  between  the  loops  leading  to 
and  awa}^  is  now  usually  prevented — gives  rise  to  but  slight,  if  any,  diffi- 
culty, and  this  is  only  perceptible  by  a  bilious  taste.  Experiments  which 
Joslin  undertook  in  the  year  1897  at  my  suggestion  revealed  decreased 
fat  digestion,  but  this,  as  ISTikolaysen  later  found,  is  only  immediately 
after  the  operation,  and  then  is  replaced  by  normal  conditions.     The  ex- 


214  GASTRIC  ULCER  AND  GASTRIC   HEMORRHAGE 

periments  at  that  time,  however,  were  made  upon  patients  who  had  not 
been  operated  upon;  what  the  results  would  be  after  this  operation  is 
still  to  be  determined. 

5.  In  case  of  perforation,  operation  whenever  possible  should  be  per- 
formed in  the  first  twenty-four  hours;  the  later,  the  worse  the  chances. 
Tn  1895  Pariser  could  report  only  43  cases. 

In  the  year  1896  Weir  and  Foote  compiled  a  table  of  the  cases  of 
perforating  gastric  ulcer  which  had  been  operated  upon,  and  this  showed 
78  cases  with  23  recoveries,  =  29  per  cent.  In  43  cases  the  perforative 
opening  was  situated  upon  the  anterior  wall  of  the  stomach,  11  times  upon 
the  posterior  wall,  and  6  times  on  the  lesser  curvature.  Accordingly,  in  the 
majority  of  cases  this  opening  may  be  found  and  sutured.  In  92  per  cent. 
of  the  cases  the  history  pointed  to  the  diagnosis  of  gastric  ulcer.  The 
importance  of  early  operation  is  very  evident,  for  in  the  cases  that  had 
existed  less  than  twelve  hours  the  mortality  was  39  per  cent.,  in  those  of 
twelve  to  twenty- four  hours  76  per  cent.,  and  in  those  over  twenty-four 
hours  87  per  cent. 

The  number  of  such  cases  rapidly  increased.  In  1900,  Mayo  Robson 
published  statistics  compiled  from  reports  of  English  and  American  hos- 
pitals, comprising  429  cases  with  a  mortality  of  55  per  cent.;  Brunner, 
however,  declares  that  some  cases  were  counted  twice.  In  the  year  1903, 
Brunner  compiled  the  statistics  of  466  cases  upon  whom  operation  for 
gastric  perforation  had  been  performed,  which  gave  a  mortality  of  50  to 
64  per  cent. ;  here  also  the  advantage  of  early  operation  was  clearly  demon- 
strated, for,  among  the  cases  in  which  operation  was  performed  in  the  first 
twelve  hours,  75  per  cent,  recovered !  It  is  well  known  that  the  chances 
of  recovery  for  the  patient  are  much  better  if  the  stomach  at  the  time 
of  perforation  is  empty. 

Unfortunately,  under  some  circumstances,  we  cannot  determine  whether 
in  the  case  in  question  we  are  dealing  with  a  perforative  peritonitis  due  to 
ulcer  of  the  stomach  or  not.  I  have  seen  a  case  of  this  kind  terminate  in 
recovery,  yet  during  its  course  and  even  later  no  positive  diagnosis  was 
possible. 

Brunner  collected  reports  of  17  cases  recovering  without  operation,  as 
against  466  who  were  operated  upon  in  the  same  period  of  time.  This 
number,  17,  has  been  increased  by  a  recent  English  report  of  a  few  cases 
{Briiish  Med.  Journal,  Feb.  20,  1904,  H.  Whiteford),  which,  however, 
is  not  quite  trustworthy. 

6.  By  some  authors  the  pure,  uncomplicated  ulcer  has  also  been  desig- 
nated as  suitable  for  surgical  treatment.  I  do  not  agree  with  this.  An 
uncomplicated  ulcer  heals  readily  under  internal  treatment;  if  healing 
does  not  thus  take  place  the  ulcer  is  not  uncomplicated,  but  is  combined 
with  changes  which  resist  the  regenerative  process.  Under  such  circum- 
stances, the  indication  for  operation  has  been  assumed  from  the  fact  that 


TREATMENT  215 

an  ulcer  may  occasionally  undergo  malignant  degeneration.  This  is  anal- 
ogous to  the  proposition  to  operate  upon  every  appendix  in  which  there 
are  signs  of  inflammation,  because  subsequently  perforation  might  result. 
But  in  the  one  instance,  as  in  the  other,  this  is  but  a  remote  possibility, 
and  in  the  case  of  ulcer  the  danger  is  very  slight,  for  the  number  of  cases 
cured  decidedly  preponderates  over  those  of  uncured  ulcer  of  the  stomach. 
As  shown  above,  this  proportion  is  about  2 : 1,  but  in  reality  only  a  small 
fractional  part  of  unhealed  cases  undergo  malignant  degeneration. 

Finally,  as  a  general  indication  for  operative  interference,  immaterial 
which  of  the  conditions  enumerated  comes  into  question,  it  must  be  borne 
in  mind  that  operation  only  removes  the  existing  pathologic  focus,  not  the 
predisposition  to  future  relapses.  Therefore,  the  appearance  of  a  new 
ulcer,  another  hemorrhage,  fresh  adhesions,  is  by  no  means  impossible 
after  a  successful  operation,  and  Braschr  has  described  a  case  in  which 
fatal  hemorrhage  occurred  immediately  after  gastroenterostomy  had  been 
performed.  Consequently  those  surgeons  are  right  who  proceed  to  operate 
only  when  all  the  remedies  of  internal  treatment  have  been  exhausted, 
that  is,  when  the  condition  of  the  patient  permits  no  further  delay.  That 
cases  of  acute  perforation  are  exceptions  to  this  is  self-evident.  In  his 
opinion,  and  also  in  the  warning  against  exaggeration  of  the  indications 
for  operation,  as  expressed  by  Sahli  before  the  Twentieth  Congress  of 
Internal  Medicine  in  1902,  I  concur  almost  absolutely. 

It  should  never  be  forgotten  that  the  process  of  healing  after  these 
operations  is  not  always  smooth  and  unbroken.  I  do  not  refer  to  the 
danger  of  the  so-called  vicious  circle,  i.  e.,  the  regurgitation  of  the  gastric 
contents  into  the  false  intestinal  loop  in  gastroenterostomy,  because  this 
perhaps  is  avoided  by  the  simultaneous  enterostomy,  but  I  must  call  atten- 
tion to  the  occasional  development  after  operation  of  peptic  intestinal 
ulcers  which  are  a  new  source  of  difficulty  and  danger  to  the  patient. 
Neumann  has  recently  reported  a  very  instructive  case  of  this  kind,  and 
in  my  opinion  given  very  valuable  advice,  which  is,  that  in  gastric  dilata- 
tion with  pylorospasm  and  hyperacidity  we  should  first  perform  jejunos- 
tomy  and  then  allow  the  stomach  to  rest.  Later,  if  necessary,  and  under 
favorable  circumstances,  gastroenterostomy  may  be  performed. 

Mineral  Spring  Treatment. — Since  remote  times  the  hot  Glauber  Salt 
Springs,  particularly  those  of  Carlsbad,  have  enjoyed  a  well  deserved  repu- 
tation, and  there  is  no  doubt  that  the  treatment  of  ulcer  at  this  resort, 
when  carefully  conducted  and  too  large  quantities  of  water  at  one  time 
are  not  consumed,  is  frequently  crowned  by  the  best  results.  When  the 
disturbances  on  the  part  of  the  digestive  apparatus  are  relieved,  the  pa- 
tient should  endeavor  to  recuperate  and  gain  strength  by  a  sojourn  at 
Franzensbad,  Elster,  Eippoldsau,  Pyrmont,  etc.,  in  the  mountains  or  at 
the  sea,  with  the  proviso  that  he  can  secure  suitable  food,  which  is  best 
when  the  family  does  its  own  cooking.     Since,  however,  many  patients 


216  GASTRIC   ULCER  AND   GASTRIC   HEMORRHAGE 

prefer  a  mineral  spring  cure  to  going  to  bed  at  home,  and  many  can  only 
avail  themselves  of  the  short  period  of  four  to  six  weeks,  Carlsbad  for 
these  is  always  the  best  place,  because  the  opportunity  there  for  dietetic 
sins  is  less  than  elsewhere.  After  Carjsbad,  Neuenahr,  Ems,  Franzensbad, 
Homburg  and  Vichy  are  to  be  recommended. 

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LITERATURE  217 

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Eysenhardl,  quoted  by,  Struppler. 
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Joum.,  November  30th,  1901. 
Frz.  Fink,  "Erfolge  der  Karlsbader  Cur  u.  s.  w."    Wien  und  Leipzig,  1903. 
L.  Fischl,  "Zur  Therapie  der  Hyperaciditat  des  Magens."    Prnger  med.  Woch- 

enschr.,  1903,  Nr.  11. 
Fleiner,   "Therapie  des  Magengeschwiirs."    XX.  Congr.  }.  innere  Med.,  Wies- 
baden, 1902. 
Friedenthal,  "  Ernahrungsschwierigkeiten  bei  Ulcus  ventriculi."    Inaug.-Dissert., 

Berlin,  1899. 
Fvtterer,  "Treatment  of  Chronic  Round  Ulcer  of  the  Stomach."     Joum.  Amer 

Med.  Association,  January,  1902. 
Gaillard,   "Syphilis  gastrique  et  ulcere  de  I'estomac."     Arch,  gener.  de  mM., 

1886. 
D.  Gerhardt,  "Ueber  geschwiirige  Processe  im  Magen."     Virchow's  Arch.,  Bd 

CXXVII,  p.  85. 
Gluczinsky,  "Ueber  die  Behandlung  des  peptischen  Magengeschwiirs."     Wiener 

klin.  Wochenschr.,  1900,  Nr.  49. 
Greenoiigh  and  Joslin,  "Gastric  Ulcer  at  the  Massachusetts  General  Hospital." 

Amer.  Joum.  of  Med.  Sciences,  August,  1899. 
Hampeln,   "  Gastro-intestinale   Blutungen."    St.   Petersburger  med.   Wochenschr., 

1891,  Nr.  8. 
Harttung,    "Ueber    Faltenbildung    und    hamorrhagische    Erosionen."    Deutsche 

Wochenschr.,  1890,  p.  847. 
Hemmeter,  "Zur  Histologie  der  Magenschleimhaut."    Arch.  f.  Verdauungskrankh., 

Bd.  IV,  p.  24. 
A.  Hirsch,  "Beitrage  zur  motorischen  Function  des  Magens."    Centralbl.  f.  klin 

Med.,  1892,  Nr.  47. 
P.  Hirsch] eld,  Discussion.     XX.  Congr.  f.  innere  Med.,  Wiesbaden,  1902. 
W.  C.  Hood,  "  Haematemesis  with  Special  Reference  to  that  Form  met  with  in 

Early  Adult  Female  Life."     London,  1892. 
Kausch,  "Ueber  functionelle  Ergebnisse  nach  Operationen  am  Magen."    Grenz- 

gebiete,  Bd.  IV,  p.  347. 
G.    Kelling,    "  Sympathischer    Reizzustand   bei    Magengeschwiir."     Wiener   med. 

Wochenschr.,  1902,  Nr.  48. 
Kocher,    "  Indicationen    zur   Operation    bei    Ulcus   ventricuH."     Correspondenzbl. 

/.  Schweizer  Aerzte,  15  October,  1898. 
G.  Kohler,  "Beitrag  zur  Kenntnis  der  Symptomatologie  bei  Ulcus  ventriculi  sim- 
plex."    Inaug.-Dissert.,  Berlin,  1895. 
Korte,   " Chirurgische   Behandlung  des  Magengeschwiirs."     Arch.  }.   klin.   Chir., 

Bd.  LXIII,  p.  1. 
Krafft,  "Beitrag  zur  Pathogenese  des  Ulcus  ventriculi."    HospUalstidende,  1900. 
Kronlein,  "Ueber  Ulcus  und  Stenosis  des  Magens  nach  Trauma."    Arch.  f.  Chir. 
L.  Kuttner,  "  Magenblutungen  und  deren  Beziehungen  zur  Menstruation."     Ber- 
liner klin.  Wochenschr.,  1895,  Nr.  7. 
Lange,  Deutsche  Klinik,  1860,  p.  90. 


i218  GASTRIC  ULCER  AND  GASTRIC   HEMORRHAGE 

Langerhans,  "  Ungewohnliche  Art  der  hamorrhagischen  Erosionen  des  Magens." 

Virchow's  Arch.,  Bd.  CXXIV,  p.  373. 
Letiille,  CompL  rend.,  1888,  Vol.  CVI. 
V.  Leube,  "Ueber  die  Erfolge  der  internen  Behandlung  des  Magengeschwiirs  und 

die  Indicationen    zum    chirurgischen  Eingreifen  in  dieselbe    Grenzgebiete," 

Bd.  II.     Rejerat  auf  dem  XXVI.  Chirurgen-Congress,  1897. 
Leuk,  "  Untersuchungen  zur  pathologischen  Anatomie  des  menschlichen  Magens," 

etc.    Zeitschr.  /.  klin.  Med.,  1899,  Bd.  XXXVII. 
Litten,  "Ulcus  ventriculi  tuberculosum."     Virchow's  Archiv,  Bd,  LXVII,  p.  615. 
L.  Lorell-Keays,"  A  case  of  Double  Perforating  Gastric  Ulcer."    Brit.  Med.  Journ. 

December  loth,  1903. 
Luxenburg  und  Jawadzki,  "  Ein  Fall  von  Ulcus  ventriculi  rotundum  auf  Grund 

syphilitischer  Gefasserkrankung."     Wiener  Med.  Presse,  1894,  Nr.  50  und  51. 
J.  N.  ^[arshall,  "Two  Gases  of  Gastric  Ulcer  in  which  Symptoms  arose  suggesting 

Perforation  of  the  Stomach."     Glasgow  Med.  Journ.,  February,  1890. 
A.  Mathieu,  "Traite  des  maladies  de  I'estomac  et  de  I'intestin."     Paris,  1901. 
Mathicu  et  Roux,  "Sur  un  cas  d'ulcerations  uremiques  de  I'estomac  et  de  I'intestin 

grele."     Arch.  gen.  de  mcd.,  Janvier,  1902. 
V.  Mering,  "Zur  Function  des  Magens."     Congr.  f.  innere  Med.,  Berlin,  1897. 
H.  Merkel,  "Ein  Fall  von  chron.  Magengeschwiir  mit  tiidtlicher  Blutung  aus  der 

arrodirten  linken  Nierenvene."     Virchow's  Archiv,  1903,  Bd.  CXXIII. 
E.  Mey,  "  Profuse  Magenblutungen  und  Hydrops  anasarca  als  initiale  Symptome 

des  Magencarcinoms."     I naug. -Dissert.,  Dorpat,  1891. 
Michailoic,  "  Ein  Fall  von  erfolgreichem  chirurgischen  Eingriff  bei  Blutungen  aus 

einem  Magengeschwiir."     Grenzgebiete,  1901,  p.  535. 
V.  Mikulicz,  "Die  chirurgische  Behandlung  des  chron.  Magengeschwiirs."     Ber- 
liner klin.  Wochenschr.,  1897,  Nr.  23. 
Minkowski,  Discussion.     XX.  Congr.  /.  innere  Med.  zu  Wiesbaden,  1902. 
tS'.  Mintz,  "Hamorrhagische  Magenerosionen."    Zeitschr.  /.  klin.  Med.,  Bd.  XLVI, 

Heft  1  to  4. 
Marfan,  "Troubles  et  lesions  gastriques  dans  la  phthisie  pulmonaire."     Paris, 

1887. 
William  Murrell,  "The  Value  of  Age  and  Sex  as  Etiological  Factors,"  etc.     Med. 

Press  and  Circular,  October  23d,  1901. 
/.  H.  Musser,  "Tubercular  Ulcer  of  the  Stomach."    Philadelphia  Hosp.  Reports, 

1890,    Vol.    I. 
0.  Midler  und  Hccker,  quoted  by  Struppler. 
Xauurrk,  "  Mykotisch-peptisches  Magengeschwiir."    MUnchener  med.  Wochenschr., 

1895,  Nr.  38  und  39. 
V.  Openchowski,  "Zur  pathol.  Anatomie  der  geschwiirgen  Processe  im  Magen- 

Darnitractus."     Virchow's  Archiv,  Bd.  CXVII,  p.  347. 
ir.  Ord,  "On  the  Diagnosis  and  Treatment  of  Gastric  Ulcer."     Amer.  Journ.  of 

Med.   Sci.,   June,    1889. 
O.'^terspey,  "Die  Blutuntersuchungen  bei  Magenkranken."    Berliner  klin.  Woch- 
enschr., 1892,  Nr.  12  und  13. 
Parisrr,  "  Discussionsbemerkungen  im  XX.  Congr.  f.  innere  Med.  zu  Wiesbaden. 

Ueber   hamorrhagische    Erosionen   der   Magenschleimhaut."    Berliner   klin. 

Wochenschr.,  1900,  Nr.  43. 


LITERATURE  219 

Paulicki,  Virchow's  Archiv,  Bd.  XLIV. 

Petersen  und  Machol,  "Beitrage  zur  Pathologie  iind  Therapie  gutartiger  Magen- 

krankheiten. "     v.  Bruns'  Beitrage  zur  klin.  Chir.,  Bd.  XXXIII,  p.  297. 
Petruschky,  "Zur  Diagnose  und  Therapie  des  primaren  Ulcus  ventriculi  tubercu- 

losum."    Deutsche  med.  Wochenschr.,  1899,  Nr.  24,  und  1901,  p.  394. 
A''.  Platter,  "Ueber  Erosionen  der  Magenschleirahaut."    I naug. -Dissert.,  Zurich, 

1901. 
Reichard,  "Freie  Vereinigung  der  Chirurgen  Berlins."    Deutsche  med.  Wochen- 

schr.,  1890,  p.  327. 
R.  Reinhard,  "Ulcus  ventriculi  simplex  mit  Tunioren."    Inaug. -Dissert.,  Berlin, 

1888. 
R.  Rencki,  "  Diagnostische  Bedeutung  der  mikroskop.  Blutuntersuchung  bei  Car- 

cinom  und  Ulcus  ventriculi."    Arch.  J.  Verdauungskrankh.,  1901.     "Ueber 

die  functionellen   Ergebnisse   nach   Operationen  am  Magen  bei  Ulcus  und 

gutartiger  Pylorusstenose."    Grenzgebiete,  1901,  Bd.  VIII. 
Rheinwald,    "Die   Behandlung   des   einfachen   Magengeschwiirs  mit   Karlsbader 

Curen."    I  naug. -Dissert.,  Tubingen,  1898. 
F.  Riegel,  "Beitrage  zur  Diagnostik  der  Magenkrankheiten."    Zeitschr.  j.  klin. 

Med.,  Bd.  XII,  Heft  5. 
Mayo  Robson,  "A  Clinical  Lecture  on  the  Complications  of  Gastric  Ulcer  and  Its 

Treatment."    Brit.  Med.  Journ.,  February  2d,  1901. 
Rosenheim,  "Ueber  seltene  Complicationen  des  runden  Magengeschwiirs."    Ber- 
liner klin.  Wochenschr.,  1889,  p.  1031.     "Ueber  die  chirurgische  Behandlung 

der  Magenkrankheiten."     Deidsche  med.  Wochenschr.,  1895,  Nr.  1. 
Schloffer,  "Operationen  bei  gutartiger  Magenerkrankung."    v.  Bruns,  Beitrage  zur 

klin.  Chir.,  Bd.  XXXII,  Heft  2. 
A.    Schmidt,    "Pathogenese    des   Magengeschwiirs."     Verhandl.    XX.    Congr.    f. 

innere  Med.,  Wiesbaden,   1902. 
Schiltz,  "Zur  Differentialdiagnose  des  Ulcus  ventriculi."     XVII.  Congr.  f.  innere 

Med.,  Wiesbaden,  1899. 
J.  Schulz,   "Ueber  Dauererfolge  der  internen  Therapie  des  Ulcus  ventriculi." 

Grenzgebiete,  1903,  Bd.  XI. 
Schwarz, "  Beitrage  zur  Pathologie  und  chirurgischen  Therapie  des  penetrirenden 

Magengeschwiirs."     Grenzgebiete,  1900. 
J.  Sigel,  "Zur  Diagnose  des  Magencarcinoms."    Berliner  klin.  Wochenschr.,  1904, 

Nr.  12  und  13.        ^ 
M.  Silberrnark,  "Rundes  Magengeschwiir  nach  Trauma."    Wiener  med.   Woch- 
enschr., 1902,  Nr.  21  und  22. 
Simmonds,    "Ueber   Tuberculose   des   Magens."    Munchener  med.    Wochenschr., 

1900,  Nr.  10. 
V.  Sohlern,  "Einfluss  der  Ernahrung  auf  die  Entstehung  des  Magengeschwiirs." 

Berliner  klin.  Wochenschr.,  1889,  Nr.  13  und  14. 
Spicker,  "Spontan  geheilte  Perforationsperitonitis  bei  Ulcus  ventriculi."  Deutsche 

med.  Wochenschr.,  1903,  Nr.  1. 
A?'.epp,  "Zur  Behandlung  des  chron.  Magengeschwurs."    Festschr.  d.  Nilrnberger 

drztl.  Vereins,  1902. 
Stern,    "Ueber   traumatische   Erkrankungen   der  Magenschleimhaut."    Deutsche 

med.  Wochenschr.,  1899,  Nr.  23. 


220  GASTRIC  ULCER  AND  GASTRIC  HEMORRHAGE 

H.  Strauss  und  Bleichroder,  "  Untersuchungen  iiber  den  Magensaftfluss."    Grem- 

gebiete,  1903,  Bd.  XII,  Heft  1. 
Struppler,  "Ueber  das  tuberciilose  Magengeschwiir."    Zeitschr.  /.  TvbercuLose  und 

Heilstdttenwesen,  Bd.  I,  Heft  4. 
Talamon-Balzer,  "Phthisie  locale;  ulcerations  tuberculeuses  de  I'estomac  et  de 

I'intestin."  •  Bullet.  Soc.  Anatom.,  1878,  p.  374. 
S.  Talma,  "Untersuchungen  iiber  Ulcus  ventriculi  simplex."    Zeitschr.  f.  klin. 

Med.,  Bd.  XVII,  Heft  1  und  2. 
M.  Tiegd,  "Beitrag  zur  Casuistik  todtlicher  Magenblutungen."    Miinchener  med. 

Wochmschr.,  1902,  Nr.  47. 
Dalla  Vedova,  "  Experimenteller  Beitrag  zur  Kenntnis  des  Ulcus  ventriculi."  Arch. 

f.  Verdauungskrankh.,  Bd.  VIII,  Heft  3. 
Walko,  "Ueber  die  Behandlung  des  Ulcus  ventriculi  mit  Olivenol."    Centralbl. 

f.  innere  Med.,  1902,  Nr.  45. 
M.  Weiss,  "  Magenblutung  bei  Typhus  abdominalis."     Wiener  Med.  Presse,  1887. 
Frz.  Wamecke,  "  Indicationen  zur  operativen  Behandlung  des  Ulcus  ventricuU." 

Preisschr.,  Gottingen,  1903. 
van  Yzeren,  "Die  Pathogenesis  des  chron.  Magengeschwiirs."    Zeitschr.  f.  klin. 

Med.,  Bd.  XLIII,  p.  181.     (Also  see  the  literature  in  Ewald's  article  "Magen- 

krankheiten,"  Eulenburg's  Real-Encyclopddie,  1897,  Bd.  XIV.) 


GASTRIC    AND    INTESTINAL   CARCINOMATA 

By  J.  BOAS,  Berlin 

When  a  case  of  gastric  or  intestinal  carcinoma  presents  itself  before 
us  to-day,  we  judge  it  by  very  different  standards  from  those  employed 
about  twenty  years  ago.  At  that  period,  i.  e.,  in  the  days  of  Billroth,  Pean 
and  Rydygier,  our  chief  endeavor  was  to  make  the  diagnosis^  and  at  that 
a  diagnosis  of  general  visceral  cancer.  Whether  the  cancer  was  located 
in  the  stomach  and  in  what  part  of  the  same,  whether  in  the  small  or 
large  intestine,  whether  in  the  omentum  or  the  liver,  in  the  gall-bladder 
or  the  pancreas,  was  of  scientific  but  not  of  therapeutic  interest.  In  every 
case  the  patient  was  doomed;  to  him  accurate  proof  that  this  or  that 
portion  of  his  viscera  showed  malignant  degeneration  was  of  no  avail. 

In  the  last  two  decades  our  views  concerning  these  affections  have 
undergone  a  complete  change  the  influence  of  which  no  physician,  however 
pessimistic  he  may  be  regarding  carcinoma  in  general,  can  withstand. 
This  change,  as  is  well  known,  has  been  brought  about  by  surgery,  and  no 
genius  has  yet  appeared  to  teach  us  how  to  cure  by  internal  remedies. 
The  knife  alone  can  permanently  remove  the  difficulty,  or,  although  very 
rarely,  bring  amelioration  which  lasts  for  years. 

This  advance,  which  is  largely  due  to  the  high  development  of  anti- 
sepsis and  asepsis,  but  also  to  an  enormous  impetus  to  the  technic  of 
abdominal  surgery,  imposes  upon  internal  medicine  new  obligations. 

The  diagnosis  must  be  made  early.  It  must  accurately  define  the  seat 
of  the  affection,  it  must — when  possible — embrace  the  consideration  whether 
the  malignant  focus  is  circumscribed  or  already  generalized.  It  must  de- 
cide whether  or  not  any  complications  are  present  which  may  influence 
the  course  of  the  operation,  and,  finally,  it  must  determine  whether  at  the 
given  moment  the  patient's  strength  will  warrant  surgical  interference. 

If  it  were  possible  in  a  case  of  gastric  or  intestinal  carcinoma  to  decide 
all  these  points  with  certainty,  the  results  of  operative  treatment  would 
be  decidedly  more  favorable  than  they  are  at  present,  and  this  would  doubt- 
less influence  strongly  our  decision  as  to  conservative  or  active  treatment. 
Although,  in  fact,  this  goal  is  still  remote,  our  chief  endeavor  must  be 
to  arrive  as  near  as  possible  to  the  previously  mentioned  postulates.  For 
this  purpose  not  only  a  comprehensive  diagnosis,  but  also  the  earliest 
recognition  of  the  affection  from  all  points  of  view  is  necessary. 

221 


222  GASTRIC   AND  INTESTINAL  CARCINOMATA 

After  these  preliminary  remarks  I  shall  describe  a  typical  case  of  gas- 
tric carcinoma,  the  delineation  of  other  less  typical  forms  will  follow  this, 
and  I  shall  then  describe  a  case  of  carcinoma  of  the  large  intestine  and 
of  the  rectum;  for  cancer  of  the  small  intestine,  on  account  of  its  rarity, 
a  brief  description  will  suffice;  in  conclusion  I  shall  summarize  the  treat- 
ment of  gastrointestinal  carcinomata. 


ETIOLOGY 

In  examining  the  history  of  this  patient  it  will  be  noted  that  he  is 
about  50  years  of  age,  and  up  to  the  time  of  his  present  affection  he  has 
usually  been  well ;  above  all,  he  has  had  no  gastric  affection.  Until  within 
the  last  few  months  he  could  eat  anything  and  digest  it.  His  present 
illness  dates  from  this  periods 

Let  us  here  pause  for  a  moment,  since  these  data  are  of  great  importance 
as  indicating  the  character  of  the  affection.  When  a  patient,  who  has 
reached  the  age  at  which  cancer  is  likely  to  occur,  tells  us  that  he  has 
never  been  ill,  while  his  appearance  denotes  the  existence  of  a  serious 
malady,  we  must  primarily  think  of  a  malignant  disease.  Not  that  this 
report  is  in  itself  of  vital  importance,  but  it  indicates  the  direction  in 
which  we  must  search  for  the  underlying  affection. 

We  have  heard  from  this  patient  how  his  ailment  gradually  developed 
to  its  present  extent.  We  are  especially  interested  in  learning  whdt  the 
first  symptoms  were,  and  whether  these  gave  any  indication  of  the  gravity 
of  the  condition. 

His  report,  in  brief,  is  the  following:  On  taking  food,  he  has  now  and 
tlien  a  sensation  of  pressure  which  is  not  actual  pain  in  the  pit  of  the 
stomacli,  occasionally  there  is  eructation  of  gas  but  not  of  food,  and  with 
this  a  gradually  increasing  loss  of  appetite.  This  is  alxtut  all.  We  see 
the  justification  of  Brinton's  expression  in  regard  to  the  onset  of  gastric 
carcinoma :  "  Obscure  in  its  symptoms."  Nevertheless,  any  one  who  has 
had  mucli  experience  in  the  realm  of  visceral  carcinomata  will  not  escape 
the  conviction  that  this  latent  and  indefinite  onset  forms  the  rule-  to  which 
there  arc,  however,  numerous  exceptions  of  practical  importance.  Among 
these  belongs  the  sudden  onset  with  severe  symptoms:  In  the  midst  of 
apparently  normal  health  the  patient  begins  to  vomit,  and  to  the  surprise 
of  those  about  him,  even  of  the  physician,  this  continues  and  steadily 
becomes  more  copious  so  that  in  a  few  days,  or  at  most  in  a  few  weeks, 
the  patient  emaciates  markedly,  loses  his  appetite,  and  becomes  feeble  and 
debilitated;  briefly,  he  shows  such  extreme  emaciation  that,  provided  no 
severe  functional  or  central  affection  is  present — in  this  connection  I  refer 
particularly  to  the  gastric  crises  and  the  periodical  vomiting  described  by 
V.  Loydon — without  more  ado  the  suspicion  of  malignant  disease  is  aroused. 

Another  mode  of  onset  of  practical  significance  is  when  gastric  car- 


ETIOLOGY  223 

cinoma  is  most  surprisingly  ushered  in  by  decided  and  threatening  hema- 
temesis  or  melena.  This  naturally  leads  us  to  think  of  a  simple  ulcer  of 
the  stomach  or  of  the  duodenum,  and  if  etiologic  factors  are  favorable,  per- 
haps also  of  cirrhosis  of  the  liver  or  some  other  form  of  disease  leading 
to  stasis  of  the  portal  vein;  but  the  further  course  shows  that  a  scarcely 
avoidable  error  has  been  made.  In  connection  with  the  hemorrhage  isolated 
symptoms  occur,  or  all  the  symptoms  of  a  malignant  course  may  be  re- 
quired to  make  the  diagnosis  of  cancer  more  positive  from  day  to  day. 
Practically  we  may  easily  assume  that  a  gastric  ulcer  is  undergoing  malig- 
nant degeneration,  but  it  has  been  proven  with  certainty  (by  May,  Ewald 
and  others)  that  such  a  course  by  no  means  always  permits  the  conclusion 
of  a  preceding  ulcer.  I  shall  refer  to  this  again  in  the  description  of 
carcinomatous  ulcer. 

But  such  occurrences  as  have  been  mentioned  are  usually  exceptional. 
The  typical  onset,  as  we  unfortunately  know,  is  usually  so  slightly  charac- 
teristic that  the  last  thing  the  patient  and  his  relatives  think  of  is  the 
development  of  a  malignant,  incurable  disease.  And  thus  it  happens  that 
at  first,  according  to  their  degree  of  education,  they  become  their  own 
physicians  and  employ  all  sorts  of  home  remedies  and  occasionally  purga- 
tives up  to  a  period  when  every  effort  at  internal  or  surgical  treatment 
is  hopeless.  But  with  careful  and  comprehensive  professional  treatment 
from  the  first,  all  concerned  will  have  an  expectant  attitude.  The  wise 
physician  will  reckon  on  the  possibility  of  a  beginning  malignant  affection, 
but  because  of  the  absence  of  definite  symptoms,  he  will  refrain  from 
expressing  his  fears,  and  not  cause  unnecessary  fright  and  distress. 

At  the  onset,  I  purposely  mention  the  difficulties  in  the  recognition 
of  the  disease.  It  will  be  seen  that  the  demand  of  many  surgeons  for  an 
early  diagnosis  is  scarcely  justified,  for  we  cannot  make  a  diagnosis  before 
we  have  the  patient.  In  the  chapter  upon  treatment  we  shall  also  consider 
the  fact  that,  even  with  an  early  diagnosis,  rapid  surgical  intervention  is 
sometimes  prevented  by  the  stress  of  circumstances. 

After  this  brief  digression,  we  return  to  the  further  course  of  the  dis- 
ease as  described  by  our  patient.  He  states  that  in  addition  to  the  slight 
difficulties  at  the  onset  disturbances  of  more  serious  nature  now  and  then 
occurred;  there  was  pressure,  also  pain  in  the  pit  of  the  stomach  which 
occasionally  extended  from  the  left  side  posteriorly  into  the  back,  radiating 
also  to  the  shoulder-blade.  Sometimes  the  patient  mentions  a  symptom 
that,  so  far  as  known  to  me,  is  nowhere  recorded — a  peculiar  grating  in 
the  gastric  region  as  of  two  surfaces  rubbing  against  each  other.  I  have 
heard  this  symptom  described  in  the  same  manner  by  several  patients, 
so  that  in  enumerating  the  subjective  disturbances  it  appears  to  me  to  be 
of  consequence.  Now  and  then  vomiting  occurs,  at  first  rarely  and  in 
slight  amount,  in  the  last  few  weeks  more  frequently  and  more  copiously. 
The  vomitus  consisted  of  the  ingested  food  which,  in  the  first  stages, 
16 


224  GASTRIC  AND  INTESTINAL  CARCINOMATA 

showed  no  alteration  in  appearance,  but  lately  it  has  now  and  then  been 
somewhat  brownish.  After  vomiting  the  patient  is  temporarily  relieved. 
At  first  he  lost  some  flesh;  in  the  last  few  weeks  the  weight  has  declined 
rapidly,  and  hand  in  hand  with  this  there  has  been  a  marked  decrease  in 
strength;  the  appetite  is  wholly  lost. 

This  is  the  stage  in  which  patients  with  carcinoma  of  the  stomach 
usually  present  themselves  to  the  physician.  Clear  as  the  course  of  the 
development  appears,  and  strongly  as  the  individual  points  favor  a  malig- 
nant disease,  we  must  not  forget  that  other  severe  but  not  actually  ma- 
lignant processes  may  have  the  same  or  a  very  similar  course  of  develop- 
ment. I  refer,  for  example,  to  the  cases,  recently  so  accurately  studied, 
of  liypertrophic  stenosis  of  the  pylorus,  the  symptoms  of  which  closely 
resemble  those  just  described.  Cicatricial  stenosis  of  the  pylorus  also 
may  remain  latent  for  a  long  time,  and  only  when,  by  a  sudden  and  occa- 
sional cause,  the  musculature  is  insufficient,  may  show  symptoms  which 
very  closely  resemble  in  severity  and  extent  closure  by  a  malignant  process. 

Only  an  accurate  clinical  analysis  of  the  case  will  decide  whether  the 
very  suggestive  reports  of  the  patient  find  their  explanation  in  the  objective 
examination.  While  the  patient  was  undressing  it  was  noted  that  the 
extraordinary  extent  of  the  disturbance  in  nutrition  was  most  obvious  from 
the  upper  to  the  lower  extremity.  The  musculature  was  soft  and  flabby, 
the  subcutaneous  connective  tissue  thin,  atrophic  and  without  fat,  the  skin 
itself  could  readily  be  lifted  in  folds.  The  tongue  was  coated  at  the  tip 
and  borders.  From  the  present  stand  of  gastric  pathology  too  much  im- 
portance cannot  be  attached  to  the  condition  of  this  organ.  Various 
factors  here  come  into  consideration  (tobacco  and  alcohol,  their  use  and 
abuse,  fissures,  inflammation  of  the  tonsils  and  pharynx,  greater  or  less 
cleanliness  of  the  oral  cavity)  so  that  the  relation  between  gastric  diffi- 
culties and  the  tongue  cannot  be  accurately  determined.  In  contrast  to 
Leser,  I  do  not  attach  much  importance  to  the  small  miliary  and  sub- 
iniliary  angiomata  which  this  patient  also  showed,  for,  in  my  experience, 
which  coincides  with  that  of  Gebele,  this  is  not  rare  in  non-carcinomatou» 
cases,  particularly  in  the  aged. 

After  the  patient  had  removed  his  clothes  he  was  systematically  ex- 
amined in  the  usual  manner.  To  avoid  taking  up  unnecessary  time  I 
shall  state  at  once  that  the  examination  of  the  heart  and  lungs  revealed 
normal  conditions. 

In  the  examination  of  the  abdomen  I  must  promptly  emphasize  the 
importance  of  inspection  of  the  abdomen,  for  this  method  furnishes  a  ful- 
ness of  diagnostic  aids  which  can  only  be  recognized  by  experience.  First, 
the  configuration  of  the  abdomen  must  be  noted,  and  the  deviations  in 
both  its  halves  carefully  compared.  To  the  right  of  the  median  line  a 
relief-like  projection  is  then  noted,  a  slight  prominence,  which  on  deep 
inspiration  descended,  and  upon  expiration  rose  again  to  its  old  position. 


ETIOLOGY  225 

I  shall  revert  io  this  later.  But  another  very  remarkable  phenomenon 
was  noted !  From  time  to  time  a  second  relief  was  seen  in  the  left  hypo- 
chondrium,  rising  suddenly  and  prominently,  almost  like  a  mound,  from 
the  level  of  the  abdomen,  and  after  a  brief  time  sinking  to  its  old  position 
of  rest. 

While  inspecting  the  abdomen  carefully,  and  at  the  conclusion  of  this 
phenomenon,  a  peculiar  gurgling  murmur  was  heard. 

What  does  this  phenomenon  mean?  It  will  perhaps  be  said  that  it 
denotes  peristaltic  unrest  of  the  stomach,  as  was  first  described  in  a  classical 
manner  by  Kussmaul,  or,  as  the  French  term  it,  "  peristaltism."  But  if 
this  sign  which  was  found  to  recur  at  brief  intervals  and  always  to  run  the 
same  course  be  more  accurately  examined,  we  may  convince  ourselves  that 
it  is  not  from  true  peristaltic  action.  On  the  contrary,  it  resembles  a 
tonic  contraction  which  does  not  develop  further  but  remains  localized. 

The  picture  is  so  fascinating  that  when  the  phenomenon  is  at  its 
height  we  cannot  refrain  from  grasping  the  prominence  with  the  hands. 
We  feel  a  hard,  contracted  mass  which  resembles  the  uterus  during  a  pain. 
No  doubt  this  is  the  fundus  of  the  stomach.  We  designate  this  process 
"gastric  rigidity/'  and  this  is  analogous  to  the  nomenclature  Nothnagel 
proposed  for  similar  processes  in  the  intestine,  to  which  we  shall  refer 
later. 

This  sign,  to  which  I  have  recently  again  called  attention,^  was  ob- 
served about  fifty  years  ago  by  no  less  a  one  than  Cruveilhier,^  and  I 
cannot  refrain  from  quoting  what  he  says  of  this  symptom  in  his  great 
"  Traite  d'anatomie  pathol.  generale,"  as  follows : 

"  La  dilatation  hypertrophique  de  I'estomac  s'observe  dans  les  cas  ou 
I'ampliation  de  I'estomac  se  faisant  graduellement,  la  contractilite  et  la 
force  elastique  de  Forgane  n'ayant  pas  ete  vaincues,  il  y  a  resistance  a  la 
distension  de  la  part  de  la  tunique  musculeuse,  qui  se  contracte  energique- 
ment  sur  les  aliments,  les  boissons  et  les  gaz,  qu'il  contient.  Cette  con- 
traction qui  se  manifeste  d'une  maniere  intermittente  est  facile  a  recon- 
naitre  pendant  la  vie  par  un  durcissement  douloureux  analogue  aux  legeres 
contractions  uterines,  qui  precedent  les  grands  douleurs  de  V accouchement. 
Pendant  toute  la  duree  de  cette  contraction  la  forme  de  Vestomac  se  dessine 
a  travers  les  parois  abdominales  et  cJiez  les  sujets  amaigris  on  peut  en  suivre 
tous  les  contours  a  I'oeil  et  au  doigt.  C'est  a  mon  avis  un  grand  moyen 
de  diagnostic." 

In  this  description  the  process  of  gastric  rigidity  is  so  masterfully 
portrayed  that  little  of  importance  can  be  added. 

My  own  experience  has  taught  me  that  several  stages  of  gastric  rigidity 
may  be  diiferentiated :  1.  Slight  contractions  extending  only  to  small  areas 

*  Boas,  Deutsche  med.    Wochenschr.,  1902,  Nr.  10. 

'Cruveilhier,  "Traits  d'anatomie  pathol.  g6n§rale,"  1852,  T.  II,  p.  857. 


226  GASTRIC  AND  INTESTINAL  CARCINOMATA 

of  the  fundus,  which  are  felt  as  increased  tonicity  lasting  but  a  few  seconds 
(abortive  gastric  rigidity) ;  2.  Distinct  contractions  conveying  the  sensa- 
tion of  marked  increase  in  tonicity,  becoming  visible  as  globular  prom- 
inences, being  contractions  of  a  greater  or  lesser  area  of  the  fundus,  and 
terminating  with  a  distinct  pressure  murmur  which  is  felt  by  the  patient 
as  a  more  or  less  painful  contraction;  3.  Decidedly  marked,  visible  and 
palpable  contractions  in  the  entire  extent  of  the  gastric  fundus,  which 
continue  for  a  long  time,  terminate  with  a  distinct  gurgle,  and  produce 
active  pain. 

This  gastric  rigidity  is  apparently  the  precursor  of  peristaltic  unrest. 
Its  relation  to  the  latter  is  that  of  tonus  to  tetanus.  Occasionally,  par- 
ticularly whfen  the  stomach  is  overloaded,  both  may  be  observed  side 
by  side. 

Gastric  rigidity  is  in  my  opinion  of  very  decided  diagnostic  importance. 
It  indicates  at  a  relatively  early  stage  that  there  is  an  obstruction  at  the 
pylorus.  Of  what  nature  this  is,  whether  purely  functional  (spastic 
contraction  of  the  pylorus)  or  organic,  whether  an  ulcer,  a  neoplasm,  a 
gastrolith,  an  adhesion  of  the  pylorus  to  neighboring  organs,  volvulus,  etc., 
can  only  be  decided  by  continued  objective  analysis  of  the  individual  case. 
But  the  fact  alone  that  the  patient  is  suffering  from  an  obstruction  at 
or  near  the  pylorus  is  not  only  of  great  import  in  the  diagnosis  but  also 
in  the  prognosis,  and  even  in  treatment. 

For  this  purpose  I  wish  to  add  a  few  remarks  of  practical  significance 
to  the  discussion  of  the  symptom  of  gastric  rigidity,  which  is  not  suffi- 
ciently considered  in  medical  literature.  "  Gastric  rigidity,"  for  obvious 
reasons,  may  be  T)est  noied  when  the  organ  is  full  and  it  may  then  be  best 
palpated;  but,  even  then,  it  can  occasionally  only  be  observed  with  marked 
friction  of  the  gastric  region,  preferably  with  a  cool  hand  or  a  hand  that 
has  been  dipped  in  ice-water.  As  gastric  rigidity  does  not  always  occur 
even  under  these  conditions  the  examination  must  be  frequently  repeated. 
A  slight  degree  of  gastric  rigidity  can  only  be  determined  by  much 
practice,  and  I  therefore  advise  that  the  students  practise  first  with  cases 
in  which  the  rigidity  is  well  developed,  so  as  to  determine  the  increased 
gastric  tonus. 

I  have  purposely  dwelt  upon  this  phenomenon  at  some  length,  for  with- 
out a  complicated  apparatus  it  at  once  gives  the  physician  reason  to  sup- 
pose that  something  is  out  of  order  in  the  motor  apparatus  of  the  stomach. 
We  have  then  a  certain  foundation  upon  which  to  proceed,  and  we  know 
what  further  steps  must  be  taken  to  clear  the  situation. 

We  shall  now  recur  to  the  previously  mentioned  visible  prominence. 
We  note  that  it  shows  inspiratory  and  expiratory  motion,  and  we  shall 
proceed  to  palpate  it.  As  may  he  readily  determined,  we  are  dealing  with 
a  hard  tumor  of  uneven  surface  and  about  the  size  of  «.  small  orange. 

Apparently  this  completes  the  diagnosis.     We  have  before  us  a  tumor 


ETIOLOGY  227 

of  the  pylorus.  But  we  must  investigate  still  further  to  ascertain  the 
nature  of  this  tumor.  Is  it  movable  or  adherent?  Can  it  be  fixed  upon 
expiration  or  not? 

The  movability  of  a  pyloric  tumor  (for  only  these  can  be  decidedly 
moved  manually)  is  so  readily  proven  that  we  really  need  say  nothing 
further  in  regard  to  it.  But  only  a  very  few  pyloric  tumors  are  movable 
in  all  directions  like  the  head  of  a  child  in  the  uterus;  in  the  majority 
of  cases  there  are  some  adhesions,  and  it  is  then  necessary  to  determine 
the  degree  of  movability. 

If  we  are  in  doubt,  it  is  well  to  inflate  the  stomach  with  carbonic  acid 
or  air,  when  it  will  be  possible  to  determine  the  position  of  the  stomach, 
especially  that  of  the  greater  curvature.  If  while  inflated  by  air  the 
tumor  is  still  movable,  certain  locomotor  excursions  downward  and  to  the 
right  will  occur,  occasionally  also  upward  and  to  the  right. 

Under  this  method  in  the  case  in  question  we  note  that  inflation  by 
CO,  (which  we  prefer  on  account  of  its  simplicity  and  particularly  because 
the  patient  has  not  yet  become  accustomed  to  the  prolonged  presence  of 
the  stomach-tube)  affects  the  position  of  the  tumor  but  little.  Therefore, 
it  is  probably  adherent  to  the  surroundings. 

At  this  point  we  must  consider  an  important  difference  between  the 
expiratory  relation  of  tumors  of  the  pylorus  and  tumors  of  the  small  cur- 
vature. The  latter,  as  was  first  determined  by  Minkowski,^  are  charac- 
terized by  expiratory  immovability.  By  this  sign  tumors  of  the  small 
curvature  may  readily  be  differentiated  from  tumors  belonging  to  other 
organs,  and  on  the  other  hand  it  is  also  an  important  factor  in  differen- 
tiating them  from  tumors  of  the  pylorus.  Yet,  tumors  of  the  small  curva- 
ture may  lose  their  expiratory  immovability  when  they  become  adherent 
to  neighboring  organs,  but  in  this  case  they  either  do  not  ascend  with 
inspiration,  or  they  slightly  descend. 

Judging  from  the  previously  mentioned  findings  the  tumor  in  this 
case  proves  to  be  a  tumor  of  the  pylorus,  and  since  it  is  hard  to  the  touch 
and  the  other  s3nnptoms  also  point  to  a  malignant  course,  we  can  hardly 
be  wrong  in  deciding  that  we  have  before  us  a  carcinoma  of  the  pylorus. 

Nevertlieless,  although  we  feel  quite  certain  of  our  opinion,  we  shall 
complete  as  far  as  possible  the  physical  examination  of  the  organ,  as  well 
as  of  the  other  abdominal  organs. 

Previously,  on  inflating  with  CO2  and  simultaneously  ascertaining  the 
movability  of  the  pyloric  tumor,  we  observed  the  position  of  the  greater 
curvature.  It  was  noted  under  these  circumstances  that  it  extended  above 
the  horizontal  umbilical  line  about  a  handbreadth.  We  were  then  unable 
to  determine  the  position  of  the  smaller  curvature  as  this  is  only  possible 
on  inflating  the  stomach  with  air  to  the  extreme  limit.     These  methods. 


Minkowski,  Berliner  klin.  Wochemchrift,  1888,  Nr.  31. 


228  GASTRIC  AND  INTESTINAL  CARCINOMATA 

therefore,  do  not  permit  us  to  ascertain  whether  the  stomach  is  enlarged 
or  descended,  or  whether  both  conditions  are  present. 

If  we  desire  accurate  knowledge,  we  must  resort  to  maximal  inflations 
with  air,  tilling  with  water,  or,  eventually,  the  illumination  of  the  stomach. 
These  tests  may  perhaps  have  a  scientific  value,  but  are  of  little  practical 
importance. 

It  is  more  serviceable  to  investigate  the  organs  adjacent  to  the  stomach, 
especially  the  liver,  the  intestines,  and  the  mesentery. 

As  the  metastases  of  carcinoma  are  principally  found  in  the  liver,  we 
should  convince  ourselves  of  an  enlargement  of  this  organ,  or  of  the  pres- 
ence of  nodules  therein,  and  should  also  palpate  the  entire  intestines  and 
the  mesentery,  in  so  far  as  they  are  susceptible  to  the  palpating  finger; 
above  all  we  must  not  fail  to  ascertain  whether  or  not  free  fluid  is  present 
in  the  abdominal  cavity. 

Finally,  we  must  palpate  for  a  moment  the  left  supraclavicular  region 
for  the  possible  presence  of  a  so-called  Virchow's  gland.  The  occurrence 
of  such  glands,  sometimes  ranging  in  size  from  that  of  a  hazelnut  to  that 
of  a  hen's  egg,  according  to  the  opinion  of  most  authors  (v.  Leube,  Ewald, 
Kiegel,  Rosenheim,  Mathieu,  Hayem  and  Lion,  Hemmeter,  Einhorn, 
Fleiner)  with  whom  I  coincide,  belongs  to  the  greatest  rarities.  In  regard 
to  the  fact  that  enlargement  of  the  supraclavicular  glands  (Tarchetti  and 
others)  unquestionably  belongs  to  a  late  period  of  carcinomatous  develop- 
ment, complete  unanimity  does  not  exist  even  among  the  few  authors  who 
ascribe  great  importance  to  this  symptom. 

That  enlargement  of  the  supraclavicular  glands  is  not  peculiar  to  gas- 
tric carcinoma  alone,  but  to  all  intestinal  carcinomata,  need  hardly  be 
mentioned.  The  condition  may  throw  light  upon  the  cases  in  which  the 
clinical  signs  of  an  intestinal  carcinoma  are  obscure.  Such  instances  have 
been  reported  in  literature,  and  every  one  of  experience  will  remember 
similar  occurrences.  Under  these  circumstances,  glandular  enlargement  of 
the  supraclavicular  region  may  aid  in  the  diagnosis. 

The  same  is  true  of  another  variety  of  glandular  enlargement  which 
has  been  observed  for  a  long  time,  especially  in  France  and  also  in  Ger- 
many, but  in  the  main  has  received  but  little  consideration:  The  enlarge- 
ment of  the  peri-  and  para-umhilical  glands.  Simultaneously,  but  even 
alone,  the  umbilicus  may  also  show  metastasis,^  so  that  we  then  speak  of 
imibilical  carcinoma.  This  complication,  which  Quenu  and  Longuet  ^  a 
few  years  ago  made  the  subject  of  a  comprehensive  study,  is  exceedingly 
rare.     Nevertheless,  in  the  course  of  years  I  have  seen  about  half  a  dozen 


'  Cases  of  primary  carcinoma  of  the  umbilicus  have  been  described  in  literature ; 
they  are,  however,  exceedingly  rare. 

-Quenu  ct  Longuet,  "Cancer  secondaire  de  rombilic."    Revue  de  Chirurg.,  1896, 

T.   U5,  p.  1897. 


ETIOLOGY  229 

of  these  metastases.  That  which  has  been  mentioned  as  clinically  impor- 
tant in  enlargement  of  the  supraclavicular  glands  is,  cceteris  paribus,  also 
true  of  carcinoma  of  the  umbilicus  and  its  surroundings. 

This  exhausts  the  leading  points  of  the  physical  examination. 

They  are  sufficient,  as  we  have  seen  in  the  case  in  question,  not  only 
for  the  diagnosis  but  also,  so  far  as  this  be  possible,  to  decide  whether  or 
not  complications  are  present.  From  an  examination  of  the  vomited 
material  and  from  its  nature  a  conclusion,  although  not  an  exhaustive 
one,  may  be  drawn  in  regard  to  the  gastric  functions,  and  it  will  be 
apparent  that  in  classical  cases  of  carcinoma  of  the  stomach  other  methods 
of  examination,  particularly  an  examination  of  the  gastric  contents,  in  a 
strict  sense,  are  superfluous. 

In  my  opinion  these  are  only  necessary  when  other  methods  yield 
insufficient  or  contradictory  results. 

As  this  is  often  the  case,  the  examination  of  the  gastric  contents  will 
be  included  with  the  physical  examination  of  the  patient  in  question, 
although  not  for  the  purpose  of  a  strict  indication,  but  for  didactic  reasons. 
The  patient  was  prepared  for  this  by  withholding  food  from  about  eight 
o'clock  of  the  preceding  evening  to  the  following  morning. 

This  method  of  procedure,  i.  e.,  the  examination  of  the  empty  stomach, 
is  very  valuable  in  daily  practice,  as  by  this  means  without  further  prepa- 
ration not  only  the  secretory,  but,  above  all,  the  motor  activity  of  the 
stomach  may  be  investigated.  In  the  majority  of  cases,  if  the  stomach 
proves  to  be  empty,  we  may  at  once  administer  a  trial  breakfast  and  an 
hour  after  its  introduction  the  gastric  contents  may  be  obtained. 

In  the  case  in  question  the  trial  breakfast  is  unnecessary,  as  the  patient's 
stomach,  even  early  in  the  morning,  contains  about  one-half  liter  of 
residue. 

We  must  first  examine  the  residue  carefully. 

It  consists  of  a  grayish,  thin  fluid,  a  mucus-containing  mass,  as  may 
be  noted  by  pouring  the  material  from  one  vessel  into  another,  and  has 
an  acid  but  not  disagreeable  odor.  If  a  portion  of  the  fluid  be  poured 
into  a  test-tube  there  is  no  obvious  change  except  that  the  solid  constitu- 
ents fall  to  the  bottom,  but  true  gas  formation  which  occurs  so  often  in 
other  cases  of  stagnated  gastric  contents,  is  not  here  visible.  If  the  attempt 
be  made  to  observe  gas  formation  in  a  ferment- tube,  no  actual  production 
of  gas  is  noted,  

Occasionally  in  the  gastric  contents  or  in  the  vomited  material  one 
or  several  particles  of  the  tumor  may  be  admixed,  and  if  microscopic 
examination  reveals  characteristic  signs  of  an  atypical  neoplasm  the  diag- 
nosis is  virtually  certain.  It  need  hardly  be  stated  that  macroscopic  exami- 
nation alone  under  no  circumstances  suffices,  since  particles  resembling 
tumor  may  upon  accurate  investigation  prove  to  be  fragments  of  mucous 
membrane,  coagulated  blood,  etc. 


230  GASTRIC  AND  INTESTINAL  CARCINOMATA 

CHEMICAL   AND    MICROSCOPICAL   INVESTIGATION   OF   THE 
GASTRIC    CONTENTS 

With  this  external  investigation  we  now  include  the  chemical  and 
microscopical  examination  of  the  gastric  contents. 

As  may  be  noted  from  the  color  reaction  (tropaeolin  paper,  Congo 
paper)  as  well  as  from  the  results  of  the  phloroglucin,  vanillin  and  resorcin 
tests,  free  hydrochloric  acid  is  not  present  in  the  gastric  contents.  It  was, 
however,  found  that  litmus  paper  was  decidedly  reddened.  The  gastric 
contents  must  contain  either  much  combined  hydrochloric  acid  or  acid 
salts  or  organic  acids,  or  all  of  these  combined  are  found.  Of  these  we 
are  chiefly  interested  in  lactic  acid,  especially  as  its  presence  may  be  most 
easily  determined.  In  fact,  as  was  demonstrated  by  the  iron  chlorid  test, 
lactic  acid  was  present  in  large  amounts.  Besides  lactic  acid,  other  volatile 
fatty  acids  are  probably  present,  but  their  exact  determination  is  difficult 
and  they  are  of  little  practical  importance. 

On  the  other  hand,  further  to  determine  the  secretory  insufficiency  of 
the  stomach,  the  proof  that  enzymes^  that  is,  proenzymes  of  the  gastric 
contents,  pepsin  and  pepsinogen,  as  well  as  lab-ferment  and  lab-zymogen, 
are  absent  is  necessary.  As  was  shown  by  the  tests  which  were  made,  the 
previously  mentioned  enzymes  are  absent  from  the  gastric  contents  of  the 
patient  in  question. 

We  conclude  the  chemical  examination  by  testing  a  portion  of  the 
gastric  contents  for  blood,  using  the  guaiac  test  modified  by  Weber. 

Test  for  Blood. — As  this  test  has  been  but  little  employed  in  practice  I 
shall  at  this  point  briefly  describe  it.  About  10  c.c.  of  unfiltered  gastric 
contents  are  mixed  in  a  test-tube  with  about  one-third  as  much  of  glacial 
acetic  acid,  and  the  mixture  is  repeatedly  shaken.  We  then  add  to  it  the 
same  quantity  of  sulphuric  ether,  after  which  we  shake  it,  and  subse- 
quently note  whether  the  mixture  shows  any  change  in  color.  If  much 
hemoglobin  be  present  in  the  gastric  contents  the  ether  soon  changes  to 
a  yellowish-brown  color  somewhat  like  diluted  Tokay  wine. 

This  yellowish-brown  discoloration  strongly  indicates  the  presence  of 
hematin.  The  ether  is  carefully  decanted,  and  ten  drops  of  guaiac  tinc- 
ture freshly  prepared  each  time  and  thirty  drops  of  old,  strong  oil  of 
turpentine  are  added.  If  hematin  is  present,  upon  long  standing  at  first 
a  grayish  and  later  a  decidedly  marked  violet  color  develops  in  the  mixture. 

We  add  to  the  mixture  a  few  cubic  centimeters  of  distilled  water  and 
from  ten  to  twenty  drops  of  chloroform.  This  rapidly  takes  up  the  blue 
coloring  matter,  and  the  reaction  soon  becomes  markedly  distinct.  From 
(lie  intensity  of  the  blue  or  violet  discoloration  we  may  draw  conclusions 
as  to  the  amount  of  dissolved  hematin  present  in  the  gastric  contents. 

The  tost  made  in  the  case  of  our  patient  revealed  an  extraordinarily 
profuse  amount  of  hematin  in  the  gastric  contents. 


MICROSCOPICAL  INVESTIGATION   OF  THE   GASTRIC  CONTENTS    231 

Finally,  a  microscopic  examination  of  the  gastric  contents  should  be 
undertaken.  Under  the  microscope  numerous  immotile  rods,  partly  iso- 
lated, partly  in  clumps  or  forming  angles,  were  observed;  these  are  lactic 
acid  hacilli,  which  were  first  described  by  me,  later  by  Oppler,  and  accu- 
rately studied  by  Kaufmann  and  Schlesinger.  Furthermore,  numerous 
transverse,  striped  muscular  fibers  were  noted  of  which  a  part  were  still 
well  retained,  now  and  then  starch  bodies,  also  fatty  acid  crystals  and  fatty 
acid  needles.  Occasionally  yeast  colonies,  isolated  or  beginning  to  sprout, 
are  noted,  but,  on  the  other  hand,  the  sarcinae  so  frequently  present  in 
these  conditions  were  absent. 

Pus  in  the  gastric  contents  is  a  significant  finding,  and  its  presence  is 
often  revealed  by  the  odor.  If  the  gastric  contents  are  spread  out  thin 
upon  a  black  pus  basin  and  carefully  examined,  as  a  rule  particles  of  pus 
will  be  discovered  which  may  be  verified  by  microscopic  examination. 

In  the  preceding  I  have  described  the  most  important  macroscopical, 
chemical  and  microscopical  findings  in  the  gastric  contents  of  the  case 
under  discussion.  Let  us  now  consider  the  collective  importance  of  the' 
individual  findings. 

The  least  weight  is  to  be  attached  to  the  macroscopic  investigation;  it 
is  true  the  coffee-ground  appearance  may  strengthen  the  suspicion  of  car- 
cinoma, yet  it  is  not  absolutely  proven.  But  the  previously  mentioned 
particles  of  tumor  tissue  unquestionably  are  in  favor  of  a  malignant 
neoplasm. 

More  valuable  is  the  chemical  finding,  and  here  primarily  the  absence 
of  free  hydrochloric  acid  and  enzymes,  the  fact  of  abnormal  lactic  acid 
fermentation,  and  the  presence  of  blood  and  pus  in  the  gastric  contents 
are  significant. 

The  absence  of  free  hydrochloric  acid  (which,  as  is  well  known,  was 
discovered  in  Kussmaul's  Clinic  in  the  year  1879  by  van  den  Velden), 
even  to-day  is  looked  upon  as  a  relatively  certain  and  decisive  sign.  It 
is  of  very  frequent  occurrence  in  gastric  carcinoma;  it  was  present  in  77.5  i 
per  cent,  of  my  cases,  and  other  observers  give  even  higher  figures.  But 
gastric  carcinoma  is  not  the  only  affection  which  shows  the  absence  of 
hydrochloric  acid.  This  symptom  is  observed  in  maladies  of  an  entirely 
benign  character:  In  chronic  gastritis,  in  amyloid  degeneration,  in  severe 
forms  of  anemia,  in  poisoning  by  sulphuric  and  hydrochloric  acids,  in 
so-called  achylia  gastrica,  in  hypertrophic  pyloric  stenosis,  and  in  rare 
cases  of  ulcer  of  the  stomach;  moreover,  deficient  hydrochloric  acid  is 
found  in  carcinoma  of  other  organs,  for  example,  of  the  esophagus,  of  the 
uterus,  of  the  breast,  and  of  the  rectum. 

Inversely,  free  hydrochloric  acid  is  occasionally  found  even  in  con- 
spicuous excess  in  well  developed  cases  of  gastric  carcinoma.  An  excess 
of  hydrochloric  acid  is  especially  frequent  in  carcinomatous  ulcer,  to  which 
we  shall  refer  later.     But  also  in  undoubted  gastric  carcinoma,  particu- 


232  GASTRIC   AND   INTESTINAL  CARCINOMATA 

laily  of  the  pylorus  and  at  the  onset  of  the  disease,  we  quite  often  find 
hydrochloric  acid. 

Of  greater  decisive  importance  is  the  occurrence  of  large  amounts  of 
lactic  acid.  Arthur  Schiff  ^  compiled  the  figures  of  Hammerschlag, 
Strauss,  Schlesinger,  Kaufmann  and  Ekehorn,  which  show  that  84.4  per 
cent,  of  gastric  affections  running  their  course  with  lactic  acid  fermentor 
Hon  are  gastric  carcinomata.  According  to  the  same  compilation,  the  in- 
vestigations of  Boas,  Hammerschlag,  Kosenheim,  Lindner,  Kuttner,  Robin, 
Strauss,  Kaufmann  and  Schlesinger  show  that  lactic  acid  occurs  in  73 
per  cent,  of  all  gastric  carcinomata.  Higher  figures  were  given  by  Croner,^ 
that  is,  78.5  per  cent.,  and  Riitimeyer,^  75  to  80  per  cent. 

On  the  other  hand,  it  cannot  be  denied  that  lactic  acid  fermentation 
in  the  stomach  occurs  in  quite  a  number  of  non-malignant  gastric  affec- 
tions; for  example,  in  hypertrophic  pyloric  stenosis,  gastritis  gravis  (Rosen- 
heim), in  pernicious  anemia  with  gastric  atrophy  (Ewald),  and  in  other 
rare  cases  which,  however,  do  not  clinically  present  the  picture  of  gastric 
carcinoma. 

As  the  presence  of  lactic  acid  occurs  only  with  stasis  of  the  gastric 
contents  and  the  absence  of  hydrochloric  acid,  it  is  obvious  that  deficiency 
in  lactic  acid  by  no  means  excludes  gastric  carcinoma. 

The  positive  finding  only  is  of  importance,  not  the  negative. 

Besides  the  chemical  changes  previously  mentioned  the  absence  of 
pepsin  and  lab-ferment  is  to  be  emphasized,  to  which  Hammerschlag, 
Ewald,  Kuttner  and  others  attach  great  value.  This,  however,  always 
occurs  when  the  presence  of  lactic  acid  is  combined  with  the  absence  of 
hydrochloric  acid,  so  that  proof  of  the  absence  of  enzymes  at  most  only 
confirms  the  previously  mentioned  anomalies  or  complements  them. 

Occult  Gastric  Hemorrhage. — In  my  experience  some  weight  must  be 
attached  to  the  evidence  of  occult  gastric  hemorrhage.  This  may  be  de- 
tected in  the  gastric  contents  or,  if  for  any  reason  not  thus  perceptible, 
may  be  demonstrated  in  the  feces  by  means  of  the  previously  mentioned 
method   (page  230). 

Since  Ewald  and  Kuttner  called  attention  to  the  occurrence  of  these 
slight  hemorrhages,  I  have  recently  had  an  opportunity  to  study  this  sub- 
ject carefully,  and  in  numerous  cases  of  gastric  carcinoma  have  deter- 
mined that  in  these  diseases  occult  hemorrhages  are  exceedingly  common. 
Thus,  associated  with  my  assistant.  Dr.  Kochmann,  in  67  cases  of  gastric 
carcinoma  we  found  65  hemorrhages,  and  in  the  overwhelming  majority 
of  eases  the  bleeding  was  occult. 

^Arthur  Schiff.  "Die  Diagnose  des  Magencarcinoma,"  "  Sammelreferat  nach  den 
Arbeiten  der  Jahren  1894-1898."  Centralbl.  f.  die  Grenzgebiete  der  Medicin  u. 
Chirurgie,  1898,  Nr.  12  and  13. 

2  Croner,  Mittheilungen  aus  den  Orenzgebieten,  1899,  Bd.  V,  p.  405. 

3  lUltimcycr,  Correspondenzbl.  f.  Schweizcr  Acrzte,  1900,  Nr.  21. 


MICROSCOPICAL  INVESTIGATION  OF  THE   GASTRIC  CONTENTS    233 

However,  this  finding  is  not  pathognomonic.  We  have  noted  the  con- 
dition in  a  large  series  of  observations,  most  numerously  in  cases  of  benign 
dilatation,  also  in  hypertrophic  pyloric  stenosis  and  in  ulcer  of  the  stomach, 
but  not,  however,  in  positive  cases  of  chronic  gastritis  and  achylia.  Natu- 
rally, even  in  these  cases,  fresh  visible  hemorrhages  may  appear  as  capillary 
hemorrhages  which,  however,  as  a  rule,  are  of  artificial  origin.  Continu- 
ous hemorrhage  in  chronic  achylia  or  gastritis  without  conditions  of  stasis 
belongs  to  the  greatest  exceptions;  in  carcinoma,  however,  it  forms  the 
rule. 

The  differentiation  of  a  benign  from  a  malignant  pyloric  stenosis  by 
demonstrating  the  presence  of  blood  is  not  readily  made.  But  we  may 
state  that  under  these  conditions  the  reaction  in  carcinoma  is  decidedly 
more  marked  (saturated  blue)  than  in  benign  processes  (delicate  violet). 

Microscopic  examination  has  a  certain  importance  inasmuch  as  it  re- 
veals the  thread  bacilli  of  lactic  acid  fermentation,  and  thus  confirms  the 
presence  of  the  latter.  Sarcinw,  in  my  experience,  are  of  no  diagnostic 
significance  in  gastric  carcinoma.  They  are  absent,  as  a  rule,  but  not 
invariabl}^  in  marked  lactic  acid  fermentation,  and,  vice  versa,  with  the 
finding  of  free  hydrochloric  acid  and  marked  stagnation  they  are  almost 
always  present  in  carcinoma. 

Pus  in  the  gastric  contents  is  by  no  means  a  rare  symptom;  usually 
it  is  found  admixed  with  blood.  Although  pus  may  occur  in  the  stomach 
from  various  causes  (gastritis  phlegmonosa,  abscesses)  and  is  especially 
prone,  to  originate  from  the ,  upper  air  passages,  the  continuous  finding 
of  amounts  of  pus,  particularly  if  the  conditions  mentioned  may  be  ex- 
cluded, is  a  valuable  sign  of  carcinoma. 

Besides  the  gastric  contents,  the  composition  of  the  blood  in  gastric 
carcinoma  has  received  considerable  attention;  in  the  main,  however,  the 
results  are  unsatisfactory.  We  often  find,  but  not  constantly,  a  marked 
diminution  of  hemoglobin  and  of  the  erythrocytes.  The  opinion  promul- 
gated a  few  years  ago  by  Schneyer  ^  that  there  is  an  absence  of  digestive 
leukocytosis  in  gastric  carcinoma  was  found  to  be  incorrect  after  further 
examination  (by  Hassmann,  Hoffmann,  Sayler  and  Taylor,  Chadbourne, 
Dolmatow,  Marchetti,  Eencki  and  others). 

From  this  description  it  follows  that  absolute  proof  of  the  presence 
of  a  gastric  carcinoma,  aside,  perhaps,  from  the  very  rare  finding  of 
particles  of  the  tumor  which  is  only  possible  in  well  advanced  cases, 
cannot  be  obtained  from  the  investigation  of  the  gastric  contents.  Only 
most  careful  consideration  of  all  the  clinical  signs,  among  them  the  phys- 
ical, particularly  the  tumor,  can  protect  us  from  an  erroneous  diagnosis. 

With  this  we  reach  the  important  and  difficult  chapter  of  the  diagnosis 
of  gastric  carcinoma. 

*  Schneyer,  Internationale  klin.  Rundschau,   1894. 


234  GASTRIC  AND  INTESTINAL  CARCINOMATA 

GASTRIC    CARCINOMA 
DIAGNOSIS 

So  long  as  we  are  dealing  with  cases  similar  to  the  one  just  described, 
tlie  diagnosis  of  gastric  carcinoma  is  one  of  the  easiest  in  the  realm  of 
internal  medicine.  Difficulties  beset  us  only  when  the  onset  is  indistinct 
and  the  course  atypical,  when  the  symptoms  differ  in  important  points 
from  those  just  described,  when  important  objective  factors  are  either 
absent  or  indistinctly  developed. 

We  may  differentiate  two  categories  of  atypical  development:  First, 
those  in  which  a  tumor  in  the  stomach  is  not  palpable  at  the  moment  of 
examination;  secondly,  if  the  tumor  be  present,  it  does  not  have  the  char- 
acteristic properties  of  a  gastric  tumor,  and  particularly  of  a  malignant 
gastric  tumor. 

We  shall  now  concern  ourselves  with  the  first  class  of  cases.  Daily 
observation  gives  us  many  examples  of  this  kind. 

We  see,  for  instance,  a  patient  who  for  a  short  time  has  complained 
of  dyspeptic  symptoms:  Gastric  oppression,  anorexia,  now  and  then  draw- 
ing pains  in  the  epigastrium  or  in  the  fundus,  occasionally  also  in  the 
back,  eructations,  emaciation,  a  feeling  of  diminished  dynamic  activity, 
etc.  Palpation  may  perhaps  reveal  slight  sensitiveness  to  pressure,  but 
other  than  this  no  objective  signs  are  observed. 

The  suspicion  of  a  pernicious  disease  is  aroused,  but  we  may  also  be 
dealing  with  a  severe  form  of  chronic  gastritis  or  even  with  one  of  those 
not  infrequent  forms  of  nervous  dyspepsia  which  in  the  course  of  time 
lead  to  an  extreme  degree  of  marasmus,  and  thus  very  closely  simulate 
the  picture  of  carcinomatous  cachexia. 

In  another  series  of  carcinomata  we  observe  an  entirely  different  course. 
Tlie  disease  begins  suddenly  as  a  severe  gastritis,  or  like  an  acute  gastric 
dilatation :  In  the  midst  of  health  the  patient  begins  to  vomit,  or,  after 
a  more  or  less  obvious  cause,  once  or  several  times  large  or  small  amounts 
of  ingesta  are  ejected;  but  notwithstanding  careful  regulation  of  the  diet 
and  the  use  of  all  remedies  calculated  to  ameliorate  the  condition,  the 
s}Tnptoms  do  not  yield  but  even  increase.  The  patient  permanently  loses 
his  appetite,  cannot  take  even  the  most  carefully  prepared  food,  and  in  a 
few  weeks  shows  a  threatening  state  of  inanition. 

Or  after  indistinct  prodromes  the  patient  is  suddenly  attacked  with 
profuse  hematemesis  or  melena.  We  first  think  of  a  latent  ulcer  and  in- 
stitute appropriate  treatment;  the  hemorrhage  ceases  but  the  patient  does 
not  recover  his  health,  he  rejects  his  food,  repeatedly  vomits,  sometimes 
food  liut  occasionally  also  fresh  blood,  and  the  case  begins  to  assume  a 
serious  aspect. 

In  other  cases,  the  patient  shows  indistinct  dyspeptic  symptoms  with 
fever  which  is  not  characteristic,  nor  does  it  conform  to  any  of  the  well- 


GASTRIC  CARCINOMA  235 

known  types.  We  think  of  cryptogenetic  pyemia  or  an  irregular  attack 
of  enteric  fever,  of  malaria,  of  tuberculous  peritonitis,  etc.,  and  finally 
section  shows  the  presence  of  a  gastric  or  intestinal  carcinoma  which 
was  insusceptible  to  palpation. 

This  shows  but  a  few  forms  under  which  carcinoma  may  be  masked. 
If  we  undertook  to  enumerate  them  all  we  should '  lose  ourselves  in  a 
chaos  of  conditions  which  could  not  be  examined. 

Somewhat  less  intricate  but  still  obscure  is  the  second  category  of  cases 
in  which  a  tumor  is  present  but  in  which  doubts  arise  as  to  whether  it 
belongs  to  the  stomach,  or  in  which  the  history  or  malignancy  is  uncertain. 
We  mention,  for  example,  the  difiicult  differentiation  of  an  old  ulcer  with 
thickened  borders  from  a  carcinoma  or  a  carcinomatous  ulcer,  further- 
more, the  recognition  of  a  callous,  indurated  perigastritis,  a  hypertrophic 
thickening  of  the  pylorus,  a  hard  gall-bladder  filled  with  stones,  a  gastro- 
lith,  a  lipoma,  a  papilloma  or  myoma,  not  to  speak  of  sarcoma  of  the 
stomach. 

In  these  and  numerous  other  cases  which  cannot  be  mentioned  here 
all  methods  of  diagnosis,  particularly  the  examination  of  the  gastric  con- 
tents, must  be  utilized,  and,  as  I  must  admit,  frequently  without  success, 
to  clear  up  these  doubtful  conditions.  But,  nevertheless,  cases  remain  in 
which  nothing  but  the  further  course  of  the  disease,  and  often  not  even 
this,  but  only  laparotomy  or  the  autopsy,  will  decide  the  question. 

To  proceed,  we  must  mention  some  other  methods  which  now  and  then 
are  employed  in  complementing  the  diagnosis. 

First  among  these  is  the  examination  of  the  patient  under  anesthesia. 
By  this  means  doubtful  tumors  whose  presence  in  the  various  abdominal 
organs  cannot  be  determined  with  certainty  may  be  better  recognized  or 
localized.  However,  in  consequence  of  more  thorough  technic  in  palpa- 
tion, examination  under  an  anesthetic  has  in  the  last  few  years  fallen  into 
disuse.  It  is  best  reserved  for  the  cases  in  which  active  tension  of  the 
abdominal  walls  from  marked  meteorism,  etc.,  makes  it  impossible  to 
obtain  a  clear  idea  of  the  condition  of  the  viscera. 

The  second  method  is  gastroscopy  which,  however,  up  to  the  present 
time  has  secured  no  permanent  place  in  the  diagnosis  of  gastric  pathology. 
Invented  by  v.  Mikulicz,  and  further  developed  by  Rosenheim,  Kuttner 
and  Rewidzoff,  this  method  has  been  chiefly  employed  in  the  last  few 
years  by  G.  Kelling.  Kelling  is  of  the  opinion  that  gastroscopy  enables 
us  to  make  the  diagnosis  in  doubtful  cases  of  gastric  carcinoma,  and  in 
other  instances  to  make  it  early  (see  below).  We  must  wait  and  see  what 
the  technic  and  possibilities  of  gastroscopy  achieve  in  the  future,  before 
we  can  look  upon  this  method  as  positive  and  decisive. 

So-called  exploratory  laparotomy  has  also  been  employed  as  a  diag- 
nostic aid.  As  a  matter  of  fact  every  laparotomy  is  an  exploratory  incision, 
as  only  this  gives  us  accurate  knowledge  as  to  the  seat  of  the  tumor,  its 


236  GASTRIC   AND  INTESTINAL  CARCINOMATA 

physical  composition,  its  relation  to  neighboring  organs,  the  existence  of 
complications,  etc. 

In  this  respect,  exploratory  incision  is  in  truth  the  best  and  most  cer- 
tain diagnostic  method.  But  this  opinion  is  not  generally  held  nor  the  fact 
recognized,  above  all  among  the  laity.  Although  with  the  great  develop- 
ment in  technic  as  well  as  in  antisepsis  and  asepsis  the  risk  is  not  great, 
nevertheless  the  method  is  rejected  even  at  the  cost  of  a  positive  diagnosis. 
In  these  instances  laparotomy  is  frequently  begun  as  a  therapeutic  meas- 
ure and  ended  as  an  exploratory  operation. 

I  believe  an  exploratory  incision  to  be  unjustifiable  when  the  diagnosis 
is  wholly  obscure  or  when  we  entertain  the  suspicion  of  a  malignant 
process  hut  cannot  possibly  determine  the  organ  affected.  Here  from  a 
simple  exploratory  incision  a  lengthy,  severe,  and  occasionally  ineffectual 
operation  may  result.  In  describing  the  indications  for  the  operative 
treatment  of  gastric  carcinoma  we  shall  again  revert  to  this  subject. 

From  what  has  just  been  stated  the  impression  will  be  given  that  in 
the  majority  of  cases  of  gastric  carcinoma  a  clear  diagnosis  can  be  made. 
Much  more  perplexing  is  it  to  determine  at  the  onset  with  certainty  or 
probability  the  exact  seat,  the  extent  of  the  process,  the  presence  of  metas- 
tasis, a  beginning  ascites  or  other  complications.  In  so  far  as  we  are  deal- 
ing with  objectively  demonstrable  changes  a  careful  examination  will  natu- 
rally assist  us.  Other  very  frequent  occurrences,  such  as  metastasis  of 
the  liver,  or  of  the  mesentery,  etc.,  sometimes  escape  recognition.  A  diag- 
nosis entirely  comprehensive  in  this  respect  is  impossible. 

Intimately  related  to  these  diflBculties  is  the  much  discussed  question 
of  the  early  diagnosis  of  gastric  carcinoma.  Even  the  prior  question, 
"  What  do  we  understand  by  early  diagnosis  ? "  is  not  easily  answered. 
It  has  been  said  "that  a  diagnosis  is  made  early  if  no  palpable  tumor  is 
present.''  This  is  generally  true.  But  the  facts  show  that  even  in  Bill- 
roth's  time  radical  operation  was  attempted  for  gastric  carcinoma,  which 
proves  that  this  requirement  was  not  absolutely  a  prior  condition  for 
successful  surgical  treatment  but  also,  inversely,  what  every  one  of  ex- 
perience knows,  that  the  impossibility  of  feeling  a  tumor  is  no  proof  of 
conditions  favorable  to  operation.  Neither  will  the  time  which  has  elapsed 
since  the  onset  of  the  disease  furnish  us  any  clue  to  the  distribution  of  the 
process,  as  groups  of  tumors  which  grow  rapidly  and  also  such  as  grow 
very  slowly  have  been  observed. 

The  chemical  findings,  particularly  the  triad,  stagnation,  absence  of 
hydrochloric  acid,  and  presence  of  lactic  acid,  will  in  some  of  the  indi- 
vidual cases  enable  us  to  make  an  early  diagnosis  even  although  the  tumor 
elude  discovery,  although  isolatedly  there  are  benign  processes  with  the 
same  chemical  finding,  and,  notwithstanding  the  fact  that  the  presence 
of  this  triad  of  symptoms  indicates  conditions  already  very  unfavorable 
for  the  removal  of  the  tumor. 


GASTRIC  CARCINOMA  237 

Nevertheless,  in  the  points  above  mentioned,  collectively  at  least,  and 
so  long  as  no  better  criteria  exist,  these  factors  in  a  large  number  of 
cases  permit  an  early  diagnosis. 

The  usually  very  decided  period  of  latency  forms  the  greatest  obstacle 
in  the  discrimination  of  gastric  carcinoma.  In  this  stage  the  patients 
have  but  relatively  few  symptoms,  do  not  consult  a  physician,  and  resort 
to  home  remedies.  Certainly  most  of  the  carcinomata  which  we  meet 
are  already  well  advanced  and  manifest  conspicuous  symptoms,  above  all, 
a  palpable  tumor.  In  this  condition  gastroscopy — even  should  the  technic 
become  more  simple — will  not  materially  aid  us,  Nothing  is  easier  than 
the  diagnosis  of  rectal,  uterine  or  mammary  carcinomata,  and  yet  in  these 
we  hear  of  precisely  the  same  perplexities  on  the  part  of  the  surgeons 
and  gynecologists  as  in  the  case  of  gastric  carcinoma. 

Nevertheless  it  would  be  a  great  mistake  to  allow  these  obstacles  to 
daunt  us,  and  to  relinquish  our  endeavors  to  make  an  early  diagnosis. 
The  marked  successes  reported  in  literature  resulting  from  early  operation 
after  an  early  diagnosis  of  gastric  carcinoma  should  encourage  us,  even 
with  the  basis  of  our  present  methods,  always  to  attempt  to  diagnosticate 
the  disease  as  soon  as  possible. 

A  special  form  of  carcinoma  still  to  be  described  is  carcinomatous 
ulcer.  Previously  investigated  by  Eokitansky  and  Dittrich,  carcinomatous 
ulcer  has  recently  been  thoroughly  studied  by  Hauser.  Opinions  as  to  the 
frequency  of  the  transformation  of  a  simple  ulcer  into  carcinoma  are 
to-day  widely  asunder.  According  to  Lebert,  9  per  cent,  of  all  gastric 
cancers  are  due  to  this  cause.  Rosenheim  found  it  only  in  5  to  6  per  cent., 
and  Ewald  has  lately  declared  carcinomatous  ulcer  to  be  far  more  fre- 
quent than  has  up  to  this  time  been  assumed. 

According  to  my  experience  a  positive  diagnosis  of  carcinomatous 
ulcer  intra  vitam  is  impossible.  The  chemical  examination  of  the  gastric 
contents  utterly  fails  us.  The  excess  of  hydrochloric  acid  which  Rosen- 
heim previously  believed  to  be  decisive  is  found,  as  we  now  know,  also  in 
carcinoma  without  ulcer.  I  have  repeatedly  observed  in  carcinomatous 
ulcer  severe,  rapidly  succeeding  gastric  hemorrhages.  Yet  even  these  are 
not  decisive.  We  should  always  think  of  carcinoma  ex  ulcere  if  positive 
symptoms  of  ulcer  have  for  a  long  time  preceded  the  process. 


COURSE 

The  course  of  gastric  carcinoma  depends  upon  various  factors,  primar- 
ily upon  the  nature  and  seat  of  the  tumor.  Experience  has  shown  that 
there  is  a  gliding  scale  for  the  malignancy  of  carcinoma;  that,  for  exam- 
ple, adenocarcinomata  grow  more  slowly  and  less  frequently  develop  me- 
tastasis than  the  rapidly  growing,  speedily  decomposing  medullary  carci- 
nomata which  readily  promote  the  carrying  of  carcinomatous  products. 


238  GASTRIC   AND  INTESTINAL  CARCINOMATA 

Scirrhus  is  again  characterized  by  its  tendency  to  advance  rapidly  and 
cause  stenosis,  colloid  carcinoma  by  its  unlimited  growth. 

Possibly  the  seat  of  gastric  carcinoma  is  of  even  greater  significance 
in  the  course.  It  was  formerly  assumed  that  the  point  of  predilection 
was  the  pyloric  region.  More  recent  experience,  as  well  as  operations  and 
autopsies,  shows  this  to  be  no  longer  true.  Carcinomata  of  the  smaller 
curvature  are  not  less  frequent  than  those  of  the  pylorus,  and  it  is  even 
likely  that,  similar  to  the  course  in  ulcer,  the  smaller  curvature  is  the 
preferred  seat  for  carcinoma. 

No  matter  how  this  may  be,  the  fact  is  generally  accepted  that  the 
nearer  the  carcinoma  to  the  pylorus  the  more  rapid  and  more  serious 
the  course  of  the  disease.  Under  these  circumstances  the  malady  may 
set  in  with  elementary  force  and  in  an  exceedingly  short  time,  even  a 
few  weeks,  cause  death  {acute  carcinoma).  In  opposition  to  this  are  the 
slowly  growing  carcinomata  with  numerous  variations  which  are  clinically 
ill-defined,  and,  according  to  whether  improvement  or  aggravation  appear, 
keep  the  patient  and  the  physician  wavering  between  hope  and  fear. 

The  cause  of  this  latency  is  easily  recognized  if  we  remember  that  in 
carcinomata  not  situated  in  the  pylorus  vomiting  is  absent  or  only  present 
to  a  slight  extent,  that  hemorrhages  also  are  but  moderate,  and  that, 
finally,  the  ingestion  of  food  and  its  assimilation  are  far  less  damaged 
than  in  the  first  mentioned  group. 

Under  such  circumstances  the  patients  may  for  a  time  gain  in  weight 
and  subjective  activity;  nevertheless,  the  outcome  shows  that  the  physician 
was  correct  in  his  grave  prognosis. 

It  need  scarcely  be  mentioned  that  the  course  of  the  pathologic  process 
is  influenced  to  a  decided  extent  by  the  most  varied  complications,  such 
as  ascites,  proliferation  into  the  peritoneum,  external  rupture  or  rupture 
into  the  intestine,  metastatic  pleurisy,  etc. 

We  see  from  this  that  in  a  given  case  the  determination  of  the  duration 
of  the  course  is  beset  with  great  difficulty.  However,  it  may  be  estimated 
on  the  average  at  a  year  to  a  year  and  a  half.  If  this  period  has  elapsed 
we  will  rarely  go  astray  in  excluding  a  malignant  process. 


COMPLICATIONS  AND   SEQUELS 

The  complications  which  may  occur  in  the  course  of  gastric  carcinoma 
are  numerous.  Some  of  these  are  due  principally  to  the  nature  of  the 
afl^ection,  and  for  this  reason  are  not  of  great  clinical  interest.  Others, 
however,  require  a  brief  description. 

I  must  first  call  attention  to  the  fever  which  occurs  in  carcinoma; 
this  was  mentioned  by  Wunderlich  in  his  well-known  text-book,  and  has 
been  more  accurately  described  by  Hampeln   (1884). 

Carcinomatous  Fever. — According  to  Freudweiler,  who  made  a  thor- 


GASTRIC  CARCINOMA  239 

ough  study  of  carcinomatous  fever  in  475  cases  of  carcinoma  in  the  Zurich 
Clinic,  this  symptom  was  present  in  117  cases  (i.  e.,  in  24.6  per  cent,),  and 
was  not  due  to  complications;  rarely  (that  is,  in  1.5  per  cent,  of  all  cases) 
the  fever  was  almost  continuous,  usually  it  was  remittent  or  intermittent 
(in  10  per  cent,  of  the  total  number  of  cases) ;  much  more  rarely  it  was 
typically  intermittent  and  resembled  malaria  (in  3.6  per  cent,  of  all  cases, 
in  14.5  per  cent,  of  febrile  carcinoma) ;  in  the  latter  case,  the  fever  was 
not  so  typical  as  in  malaria,  often  it  was  of  an  inverse  type,  the  time  of 
its  appearance  varying  on  different  days  as  did  the  duration  of  the  febrile 
period;  in  a  number  of  cases  the  temperature  rose  but  gradually  instead 
of  suddenly  as  in  malaria.  With  relative  frequency  (in  38.5  per  cent,  of 
the  fever  cases  and  in  9.3  per  cent,  of  all  cases  of  carcinoma)  there  were 
isolated  rises  in  temperature  which  did  not  last  longer  than  three  days. 

In  the  majority  of  the  patients  the  condition  was  that  of  ulcerative 
carcinoma  so  that  the  fever  was  attributed  to  secondary  infection;  in  the 
minority,  however,  no  ulceration  could  be  detected  at  the  autopsy.  There- 
fore, carcinoma  in  itself,  similar  to  tuberculosis  and  lympho-sarcoma,  has 
pyrogenetic  properties. 

Inversely,  as  Freudweiler  has  shown,  carcinoma  may  also  run  its  course 
with  subnormal  temperature.  In  47.8  per  cent,  of  his  cases  temperatures 
below  96.8°   F.  were  repeatedly  found. 

Coma  Garcinomatosnm. — A  second  important  complication  is  coma  car- 
cinomatosum  which  was  first  described  by  v.  Jaksch,  then  by  Senator, 
Eiess,  G.  Klemperer  and  others.  Acetone  was  first  found  by  v.  Jaksch  in 
the  distillate  from  the  urine,  and  Klemperer  later  detected  oxyhutyric  acid. 
Coma  carcinomatosum  resembles  diabetic  coma  except  that,  in  my  experi- 
ence, its  course  is  not  so  rapid.  In  one  of  my  patients  with  rectal  car- 
cinoma, in  whom  a  few  months  previously  colostomy  had  been  performed, 
the  comatose  condition  lasted  very  nearly  two  months.  Whether  in  these 
cases,  as  is  exceedingly  likely  in  diabetes,  there  is  an  acid  intoxication, 
or  whether  specific  toxins  generated  by  the  carcinomatous  poison  are  opera- 
tive, is  not  yet  known. 

Tetany  is  very  much  more  rare  than  the  two  complications  just  men- 
tioned. This  form  of  tetany  does  not  differ  from  that  occurring  in  benign 
pyloric  stenosis. 

In  conclusion  we  must  mention  the  dropsical  symptoms  in  carcinoma 
(edema  and  ascites),  venous  thrombosis  and  metastases  in  the  liver  which, 
according  to  Lebert,  occur  in  50  per  cent,  of  all  the  cases,  also  metastases 
of  the  pleura  and  of  the  lungs,  and  finally  the  appearance  of  multiple 
neuritis. 

PROGNOSIS 

The  prognosis,  as  I  need  hardly  mention,  is  very  unfavorable  provided 
surgical  intervention  does  not  soon  interrupt  the  course  for  a  time  (un- 

17 


240  GASTRIC  AND  INTESTINAL  CARCINOMATA 

fortunately,  however,  not  for  a  very  long  time).  As  we  shall  show  in 
the  chapter  upon  therapy,  internal  treatment  may  bring  about  ameliora- 
tion of  many  of  the  symptoms  and  increase  the  strength,  but  the  unfavor- 
able outcome  cannot  be  averted.  When  no  complications  are  present,  the 
prognosis  depends  mainly  upon  the  nature  and  seat  of  the  tumor.  As  I 
have  already  mentioned,  carcinomata  which  do  not  implicate  the  pylorus 
run  a  much  slower  course,  I  might  almost  say  a  more  benign  course,  than 
carcinomata  which  cause  stenosis.  As  regards  danger  to  life,  such  car- 
cinomata may  be  prognostically  designated  as  more  favorable,  but  with 
the  limitation  that  under  a  radical  operation  the  chances  of  success  are 
even  less  than  in  those  of  the  pylorus. 


CARCINOMA    OF   THE   INTESTINES 

Proceeding  downward  from  the  stomach  we  meet  with  carcinomata 
everywhere  but — and  this  is  of  great  importance — by  no  means  with  the 
same  frequency.  While  carcinomata  of  the  small  intestines  are  extremely 
rare,  carcinomata  of  the  rectum  are  about  as  numerous  as  those  of  the 
esophagus.  Between  these,  carcinomata  of  the  large  intestine  are  found; 
and  here  also  the  curvatures  are  the  points  of  predilection.  From  this 
it  is  evident  that,  a  fact  to  which  Virchow  called  our  attention,  those  por- 
tions of  the  digestive  canal  through  which  the  contents  move  but  slowly 
and  sluggishly  are  particularly  predisposed  to  the  development  of  malig- 
nant tumors. 

SYMPTOMS 

I  shall  first  describe  a  typical  case  of  carcinoma  of  the  large  intestine, 
then  one  of  the  rectum,  and  in  connection  with  these  shall  briefly  delineate 
the  symptomatology  of  carcinoma  of  the  small  intestine. 

The  patient  was  a  man  in  the  forties  and,  except  for  the  diseases  of 
childhood  and  other  mild  affections,  he  had  up  to  the  present  time  always 
been  well.  In  particular  he  had  never  complained  of  gastrointestinal 
disturbance.  Here  we  observe  the  abrupt  onset  in  the  midst  of  perfect 
health  to  which  I  called  attention  when  describing  carcinoma  of  the 
stomach. 

The  patient  stated  that  the  first  symptom  was  stubborn  constipation, 
so  tliat  at  the  onset  of  the  affection  he  was  compelled  to  resort  to  active, 
purgatives  to  regulate  the  function  of  his  bowels.  Following  the  consti- 
pation attacks  of  severe  colic  soon  appeared,  first  at  long  intervals,  and 
later  every  two  or  three  days.  Finally,  he  complained  of  marked  loss  of 
weight,  lassitude  and  inability  to  follow  his  occupation. 

It  is  evident  here  that  the  onset  of  the  affection  was  but  slightly 
characteristic. 

At  first  a  mild  coprostasis,  a  flatulent  colic  appears,  such  as  we  are 


CARCINOMA  OF  THE   INTESTINES  241 

accustomed  to  see  every  day.  But,  under  these  circumstances,  it  is  well 
not  to  be  too  optimistic,  even  in  cases  in  which  there  is  no  serious  indica- 
tion of  a  malignant  affection,  particularly  when  an  obvious  loss  of  weight 
cannot  be  attributed  to  alimentary  processes. 

In  every  case  it  is  well  to  bear  the  patient  in  mind.  Repeated  weigh- 
ings should  be  made,  and  the  physician  should  not  be  content  until  he  has 
decisive  evidence  whether  a  mild,  or,  vice  versa,  a  very  serious  malady 
is  present.  Too  great  pessimism  will  do  no  harm,  especially  if  it  should 
later  give  way  to  positive  optimism. 

So  much  as  to  the  onset  of  the  disease.  Let  us  now  discuss  its  further 
development.  In  the  last  few  weeks  the  intestinal  cramp  increased  to  an 
unbearable  degree.  The  patient  was  compelled  to  take  narcotics.  Purga- 
tives which  at  first  had  been  active  were  now  ineffectual  even  in  large  doses. 
Stronger  drugs  were  all  the  time  taken,  and  finally  drastics  were  employed, 
without  relief.  The  feces  no  longer  appeared  in  solid,  cylindrical  masses 
as  formerly,  but  in  the  shape  of  small  scybala,  frequently  admixed  with 
mucus  or  as  a  small  quantity  of  thin  fluid,  or,  finally,  in  this  or  that 
form.  The  patient  has  not  noticed  blood  in  the  dejecta.  Upon  being 
questioned  he  reports  that  he  frequently  noted  simultaneously  with  the 
attacks  of  pain,  but  often  also  without  these,  a  distinct,  intestinal  rumbling 
similar  to  the  dripping  of  a  fluid,  and  that  this  was  even  audible  at  some 
distance.  Very  observant  patients  will  occasionally  state,  upon  being  asked, 
that  occasionally,  especially  if  active  pains  are  present,  the  prominence  of 
some  portions  of  the  intestines  has  been  perceived. 

Although  these  symptoms  are  by  no  means  positive  signs  of  the  nature 
of  the  affection,  nevertheless  it  is  wise  not  to  place  too  low  an  estimate 
upon  them.  I  can  positively  state  that,  from  a  history' of  this  kind  all 
the  details  of  which  have  been  taken  into  consideration,  I  have  made  a 
diagnosis  of  carcinoma  of  the  large  intestine  even  before  the  patient  un- 
dressed himself  for  a  physical  examination. 

Absolute  certainty,  above  all,  is  furnished  by  the  clinical  findings.  I 
shall  not  allude  to  the  general  s3niiptoms,  which  were  discussed  in  the 
previous  chapter  on  visceral  carcinoma,  but  shall  only  consider  what  may 
be  demonstrated  locally. 

In  intestinal  carcinoma  the  finding  of  a  well-characterized  tumor  is 
unquestionably  the  most  positive  and  decisive  symptom. 

Let  us  discuss  the  local  findings  in  the  patient  in  question.  As  was 
readily  observed,  there  was  an  apparently  hard  but  slightly  movable  tumor 
about  the  size  of  a  mandarin  in  the  cecal  region,  and  this  could  be  palpated. 

Does  the  tumor  belong  to  the  intestine,  and  to  which  part?  Are  we 
dealing  with  a  malignant  tumor?  What  is  its  degree  of  movability?  As 
these  questions  arise  in  every  case  that  is  not  absolutely  clear,  their 
immediate  investigation  is  imperative. 

The  fact  that  the  tumor  belongs  to  the  intestinal  canal  may,  as  a  rule, 


242  GASTRIC   AND  INTESTINAL  CARCINOMATA 

be  determined  without  great  difficulty  from  the  history  in  connection  with 
the  other  clinical  findings.  Nevertheless,  sometimes  perplexities  arise 
which  greatly  annoy  the  diagnostician.  A  displaced  lobe  of  the  liver, 
liepatoptosis,  with  a  gall-bladder  full  of  stones  or  showing  carcinomatous 
degeneration  or  dropsy,  normal  but  low-lying  kidneys,  renal  tumors,  tu- 
mors of  the  omentum,  and  even  tumors  of  the  pylorus  may,  under  some 
circumstances,  simulate  neoplasms  of  the  large  intestine.  In  the  chapter 
devoted  to  diagnosis  I  shall  enter  upon  these  details  more  minutely. 

To  prove  whether  a  benign  or  a  malignant  process  is  present  is  by 
no  means  always  easy.  Chronic  perityphlitis  with  decided  induration, 
tuberculous  thickening  of  the  cecum,  not  to  speak  of  other  benign  tumors 
(fibromata,  lipomata,  myomata,  etc.),  may  resemble  malignant  neoplasms 
to  such  an  extent  that  the  true  condition  is  recognized  only  after  pro- 
longed observation,  often  only  at  the  operation  or  at  the  post  mortem. 

In  regard  to  movability,  the  law  generally  obtains  that  in  intestinal 
tumors  this  should  exist  to  a  high  degree.  This  general  rule  does  not 
coincide  with  my  experience.  I  can  only  admit  that  the  most  extreme 
grades  of  movability  are  observed  in  carcinomata  of  the  large  intestine; 
yet,  when  a  great  number  of  cases  are  studied,  we  find  only  slight,  passive 
locomotion  to  be  present.  In  the  development  of  the  tumor  adhesions  to 
neighboring  organs  very  soon  form. 

For  distinct  passive  movability  in  inflation  of  the  rectum  with  gas 
we  have  a  method  which  is  usually  serviceable,  but  the  intestines  must 
not  be  too  greatly  distended  with  gas  for,  if  this  be  the  case,  the  tumor 
is  covered  by  the  intestines  and  is  palpated  with  great  difficulty. 

In  the  case  in  question  it  was  readily  determined  that  the  tumor  was 
liardly  movable,  and  I  may  add  that  upon  repeated  investigation  its  posi- 
tion was  unchanged.  The  inflation  of  the  intestines  per  rectum  gave  no 
other  results. 

Where  there  is  undoubtedly  a  hard  tumor  of  the  large  intestine,  as 
well  as  other  points  in  the  clinical  history,  the  clinical  picture  of  carcinoma 
of  the  large  intestine  is  sufficiently  characteristic;  there  can  be  no  doubt 
of  the  diagnosis.  Other  factors  which  we  shall  later  consider  at  most 
serve  to  complement  the  pathologic  picture. 

Very  frequently,  however,  the  symptoms  are  complicated.  A  tumor 
is  aljsent.  There  are  signs  of  a  malignant  intestinal  affection  but  without 
])ositive  indications  as  to  its  nature.  Frequently  we  note  a  symptom  which 
we  also  find  in  the  case  under  consideration :  The  picture  of  chronic  intes- 
tinal stenosis.  As  we  have  in  this  volume  a  masterly  description  by  Noth- 
nagel  of  chronic  intestinal  stenosis  (which  see)  I  limit  myself  to  a  few 
salient  points  which  relate  particularly  to  carcinoma  of  the  intestine. 

Intestinal  Rigidity, — In  this  condition  the  severe  attacks  of  obstruc- 
tion accompanied  by  severe  colic,  occasionally  by  vomiting,  which  have 
already   been  described  are  subjectively  decisive.      Objectively,  we  must 


CARCINOMA  OF  THE   INTESTINES  243 

consider  meteorism,  suprastenotic  succussion,  and  the  visible,  tetanic,  in- 
testinal contractions  to  which  Nothnagel  has  given  the  appropriate  name 
of  "  intestinal  rigidity." 

In  well-developed  cases  of  intestinal  stenosis  meteorism  is  rarely 
absent,  but  is  present  in  varying  degree  according  to  the  individual  case. 
Sometimes  it  is  localized,  and  permits  a  somewhat  accurate  recognition 
of  the  seat  of  the  intestinal  stenosis,  or  it  may  be  general  in  the  stage 
of  intestinal  paralysis,  that  is,  of  threatening  ileus,  and  may  then  be 
indistinct  or  obliterated. 

Intestinal  rigidity  is  the  clearest  and  the  most  objective  symptom  of 
intestinal  stenosis.  In  well-developed  cases  we  note  from  time  to  time  that 
the  coils  of  the  intestine  above  the  stenosed  area  contract  tetanically  with 
sensations  of  actual  pain,  they  become  hard  and  stiff,  and  remain  in  this 
condition  for  some  time.  With  a  distinctly  audible  murmur  that  I  have 
designated  a  pressure  murmur,  this  contraction  suddenly  relaxes,  or  to 
a  certain  extent  remains  permanentl3^  These  are  the  classical  types  of 
intestinal  rigidity,  but  there  are  numerous  deviations.  The  intestine  may 
contract,  for  example,  but  not  tetanically,  it  may  become  hard  and  only 
show  an  increase  of  tonicity  similar  to  what  we  have  observed  in  the 
stomach,  or  it  rises  slightly  in  the  abdominal  wall  and  rapidly  sinks  without 
producing  acoustic  phenomena  in  its  state  of  relaxation. 

The  extent  of  the  stiffened  intestinal  areas  varies  greatly,  according  to 
the  seat  and  the  extent  of  the  stenosis.  Where  stenosis  is  very  marked  and 
provided  the  seat  is  in  the  cecum  or  in  the  ascending  colon,  although  rarely 
when  deeper,  we  note  how  the  small  intestines  rise  one  above  another  like 
the  pipes  of  an  organ,  covering  the  entire  abdominal  surface,  as  has  been 
graphically  described  by  Nothnagel. 

It  is  scarcely  possible  to  confound  this  intestinal  rigidity  with  the  in- 
distinct peristaltic  motion  which  we  meet  with  physiologically  in  well- 
developed  diastasis  of  the  recti,  or  in  motility  neurosis  of  the  intestine 
(tormina  ventric.  nervosa,  Kussmaul).  The  absence  of  pain,  of  rigidity, 
of  constipation,  of  intestinal  splashing,  of  a  pressure  murmur,  indicates 
without  further  consideration  the  marked  difference. 

Although  intestinal  rigidity  points  only  to  the  existence  of  stenosis, 
and  only  exceptionally  to  its  seat,  we  are  frequently  able  to  make  a  diag- 
nosis of  intestinal  carcinoma  as  well  as  from  the  remaining  clinical  course 
even  in  the  absence  of  a  tumor.  Naturally,  this  is  not  always  an  early 
diagnosis  but,  under  some  circumstances,  the  conditions  may  be  so  favor- 
able as  to  permit  a  radical  operation  which  may  bring  relief  to  the  patient 
for  a  long  time. 

In  another  group  of  intestinal  carcinomata  we  find  no  symptoms  of 
intestinal  stenosis;  these  are  the  cases  which  from  the  onset  show  no 
annular  band  formation  with  cicatrization,  but  in  which  diffuse,  infiltrat- 
ing, ulcerating;  tumors  are  found,  as  in  the  curvatures  of  the  stomach. 


244  GASTRIC   AND   INTESTINAL  CARCINOMATA 

The  symptoms  in  these  cases — provided  a  well-developed  localized  tumor 
be  absent — vary  greatly,  according  to  the  stage,  the  seat,  and  the  extent 
of  the  process.  It  may  happen  that  for  weeks  and  even  for  months  positive 
intestinal  symptoms  are  entirely  lacking.  Or,  if  they  are  present,  they 
point  to  a  severe  intestinal  affection  the  nature  of  which  for  a  long  time 
cannot  be  discerned. 

In  such  cases  periodic,  persistent  investigation  of  the  feces  may  in  the 
course  of  time  show  the  true  nature  of  the  condition. 

The  investigation  of  the  feces  in  intestinal  carcinoma  has  not  the  same 
clinical  importance  as  the  examination  of  the  gastric  contents  in  the  diag- 
nosis of  gastric  carcinoma.  But  a  few  factors  are,  nevertheless,  significant. 
Among  these  is  the  single  or  repeated  admixture  of  blood  with  the  feces. 
This  may  introduce  intestinal  carcinoma,  or  may  appear  in  its  course,  or 
may  form  the  terminal  symptom. 

The  hemorrhages  may  be  copious,  or  may  appear  as  small  specks  which 
are  hardly  visible,  or,  finally,  they  may  be  occult  and  only  detected  by 
chemical  examination  (guaiac  test)  or  by  the  spectroscope.  Kochmann 
and  I  observed  such  occult  hemorrhages  in  two  cases  of  carcinoma  of  the 
colon,  and  greater  attention  will,  therefore,  subsequently  be  devoted  to  this 
symptom. 

In  the  main,  however,  copious  intestinal  hemorrhages  are  not  common 
symptoms  of  intestinal  carcinoma.  Such  an  experienced  investigator  as 
Treves  ^  calculates  their  frequency  at  only  15  per  cent.  Whether,  however, 
smaller  hemorrhages  which  readily  escape  recognition  by  the  patient  and 
the  physician  are  not  more  frequent  is  yet  to  be  determined. 

Besides  pure  hemorrhages,  admixtures  of  hlood  and  pus  have  been 
observed  by  other  authors  as  well  as  by  myself.  I  have  repeatedly  noticed 
these  in  deep-seated  intestinal  carcinomata  (in  the  sigmoid  flexure)  which 
offer  more  favorable  conditions  for  the  retention  of  pus  corpuscles  than, 
for  instance,  the  cecum  or  even  the  small  intestine. 

That  mucus  also  is  sometimes  admixed  with  the  feces  is  readily  con- 
ceivable if  we  remember  that  the  carcinomatous  neoplasm  produces  in  a 
large  portion  of  the  intestinal  tube  a  condition  of  catarrhal  inflammation. 
In  a  case  of  carcinoma  of  the  ascending  colon  near  the  cecum,  deter- 
mined at  the  autopsy,  I  observed  even  a  well-developed  membranous 
colitis. 

In  regard  to  the  form  of  the  feces,  it  has  previously  been  briefly  stated 
that  various  deviations  from  the  normal  may  be  observed. 

Thin,  flattened,  tape-like  feces  have  been  designated  as  typical  of  steno- 
sis. Wc  know  to-day  that  this  is  untrue,  not  because  normal  feces  may 
ic'injiorarily  appear  in  stenosis  nor  because  the  changes  mentioned  indicate 
Iho  formation  of  stenosis.     Only  one  condition  of  the  feces  is  never  found 

*  Treves,  "  Intestinal  Obstruction,"  London,  1899. 


CARCINOMA  OF  THE   INTESTINES  245 

in  carcinoma  causing  stenosis,  namely,  a  persistently  well-formed,  cylin- 
drical shape. 

In  very  isolated  cases  of  intestinal  carcinoma,  just  as  in  gastric  car- 
cinoma, shreds  of  the  tumor  are  found  in  the  feces.  The  few  observations 
at  hand  do  not  permit  a  conclusion  as  to  the  clinical  value  of  this  symp- 
tom; nevertheless,  this  much  is  certain,  that  sequestration  only  occurs  in 
well  advanced  cases. 

In  this  description  I  have  considered  mainly  the  high-seated  carci- 
nomata  of  the  large  intestine.  The  deeply-seated  ones,  therefore  those 
from  the  flexura  colico-lienalis  downward,  are  marked  by  certain  peculiar- 
ities which  I  must  briefly  indicate. 

Here  tenesmus,  which  we  must  consider  in  detail  under  the  descrip- 
tion of  carcinomata  of  the  rectum,  becomes  prominent,  not  only  tenesmus 
recti  alone  but  combined  with  tenesmus  vesicae. 

Rectal  Carcinomata. — Occasionally  the  latter  may  be  so  prominent  that 
we  are  inclined  to  think  of  an  affection  of  the  bladder.  If  a  tumor  be 
present  it  is  situated  either  in  the  region  of  the  sigmoid  flexure  or  closely 
adjacent  to  the  bladder  where  it  may  be  felt  below  or  beside  this  organ. 
In  one  of  my  cases  the  tumor  was  situated  at  the  right  side  of  the  bladder, 
and  was  therefore  thought  to  be  a  cecal  tumor.  Occasionally,  however, 
carcinomata  of  the  sigmoid  flexure,  as  Korte  correctly  remarks,  are  not 
susceptible  to  palpation,  that  is,  when  their  situation  is  intermediate,  or 
just  above  the  rectum.  They  cannot  be  reached  by  digital  examination 
either  from  above  or  below,  and  offer  great  difficulty  in  diagnosis  as  well 
as  in  surgical  operations.  Carcinomata  of  the  sigmoid  flexure  lead  imme- 
diately to  the  description  of  the  most  deep-seated  intestinal  carcinomata, 
those  of  the  rectum.  We  shall  proceed  to  consider  these  by  quoting  a 
concrete  case. 

The  patient,  as  was  at  once  apparent,  showed  no  cachexia,  nevertheless 
the  history  denoted  that  we  were  dealing  with  a  serious  affection.  He  was 
52  years  of  age.  He  stated  that  his  mother  perished  after  several  operations 
for  a  tumor  of  the  uterus,  his  father  died  from  apoplexy.  The  patient 
gave  an  excellent  history  of  himself  up  to  the  time  of  the  present  disease, 
which  began  about  five  months  ago  with  a  slight  sensation  of  pressure  and 
inability  to  evacuate  the  bowels  naturally.  The  feces  were. very  frequently 
admixed  with  mucus,  gradually  tenesmus  became  more  marked,  and  every 
three  or  four  hours  the  patient  was  compelled  to  seek  the  toilet,  frequently 
without  other  result  than  thin  fluid  feces  admixed  with  mucus,  and  even 
then  showing  traces  of  blood. 

Thinking  he  had  intestinal  catarrh  he  resorted  to  a  diet  consisting  of 
non-irritating  gruels  and  soups  with  the  result  that  tenesmus  was  produced 
and  his  strength  and  weight  decidedly  decreased. 

Among  the  symptoms  tenesmus  became  prominent  and  this  at  once 
indicated  that  the  seat  of  the  affection  was  in  the  rectum.     Of  course  in  all 


246  GASTRIC  AND  INTESTINAL  CARCINOMATA 

cases  in  which  this  symptom  is  mentioned  we  do  not  invariably  at  once 
think  of  carcinoma,  as  the  same  is  complained  of  by  patients  with  hemor- 
rhoids, with  acute  and  chronic  proctitis,  with  ulceration  in  the  rectum, 
with  prolapse  of  the  rectum,  with  so-called  fecal  impaction,  and  even  in 
purely  nervous  spasm  (proctospasm)  this  symptom  is  by  no  means  rare. 
Nevertheless,  whenever  we  have  the  symptom  of  tenesmus  a  careful  digital 
or  ocular  exploration  of  the  rectum  should  at  once  be  made. 

Before  describing  the  patient's  condition  we  shall  first  determine  whether 
physical  examination  of  the  thoracic  organs  and  external  palpation  revealed 
any  anomaly.  This  was  not  the  case  except  for  one  suspicious  point.  We 
found  that  the  liver  was  decidedly  enlarged.  It  projected  beyond  the 
border  of  the  ribs  about  three  fingerbreadths,  and  the  border  was  con- 
spicuously hard  to  the  touch  but  not  otherwise  painful.  Digital  examina- 
tion confirmed  our  suspicion.  High  up  in  the  rectum  a  hard,  nodulated, 
scarcely  movable  tumor  was  felt,  and,  as  was  observed  when  the  finger 
was  withdrawn  covered  with  blood,  an  ulcerative  tumor. 

This  made  the  diagnosis  in  our  case  positive.  The  only  question  which 
remained  was  whether  the  enlargement  of  the  liver  was  connected  with  this 
carcinoma  of  the  rectum.  I  believe  we  must  answer  this  in  the  affirmative 
as  rectal  carcinoma  is  especially  prone  to  cause  metastatic  processes  by 
means  of  the  hemorrhoidal  veins. 

To  complement  the  examination  of  the  tumor  we  may  view  the  morbid 
focus  directly  by  means  of  a  speculura  which  is  frequently  employed  for 
this  purpose.  However,  I  regard  digital  examination  as  decisive  and  usu- 
ally sufficient.  The  conditions  are  different  with  high-situated  tumors 
which  are  difficult  or  impossible  to  palpate  with  the  finger.  Here,  as  I 
have  convinced  myself,  the  diagnosis  may  sometimes  be  made  by  an  exam- 
ination with  the  speculum.  If  this  also  fails,  examination  under  an 
anesthetic  should  never  be  omitted. 

In  carcinoma  of  Jthe  rectum  in  which  a  tumor  can  be  palpated  exam- 
ination of  the  feces  is  of  secondary  importance.  Where  the  tumor  is 
located  high,  and  inspection  and  palpation  give  no  result,  careful  and 
systematic  examination  of  the  feces  may  guide  us  to  a  correct  diagnosis, 
from  the  fact  that  very  frequently  or  constantly  blood,  mucus  and  pus,  and 
occasionally  desquamated  shreds  of  tumor,  are  found.  At  all  events  we 
should  not  rest  until  we  have  satisfactorily  explained  these  very  conspicu- 
ous changes. 

Various  deviations  from  the  condition  just  described  may  mislead  the 
|)]iysician  who  is  not  familiar  with  these  symptoms.  I  can  quote  a  few 
fiom  my  own  rich  experience  without  by  any  means  exhausting  them. 
In  some  patients  the  disease  sets  in  with  decided  hemorrhage  which,  having 
once  occurred,  is  soon  repeated.  The  patient  believes  that  the  bleeding  is 
from  a  hemorrhoid,  and,  assisted  by  popular  literature  or  by  his  physician, 
is  content  with  his  "golden  vein."     In  other  cases  marked  diarrhea  or 


CARCINOMA  OF  THE   INTESTINES  247 

actual  tenesmus  do  not  point  to  the  rectum  but  to  higher  portions  of  the 
intestine.  In  still  other  instances  I  have  observed  how  accidental  compli- 
cations such  as  minor  genital  affections  (in  one  case  uterine  retroflexion) 
so  engrossed  the  attention  of  the  physician  that  the  affection  of  the  rectum 
was  entirely  overlooked. 

In  three  of  my  cases  pregnancy  was  present,  and  the  patient's  symptoms 
were  attributed  to  this  until  digital  examination  revealed  the  existence 
of  a  rectal  carcinoma.  In  two  of  these,  fortunately,  extirpation  was 
possible. 

Simple  as  the  condition  appears,  the  recognition  of  a  carcinoma  of 
the  rectum  is  difficult  when  the  affection  has  not  developed  along  normal 
lines,  and  when  it  can  only  be  recognized  by  careful  digital  examination, 
which  is  necessary  in  every  such  case  of  intestinal  disturbance. 

Cancer  of  the  Small  Intestine. — In  carcinoma  of  the  small  intestine 
we  are  on  much  more  uncertain  ground.  Carcinoma  of  the  duodenum 
shows  such  similarity  to  the  clinical  picture  of  gastric  carcinoma  that  a 
differentiation  between  them  is  simply  impossible.  At  all  events,  in  car- 
cinomata  situated  below  the  papilla  of  Vater  with  the  constant  regurgita- 
tion of  bilious  masses,  we  may  assume  a  stenosis  in  the  region  of  the 
pars  descendens  duodeni  and  not  beyond  this  unless,  exceptionally,  a 
clearly  localized,  easily  palpable,  and  otherwise  characteristic  tumor  points 
to  the  nature  of  the  affection. 

The  recognition  of  so-called  papillary  carcinomata,  i.  e.,  those  situated 
and  growing  around  the  papilla,  is  extremely  perplexing.  Jaundice  devel- 
ops very  rapidly,  but  it  is  simply  impossible  to  determine  its  cause  on 
account  of  the  many  conditions  which  are  here  present.  If  a  tumor  can 
be  palpated,  sometimes  even  without  this,  the  diagnosis  of  a  malignant 
affection  may  be  more  or  less  accurately  made  from  the  course  of  the 
disease.  The  determination  of  its  seat  is,  however,  always  accidental.  In 
all  carcinomata  of  the  duodenum  gastric  disturbances  are  the  most  promi- 
nent, particularly  vomiting,  while  symptoms  attributed  to  the  intestine 
are  of  a  secondary  nature. 

What  is  true  of  papillary  carcinomata  is,  in  the  main,  true  of  the 
exceedingly  rare  carcinomata  of  the  jejunum  and  ileum,  especially  as  these 
only  exceptionally  lead  to  the  formation  of  a  tumor.  When  a  tumor  is 
present  it  is  distinguished  by  its  great  movability.  Occasionally,  when 
symptoms  of  stenosis  develop  with  constant  vomiting  of  fecal  or  fecaloid 
masses,  we  may  diagnosticate  the  seat  of  the  tumor  as  in  the  jejunum. 
The  appearance  of  intestinal  hemorrhages  may  then  be  a  further  indica- 
tion of  the  nature  of  the  disease.  The  subjective  symptoms,  in  the  main, 
do  not  differ  from  those  of  deeply  situated  duodenal  carcinomata. 


248  GASTRIC   AND   INTESTINAL  CARCINOMATA 


DIAGNOSIS 

The  diagnosis  of  intestinal  carcinomata,  as  is  evident  from  the  fore- 
going, meets  with  great  and  occasionally  insurmountable  obstacles.  We 
shall  not  refer  to  these  again,  nor  shall  we  enumerate  all  the  errors  which 
may  diagnostically  come  into  question,  as  it  is  impossible  to  exhaust  the 
list.  We  hold  that  the  decisive  and  most  important  symptom  is  the  finding 
of  a  tumor  in  the  intestine,  and  even  this,  aside  from  the  difficulty  of  its 
positive  localization,  does  not  confer  absolute  certainty.  Thus,  for  exam- 
ple, a  frequent  source  of  error  which  has  lately  been  much  discussed  is 
found  in  inflammatory  tumors  of  the  cecum. 

Here,  primarily,  the  differentiation  of  intestinal  carcinomata  from  tu- 
bercular ulcers  comes  into  question, 

Obrastzow  ^  mentions  the  following  points  in  the  differential  diagnosis 
of  these  conditions:  In  carcinoma  of  the  cecum  the  intestines  themselves 
cannot  be  palpated,  but  the  tumor  with  the  cylindrical  mass  attached  to  it 
and  extending  downward  as  well  as  the  ascending  colon  passing  upward  is 
palpated.  In  contrast  with  this,  in  tuberculosis  of  the  cecum  the  intestine 
with  its  characteristic  peculiarities  is  for  the  most  part  susceptible  to 
palpation,  but  its  walls  appear  thickened  and  infiltrated.  Moreover,  pal- 
pation usually  shows  the  tumor  of  carcinoma  to  have  sharply  defined 
borders,  while  in  tuberculosis  the  infiltration  more  or  less  gradually  dis- 
appears.    Finally,  in  carcinoma  of  the  cecum  stenosis  very  soon  occurs. 

These  points  may  be  unquestionably  looked  upon  as  auxiliary  factors, 
but  it  is  doubtful  whether  in  the  majority  of  cases  they  enable  us  to 
reach  a  positive  decision. 

The  constant  finding  of  tubercle  hacilli  in  the  feces  without  simul- 
taneous pulmonary  tuberculosis,  as  mentioned  by  Obrastzow,  is  far  more 
decisive.  If  this  is  confirmed  we  will  have  an  additional  diagnostic  cri- 
terion. Besides  this,  the  age,  the  duration  of  the  disease,  the  state  of  the 
lungs  and  the  course  of  the  fever  will  aid  in  the  diagnosis.  Collectively 
in  isolated  cases  they  make  a  definite  opinion -possible,  in  others  this  will 
be  tentative,  and  will  remain  so  until  later  clinical  signs  (ascites,  etc.) 
or  laparotomy  remove  all  doubts. 

Besides  cecal  tuberculosis  other  inflammatory  processes  from  the  vernji- 
form  appendix,  and  occasionally  also  from  the  typhlon,  may  assume  a 
tumor-like  character  so  that  in  deciding  as  to  their  nature  certain  doubts 
arise.  Errors  in  diagnosis  are  frequently  made  in  surgical  cases  from  the 
fact  that  malignant  tumor  has  been  assumed  where  a  simple  exudate  is 
present,  and  vice  versa.  But  by  careful  clinical  observation  these  errors, 
as  a  rule,  may  bo  avoided. 

The  same  is  true  of  the  exceedingly  rare  cases  of  benign  tumors  in  the 

'  Obrastzow,  Arch.  f.  V erdwuurigskrankheiten,  Bd.  IV,  1898. 


CARCINOMA  OF  THE  INTESTINES  249 

cecum  (myomata,  lipomata,  fibromata,  etc.),  while  the  differentiation  from 
sarcomata  is  only  possible  under  very  favorable  clinical  circumstances. 

Benign  infiltrations  may  occur  in  the  sigmoid  flexure  as  well  as  in  the 
cecum  (sigmoiditis) ;  occasionally  they  are  of  the  consistence  of  a  neoplasm 
and  thus  make  the  diagnosis  difficult  or  impossible. 

Spastic  contractures  of  the  colon  must  here  be  referred  to;  they  are 
frequently  associated  with  obstinate  habitual  constipation,  and  are  found 
particularly  in  the  transverse  colon,  in  the  cecum,  and  are  occasionally 
very  conspicuous  in  the  descending  colon  and  the  sigmoid  flexure.  As  a 
rule,  however,  it  is  possible  at  once  to  determine  a  functional  spasm  by 
inflation  or  by  filling  the  intestine  with  water.  By  this  means  the  spasm 
completely  disappears  to  develop  anew  after  a  short  time. 

"We  are  here  upon  more  positive  ground  than  in  the  diagnosis  of  tumors 
of  the  rectum.  In  so  far  as  they  may  be  reached  by  the  finger  or  the 
speculum,  they  rarely  cause  confusion,  and  above  all,  benign  neoplasms  and 
syphilitic  strictures  here  come  into  question.  In  regard  to  the  first,  with 
the  exception  of  polypi,  which  are  extremely  rare,  we  observe  that  benign 
tumors  of  the  rectum  never  produce  ulceration,  while  these  as  a  rule  occur 
very  early  in  carcinomata  of  the  rectum;  nor  does  stenosis  occur,  at  least 
not  the  very  characteristic,  rigid  stenosis  of  carcinoma.  I  must  not  fail 
to  mention,  however,  that  benign  tumors  of  the  rectum,  particularly  polypi 
and  papillomata,  not  rarely  in  later  years  lay  the  foundation  for  carcinoma. 
I  have  observed  a  case  of  this  kind. 

Well  developed  syphilitic  stenoses  present  an  'entirely  different  appear- 
ance from  carcinomatous  ones.  As  Kraske  ^  correctly  states,  syphilitic 
ulcerations  never  have  the  coarse,  tumorous  border  of  the  malignant,  and, 
unlike  these,  are  usually  multiple  and  separated  from  one  another  by  areas 
of  normal  or  cicatricially  altered  mucous  membrane.  In  doubtful  cases 
the  diagnosis  may  also  be  made  by  microscopic  examination  of  a  small 
excised  particle  or  a  portion  that  has  been  detached  by  the  finger. 

Diagnosis  of  Cancer  of  the  Small  Intestine. — The  diagnosis  of  carci- 
noma of  the  small  intestine,  even  when  tumor  is  present,  is  most  difficult. 
So  long  as  we  are  dealing  with  the  upper  portion  of  the  duodenum  and 
on  account  of  the  identity  of  the  clinical  course,  the  differentiation  from 
gastric  carcinoma,  as  has  already  been  mentioned,  is  simply  accidental. 
Lower  down,  particularly  in  the  descending  part  of  the  duodenum,  the 
conditions  are  somewhat  more  favorable,  as  the  permanent  regurgitation 
of  bile  is  a  valuable  point  in  regard  to  the  seat  of  the  tumor.  Still  further 
down,  however,  the  clinical  symptoms  again  become  indistinct,  and  only 
exceptionally  permit  a  well-founded  opinion. 

The  nearer  the  carcinoma  of  the  small  intestine  is  to  the  ileo-cecal 


*  Kraske,    "  Erfahrungen    iiber    den    Mastdarmkrebs."      Volkmann's    Sammlung 
klin.  Vortrdge.     1883-84,  p.  789. 


250  GASTRIC   AND  INTESTINAL  CARCINOMATA 

valve,  the  more  closely  does  the  clinical  picture  resemble  that  of  carcinoma 
of  the  large  intestine,  and  it  becomes  impossible  positively  to  diagnosticate 
the  condition. 

All  this  is  true  of  intestinal  carcinomata  with  determinable  tumor  for- 
mation. Where  this  is  absent  the  conditions,  as  a  rule,  are  still  more  com- 
plex. Not  that  the  diagnosis  under  these  circumstances  is  impossible; 
on  the  contrary,  for  example,  stenosed  carcinomata  of  the  large  intestine, 
even  without  palpable  tumors,  may  furnish  typical  cases.  In  others — 
at  least  as  far  as  the  determination  of  a  stricture  of  the  large  intestine 
and,  proceeding  from  this  fact,  a  reflection  of  the  entire  clinical  picture — 
a  probable  and  even  a  positive  diagnosis  of  carcinoma  of  the  intestine  may 
be  made.  Nevertheless,  complicating  factors  frequently  mislead  the  diag- 
nostician, so  that  great  care  is  necessary. 

We  waver,  however,  in  our  opinion  when  a  palpable  tumor  and  symp- 
toms of  stenosis  are  absent.  In  this  case  the  clinical  impression  can  at 
most  only  indicate  the  correct  direction,  and  this  impression  is  further 
strengthened  by  certain  episodes,  for  example,  the  onset  of  severe  hemor- 
rhage, the  discharge  of  particles  of  the  tumor,  the  appearance  of  palpable 
metastases,  ascites  and  edema,  perforation  into  neighboring  organs  which 
usually  occurs  at  a  very  late  stage,  and  is  unfavorable  for  "  operative " 
treatment.  Examination  of  the  feces  may  mislead  us,  especially  as  the 
finding  of  blood  and  pus  is  susceptible  of  many  explanations,  and  does 
not  permit,  for  example,  a  differentiation  from  ulcerative  colitis. 


COMPLICATIONS   AND   SEQUELS 

The  complications  and  sequels  of  carcinoma  of  the  intestine  in  many 
respects  resemble  those  of  carcinoma  of  the  stomach.  In  one  as  in  the 
other  febrile  conditions  may  appear,  usually  in  the  advanced  stages  of  the 
affection.  Coma  carcinomatosum  has  also  been  observed  in  cancer  of  the 
intestine.  Metastasis  of  the  liver,  ascites,  pleurisy,  peritoneal  carcinosis, 
external  or  internal  ruptures  occur — particularly  into  the  peritoneum,  the 
bladder  and  the  female  genital  organs.  Other  sequels  belong  to  the  realm 
of  casuistics,  and  therefore  do  not  need  especial  mention  at  this  place. 

The  chief  complication  of  stenotic  carcinoma  requires  a  thorough  de- 
scription: The  transition  of  partial  into  complete  obstruction.  This  may 
increase  slowly  and  gradually  to  total  occlusion,  or  it  occurs  suddenly  in 
a  previously  permeable  intestine  and  may  astonish  the  patient  as  well  as 
the  physician.  The  latter  may  be  due  to  several  causes:  Either  the  power 
of  the  liypertrophied  suprastenotic  musculature,  which  has  functioned  well, 
ceases  suddenly  and  completely,  or  in  and  immediately  above  the  stricture 
obstructing  fecal  plugs  or  a  residue  of  food  have  accumulated  which,  not- 
withstanding sufficient  muscular  power,  make  propulsion  impossible,  or, 
finally,  a  quantity  of  stagnating  fecal  masses  may  produce  volvulus. 


TREATMENT   OF  CARCINOMATA  251 

In  these  cases  a  fulminant  intestinal  occlusion  occurs  with  threatening 
danger  which  can  only  be  averted  by  an  early  operation.  Pseudo-ileus 
may,  however,  also  be  present.  The  patient  presents  the  severe  picture  of 
absolute  intestinal  occlusion.  Internal  treatment  is  entirely  without  result 
but,  nevertheless,  contrary  to  our  expectations,  the  intestines  may  again 
become  open,  the  patient  may  pass  gas  and  feces,  and  is  for  the  moment 
saved.  But  only  for  the  moment !  For  the  next  or  a  succeeding  obstruc- 
tion may  become  complete  and,  in  spite  of  medical  treatment,  pursue  its 
fatal  course  unless  surgery  again  intervene  at  the  proper  time. 

PROGNOSIS 

The  prognosis  of  cancer  of  the  intestine,  as  need  scarcely  be  reiterated, 
is  in  the  main  just  as  grave  as  that  of  other  carcinomata.  But,  in  the 
opinion  of  numerous  surgeons,  the  tendency  to  the  formation  of  metastasis 
is  not  so  great  as  in  cancer  of  the  stomach,  so  that  operation  performed 
at  the  right  time  offers  in  the  main  better  chances  than  in  the  latter 
affection.  And,  as  we  shall  point  out  in  the  chapter  devoted  to  treatment, 
the  possibility  of  total  extirpation,  for  example,  in  carcinoma  of  the  colon 
and  of  the  rectum,  is  more  frequent  than  in  carcinoma  of  the  stomach; 
the  circumstance  also  that  in  carcinoma  of  the  colon  and  of  the  rectum  the 
nutrition  is  relatively  but  little  affected  makes  the  prognosis  somewhat 
more  favorable  than  in  carcinoma  situated  higher  up. 

TREATMENT    OF    CARCINOMATA    OF    THE    STOMACH   AND    OF 

THE    INTESTINES 

This  combined  description  of  the  treatment  of  carcinomata  of  the 
stomach  and  intestines  has  not  been  without  a  purpose.  The  fundamental 
laws  of  internal  as  well  as  of  operative  treatment  present  in  both  such 
numerous  points  of  contact  that  a  collective  presentation  is  by  far  the 
best  to  answer  didactic  requirements. 

Complete  cure  of  a  gastric  or  intestinal  carcinoma  is  unknown,  not 
even  by  means  of  the  knife.  The  latter  by  radical  or  palliative  procedures 
may  decidedly  prolong  life,  not,  however,  or  at  least  very  exceptionally,  up 
to  the  normal,  probable  duration  of  life  of  the  individual  in  question; 
but  even  with  the  highly  developed  surgical  technic  of  to-day  and  the 
popularity  of  operations  on  the  intestinal  canal,  this  prolongation  of  life 
occurs  only  in  a  small  fractional  number  of  the  patients.  "According  to 
the  statistics  of  G.  Heimann  ^  made  in  Prussian  hospitals  in  the  years 
1885  and  1886,  14.4  and  15.9  per  cent,  respectively  of  patients  with 
cancer  of  the  stomach  were  treated  by  operation,  and  even  in  cancer  of 
the  rectum  in  the  same  years  only  45  per  cent.,  at  most  50  per  cent.,  of 


1  0.  Heimann,  Arch.  f.  klin.  Cliirurgie,  Bd.  LVII,  p.  4. 


252  GASTRIC  AND  INTESTINAL  CARCINOMATA 

the  cases  were  operated  upon.  We  cannot  be  far  wrong  in  assuming  that 
the  remaining  number  were  already  in  such  a  hopeless  condition  that 
operation  appeared  to  be  useless. 

Therefore,  the  majority  of  patients  with  cancer  of  the  stomach,  even 
to-day,  must  he  treated  by  internal  means  and  in  no  inconsiderable  num- 
ber of  those  operated  upon  this  is  necessary  after  the  operation  {palliative 
or  radical). 

Internal  Treatment. — The  objects  of  internal  treatment  depend  in  gen- 
eral upon  the  following  considerations:  As  an  actual  cure  is  impossible 
it  becomes  necessary,  just  as  in  other  internal  conditions  (gall-stones,  dia- 
betes) to  keep  the  affection  latent  as  long  as  possible,  and  to  ameliorate 
or  remove  the  subjective  and  objective  disturbances  which  arise.  This 
may  suffice  for  a  certain  time  but  permanently  it  is  inadequate,  and  the 
reasons  for  this  are  manifold. 

Primarily,  we  must  consider  the  mechanical  disturbances  which  fre- 
(luently  arise  in  gastrointestinal  carcinoma,  then  certain  toxic  products 
which  are  produced  by  the  carcinoma,  subsequently  the  hemorrhages  which 
mediately  or  immediately  are  caused  by  the  carcinoma,  also  metastasis, 
and,  finally,  the  disturbances  of  metabolism  which,  even  though  not  wholly, 
are  nevertheless  in  great  part  the  consequence  of  carcinoma. 

In  regard  to  the  latter,  the  accurate  investigations  of  F.  Kraus,  Fr. 
IMiiller,  and  Klemperer,  to  which  those  of  v.  Noorden-Gartig  must  be  added, 
liave  given  us  full  information.  They  have  unanimously  shown  that  a 
number  of  patients  with  cancer,  notwithstanding  plentiful  food  and  a 
liigh  amount  of  albumin,  permanently  lose  N.  Fr.  Miiller  found  that  on 
increasing  the  administration  of  food  the  conditions  remained  unchanged. 
Tlic  N-excretion  was  invariably  greater  than  the  IST-intake.  The  increase 
of  acetone  observed  by  F.  Blumenthal  in  severe  carcinomatous  cachexia 
points  to  an  increased  decomposition  of  albumin.  The  more  these  products 
increase,  the  more  marked  and  persistent  is  the  loss  of  strength,  and 
vice  versa. 

It  is,  therefore,  evident  that  the  nourishment  of  patients  with  cancer 
is  extremely  difficult.  In  addition  to  this,  the  appetite  in  the  course  of 
carcinoma  is  very  frequently,  although  fortunately  not  always,  decidedly 
decreased,  chiefly  so  in  carcinoma  of  the  stomach  and  small  intestine,  and 
to  a  somewhat  slighter  degree  in  carcinoma  of  the  colon  and  rectum. 

We  must  always  bear  in  mind  the  importance  of  nourishing  patients 
with  cancer  as  plentifully  as  possible.  Our  individual  points  of  view  must 
depend  upon  the  position  and  the  nature  of  the  carcinoma,  and  the  stage 
in  wliicli  tlie  patient  comes  under  professional  observation. 

Let  us  begin  with  cancer  of  the  stomach.  We  find  the  conditions 
vastly  different  according  to  whether  the  carcinoma  runs  its  course  with 
or  without  very  decided  motor  disturbance,  or,  vice  versa,  severe  symp- 
toms of  stagnation  are  present;  in  the  latter  case,  as  a  rule,  vomiting 


TREATMENT   OF  CARCINOMATA  253 

dominates  the  scene.  In  the  former  case,  a  decided  limitation  of  diet 
is  not  indicated,  or  to  but  very  slight  extent.  Albumin,  carbohydrates,  and 
fat,  naturally  most  carefully  prepared,  are  permissible,  and  above  all  milk 
and  milk  preparations  in  the  most  varied  form  and  according  to  the  indi- 
vidual circumstances  and  the  wishes  of  the  patient. 

With  a  fairly  good  appetite  and  the  careful  combination  of  foods,  it 
may  be  possible  to  keep  the  patient  for  weeks  and  months  in  good  condi- 
tion, and  now  and  then  even  to  increase  his  weight.  Occasionally  the 
patients  are  subjectively  better,  and  their  courage  revives,  a  fact  to  which 
the  gain  in  weight  conduces  not  a  little. 

It  is  unfortunate  that  most  patients  with  cancer  of  the  stomach  have 
a  distinct  repugnance  to  meat  and  meat  derivatives  (therefore  to  bouillon 
and  meat  extracts).  Hence  the  administration  of  meat  cannot  be  insisted 
upon,  but  an  attempt  should  be  made  to  administer  other  albumin  bodies, 
with  eggs,  carbohydrates  rich  in  albumin,  dishes  prepared  with  milk,  etc. 
After  a  prolonged  abstinence  from  meat  an  attempt  may  be  made  again  to 
administer  it  in  some  form,  but  usually  without  success. 

The  nourishment  of  the  patient  is  much  more  difficult  in  carcinoma 
at  or  near  the  pylorus.  Here,  as  a  rule,  we  are  limited  to  fluid  food,  and 
often  but  small  quantities  will  pass  through  the  pylorus.  Above  all,  milk 
preparations,  soup  with  the  yolk  of  an  egg,  the  various  leguminous  vege- 
tables, and  cereals  in  convenient  form,  may  prove  serviceable.  That  only 
small  quantities  should  be  administered  will  be  understood.  From  the 
quantity  of  urine  voided,  and  by  comparing  the  amount  of  material  found 
in  the  stomach  by  lavage  in  the  early  morning  with  the  amoimt  of  fluid 
introduced,  we  can  practically  estimate  the  amount  absorbed. 

It  is  perhaps  well  at  this  point  to  touch  upon  the  value  of  artificial 
food  preparations  in  cancer  of  the  stomach.  We  may  to-day  regard  it 
as  certain  that  they  have  no  beneficial  effect  on  the  nutrition. 

Their  value  consists  solely  in  the  fact  that  the  patients  who  have  no 
appetite  for  food,  but  actual  repugnance,  regard  the  intake  of  these  sub- 
stances mixed  with  nutritive  preparations  as  a  duty  to  which  they  submit 
as  willingly  as  to  that  of  taking  medicine.  From  this  standpoint  it  is 
quite  immaterial  what  artificial  food  we  administer  to  cancer  patients. 
The  individual  taste  will  best  decide.  According  to  my  personal  experi- 
ence the  most  suitable  preparations  are :  Puro,  meat  jelly,  somatose,  sanato- 
gen,  roborat.     These  products  will  also  furnish  a  sufficient  variety. 

Luxuries,  substances  which  tempt  and  stimulate  the  appetite  (v.  Ley- 
den),  are  just  as  important  as  nutritive  preparations.  What  has  been 
said  above  is  also  true  of  these.  By  their  aid  it  is  often  possible  for  a 
long  time  to  keep  the  patient  away  from  the  cliffs  of  inanition.  What  is 
advisable  in  the  individual  case  depends  upon  the  social  position,  upon 
the  habits,  and  finally  upon  the  wishes  of  the  patient.  At  all  events  by 
being  too  strict  we  may  do  more  harm  than  good. 


254  GASTRIC   AND  INTESTINAL  CARCINOMATA 

Among  the  auxiliary  dietetic  measures  belong  artificial,  or,  as  it  has 
lately  been  called,  extra-buccal  nutrition.  For  the  technic  and  other  details 
we  must  refer  to  von  Leube's  excellent  description.  It  only  remains  for 
us  briefly  to  mention  the  value  of  this  in  carcinoma  of  the  stomach. 
Unquestionably  the  mere  introduction  of  fluid  to  prevent  a  too  dry  con- 
dition of  the  organism  may  also  prevent  threatening  tetany  and  the  accu- 
mulation of  toxic  products,  and  the  intake  of  even  a  few  calories  is  a  gain 
which  should  never  be  undervalued. 

No  one  will  claim  that  extra-buccal  nutrition  decidedly  prolongs  the 
life  of  the  patient  with  cancer.  The  simplest  method  and  the  one  most 
in  use  is  by  means  of  nutritive  enemata;  subcutaneous  methods  (oil-sugar 
solutions),  no  matter  upon  what  scientific  principle  they  are  based,  have, 
as  yet,  not  found  general  acceptance. 

What  is  true  of  cancer  of  the  stomach  is  also  true  of  carcinoma  of  the 
S77iaU  intestine. 

In  carcinoma  of  the  large  intestine  other  points  of  view  arise,  and, 
above  all,  it  is  here  an  absolute  law  that  we  should  avoid  everything  in 
diet  which  may  obstruct  or  delay  the  passage  of  the  feces.  Avoidance  of 
all  substances  ivith  sJchis  containing  residue  unsuitable  to  the  gastric  and 
intestinal  juices  is  therefore  a  leading  principle.  Then  the  nutrition  must 
be  calculated  directly  to  stimulate  intestinal  peristalsis.  This  may  be 
attained  by  physiologic  aperients:  Honey,  milk  sugar,  sour  milk,  stewed 
fruit,  lemonade,  wines  made  from  fruit,  marmalade,  and  fruit  jellies. 
Other  foods  may  be  given  in  the  form  and  manner  mentioned  under  the 
consideration  of  cancer  of  the  stomach. 

In  ulcerating  carcinomata  which  do  not  run  their  course  with  the 
formation  of  stenosis,  we  must  be  particularly  careful  of  the  diet.  The 
most  suitable  articles  here  are  milk  and  milk  preparations,  soups  made 
from  leguminous  vegetables,  soups  containing  eggs,  meat  jelly,  etc.  In 
extreme  stenosis  from  obstruction  the  introduction  of  food  is  most  diflBcult 
on  account  of  the  mechanical  hindrance  to  the  passage  of  feces.  Under 
these  circumstances  we  must  limit  ourselves  to  small  amounts  of  highly 
concentrated  food. 

The  artificial  introduction  of  food  in  carcinoma  of  the  large  intestine 
is  only  permissible  provided  the  neoplasm  does  not  extend  lower  down 
than  the  cecum  or  the  flexura  colico-hepatica.  Below  this  it  will  irritate 
ratlier  tlian  benefit  the  nutrition.  In  carcinoma  of  the  sigmoid  flexure 
tliere  can  naturally  be  no  question  of  rectal  alimentation.  Reports  in 
regard  to  subcutaneous  nutrition,  which  is  here  indicated,  are  not  to  my 
knowledge  at  hand. 

Drug  Treatment. — To  ameliorate  the  sufferings  which  carcinomata  of 
the  stomach  and  intestines  bring  in  their  train  drugs  are  often  useful, 
occasionally  even  indispensable. 

One  of  the  most  frequent  causes  of  distress  in  gastric  and  occasionally 


TREATMENT   OF  CARCINOMATA  255 

also  in  intestinal  carcinoma  is  loss  of  appetite.  Often  this  can  be  relieved 
for  a  time  by  the  so-called  stomachics,  by  condurango  as  well  as  by  other 
bitters;  as  a  rule,  however,  they  fail.  In  so-called  achylia  gastrica,  which, 
as  before  stated,  very  frequently  occurs  in  gastric  cancer,  we  may  employ 
hydrochloric  acid  and  also  pancreatic  preparations  to  improve  the  digestion. 
Recently  pankreon  has  been  much  employed  in  the  form  of  tablets  each 
containing  one  gram. 

Pain  in  the  region  of  the  stomach  and  particularly  of  the  intestine 
also  calls  for  relief.  In  gastric  pain,  as  a  rule,  mild  narcotics  (codein, 
dionin)  suffice.  In  severe  cases  of  obstruction,  in  intestinal  carcinoma, 
the  most  powerful  narcotics  are  necessary.  First  among  these  is  opium 
in  the  form  of  the  tincture  of  thebain,  or  pure  opium  (0.03-0.05)  perhaps 
in  combination  with  belladonna  (extract  of  belladonna  0.01-0.03),  then 
morphin  as  a  powder,  in  solution,  by  suppositories  or  subcutaneously. 

Obstinate  constipation  by  no  means  contraindicates  the  administra- 
tion of  opium;  on  the  contrary  we  frequently  see  that  after  complete  in- 
testinal rest  normal  intestinal  peristalsis  again  sets  in. 

Opiates  act  remarkably  well  in  the  severe  rectal  and  vesical  tenesmus 
which  we  have  learned  to  recognize  as  regular  accompaniments  of  deep- 
seated  carcinoma.  By  the  influence  of  these  drugs  the  patients  may  be 
spared  these  distressing  symptoms  for  many  hours  during  the  day  or 
during  the  night. 

Purgatives  play  an  important  role  in  the  treatment  of  gastric  and 
intestinal  carcinomata.  In  the  former  purgatives  will  only  rarely  be 
administered,  preference  being  given  to  lavage.  If  aperients  are  indi- 
cated, fluids  or  substances  readily  soluble  in  water  are  preferable  to  pills 
and  also  to  tablets  which  are  frequently  dissolved  with  difficulty  or  not 
at  all. 

In  the  stage  of  intestinal  rest  in  carcinoma  of  the  intestine,  purgatives 
are  usually  indispensable,  and  here  also  purgatives  that  are  easily  soluble 
yet  at  the  same  time  are  mild  and  act  quickly  are  the  best.  As  most  suit- 
able remedies  for  this  purpose  I  advise:  Fluid  extract  of  cascara,  com- 
pound licorice  powder,  castor  oil,  magnesium,  rhubarb,  flowers  of  sulphur 
and,  finally,  mineral  waters  in  small  doses.  In  intestinal  carcinoma  it  is 
wise  to  keep  the  bowels  regulated  by  the  continuous  use  of  a  suitable 
purgative  and  thus  avoid  being  surprised  by  the  sudden  cessation  of  peri- 
staltic action. 

Mechanical  Treatment  (gastric  lavage). — Gastric  lavage  in  cancer  of 
the  stomach  and  small  intestine  may  prove  useful  and  palliative,  but  even 
here  we  must  individualize  strictly.  This  should  not  be  resorted  to  so 
long  as  the  motor  activity  of  the  stomach  is  unimpaired.  It  is  true  that 
lavage  acts  favorably  upon  the  pain,  also  occasionally,  when  stagnation 
exists,  upon  the  appetite. 

But  even  when  this  is  the  case,  the  nature  of  the  carcinoma,  its  stage, 
18 


256  GASTRIC  AND  INTESTINAL  CARCINOMATA 

and  the  strength  of  the  patient  must  be  carefully  considered.  In  stagna- 
tion not  too  far  advanced  lavage  may  be  employed,  provided  pain,  a  sensa- 
tion of  pressure,  nausea,  vomiting  and  anorexia  are  present.  Stagnation 
itself,  in  my  experience,  does  not  necessitate  the  employment  of  lavage. 
In  the  course  of  years  I  have  seen  numerous  patients  with  cancer  of  the 
stomach  vi'ho,  in  spite  of  moderate  stagnation,  remained  in  fair  condition 
for  quite  a  long  time. 

With  severe  stagnation  and  coffee-ground  contents  I  no  longer  employ 
gastric  lavage,  because  I  have  observed  that  the  patients  are  much  worse 
after  this  treatment  than  before.  If  it  be  necessary  to  remove  the  stagnant 
masses,  an  expression  limited  to  a  few  minutes  is  sufficient.  But  even  in 
incipient  cases  I  believe  it  wise  to  resort  to  gastric  lavage  as  little  as 
possible.  With  care  in  the  diet  we  are  frequently  able  to  prevent  abnormal 
collections  of  material. 

Indications  for,  and  Results  of,  Operative  Treatment. — The  physician 
is  to-day  in  duty  bound  carefully  to  study  the  indications  for,  and  the 
results  of,  abdominal  surgery.  In  advising  or  rejecting  operation,  he  is 
often  held  responsible  both  for  what  is  done  and  what  remains  undone. 
He  will  base  his  opinion,  in  the  first  place,  upon  statistics  of  large  groups 
of  cases,  and  then  upon  personal  experience.  In  any  event,  no  matter 
how  the  individual  case  may  present  itself,  the  following  questions  are 
sure  to  arise: 

1.  Is  surgical  interference  indicated  in  the  stage  in  which  this  patient 
presents  himself? 

2.  If  this  be  the  case,  what  operation  is  indicated,  and  what  are  the 
probabilities  of  success? 

In  some  individuals  the  answer  to  the  first  question  is  easy,  in  others 
difficult  or  even  impossible.  The  decision  may  be  quickly  made  in  dealing 
with  very  cachectic  individuals,  also  in  those  cases  in  which  diffused  edema, 
ascites,  diabetes,  hepatic  metastases,  or  serious  complications  on  the  part 
of  the  heart,  the  lungs  or  the  kidneys  exist.  Under  these  circumstances, 
naturally,  any  surgical  interference  will  only  hasten  the  end.  Nor  will 
we  resort  to  operation  if,  for  example,  there  is  a  very  circumscribed  carci- 
noma of  the  small  curvature,  which  neither  subjectively  causes  severe 
symptoms,  nor  objectively  produces  serious  motor  disturbance.  Experi- 
ence teaches  us  that  in  such  cases  the  duration  of  the  patient's  life  is  no 
less  than  after  operation,  provided  that  exceptionally  a  radical  removal 
is  indicated  by  the  position  of  the  growth.  According  to  my  experience 
the  prognosis  is  very  serious  in  those  cases  of  carcinoma  (usually  at  the 
pylorus)  in  which  the  vomited  material  or  the  evacuated  gastric  contents 
resemble  coffee-grounds.  The  results  which  I  have  seen  after  even  pallia- 
tive operation  can  scarcely  be  called  good. 

In  carcinoma  of  the  large  intestine  and  rectum  the  conditions  are 
quite  similar,  but  the  lower  down  the  growth  is  situated,  the  more  favor- 


f 


TREATMENT   OF  CARCINOMATA  257 

able  are  the  prospects  of  a  radical  operation.  We  shall  revert  to  this 
later. 

In  regard  to  the  second  question,  if  there  are  no  contra-indications 
such  as  have  been  mentioned,  surgical  interference  becomes  necessary  and 
we  must  now  consider  the  question:  What  operation  is  to  be  performed, 
shall  it  be  the  radical  removal  of  the  tumor  or  merely  palliative  treatment, 
i.  e.,  the  removal  of  the  motor  disturbance  ? 

Let  us  begin  with  the  stomach.  In  the  first  place,  we  must  confess 
that  an  absolutely  positive  decision  as  to  whether  extirpation  or  gastro- 
enterostomy is  indicated  is  most  difficult  to  answer  prior  to  the  laparotomy. 
No  matter  how  favorable  the  location  of  the  tumor,  laparotomy  may  show 
such  a  general  extension  of  the  carcinoma  that  a  radical  removal  of  the 
tumor  is  simply  impossible,  v.  Mikulicz  and  Kausch  ^  therefore  very 
properly  remark  that  every  operation  is  primarily  an  exploratory  laparot- 
omy, and  a  definite  plan  of  operation  depends  upon  what  is  found  on 
opening  the  abdominal  cavity. 

In  many  cases  we  may  at  once  exclude  the  possibility  of  total  extirpa- 
tion, for  example,  when  the  tumors  are  large  and  immovable  or  when  the 
tumor  is  movable  but  the  patient  has  not  sufficient  strength. 

In  non-palpable  tumors  the  decision  is  still  less  possible  prior  to  ex- 
ploratory incision.  When  we  have  reason  to  assume  that  a  pyloric  car- 
cinoma causes  stenosis,  a  radical  operation  is  at  least  possible.  In  other 
cases,  however,  even  with  a  positive  diagnosis,  such  an  operation  can  hardly 
be  advised. 

Besides  gastroenterostomy,  as  a  palliative  procedure  we  should  also 
consider  jejunostomy  which  is  particularly  advised  by  v.  Maydl.  He 
introduced  this  operation  for  the  cases  of  gastric  disease  in  which  a  great 
portion  of  the  stomach  was  destroyed,  and  in  which  it  was  impossible  to 
supply  sufficient  nutrition. 

Recently  this  surgeon  has  advised  us  to  employ  jejunostomy  in  place 
of  gastroenterostomy,  as  the  former  is  much  more  thorough,  and,  besides, 
meets  the  important  requirements  of  the  case  by  sparing  the  diseased 
organ  and  protecting  the  neoplasm  from  all  irritation. 

However,  this  operation  has  been  employed  by  surgeons  only  to  a 
limited  extent,  chiefly  for  the  reason  that,  like  all  operations  for  fistula, 
cosmetically  it  is  not  fully  satisfactory.  The  prolongation  of  life,  too, 
is  less  than  after  gastroenterostomy. 

As  a  very  thorough  operation,  total  extirpation  of  the  stomach,  the 
union  of  the  upper  duodenum  and  the  cardia,  or  the  lowest  portion  of 
the  esophagus,  which  was  first  successfully  performed  by  Schlatter  in 
Zurich,  comes  into  question.     Although  to-day  quite  a  number  of  favor- 

'  V.  Mikulicz  und  Kausch,  "  Handbuch  der  praktischen  Chirurgie,"  Separatab- 
druck,  p.  147. 


258  GASTKIC  AND  INTESTINAL  CARCINOMATA 

able  results  are  reported  in  surgical  literature,  nevertheless,  as  v.  Mikulicz 
and  Kausch  ^  state,  metastatic  lymph-glands  are  rarely  absent  in  any  case 
of  gastric  carcinoma,  and,  therefore,  we  should  not  indulge  in  too  great 
expectations  of  the  results  of  this  heroic  treatment.  On  the  other  hand, 
it  must  be  admitted  that  some  remarkable  successes — for  instance,  the  last 
case  operated  upon  by  Fedor  Krause — favor  the  radical  removal  of  the 
neoplasm.  At  the  present  time,  however,  the  definite  results,  the  failures 
and  successes,  cannot  be  positively  recorded. 

In  the  main,  gastroenterostomy  and  resection  of  the  pylorus  are  the 
operations  at  this  time  most  frequently  performed. 

With  the  results  of  these  methods  we  are  comparatively  well  acquainted, 
a  large  number  of  statistics  being  available,  as  well  as  the  individual 
reports  of  eminent  surgeons.  Thus,  Terrier  and  Hartmann  have  collected 
the  statistics  of  abdominal  operations  performed  by  distinguished  surgeons 
(Czerny,  Kronlein,  Carle,  v.  Mikulicz,  Kocher,  and  Hartmann)  and  from 
127  resections  of  the  pylorus  have  calculated  a  mortality  of  26  per  cent.; 
but  this  varies  greatly.  For  example,  Lindner  has  lately  estimated  the 
mortality  at  50  per  cent.  In  the  main,  however,  the  results  of  resection 
ill  the  course  of  the  last  twenty  years  have  gradually  improved,  v.  Miku- 
licz^ computed  the  total  of  radical  cures  at  17  per  cent. 

If  this  estimate  is  compared  with  the  total  number  of  cures  of  other 
carcinomata  we  are  by  no  means  hopeless.  According  to  v.  Mikulicz,  the 
cases  of  carcinoma  of  the  breast  permanently  cured  amount  to  from  10 
to  15  per  cent.,  with  curettage  of  the  axillary  cavity  to  25  to  30  per  cent., 
in  carcinoma  of  the  uterus  30  to  35  per  cent.,  in  carcinoma  of  the  rectum 
10  to  20  per  cent.,  in  carcinoma  of  the  tongue  10  to  20  per  cent.  If 
we  compare  these  with  the  results  of  gastroenterostomy,  the  latter,  on 
account  of  a  more  complete  technic,  and,  above  all,  by  the  avoidance  of  the 
so-called  vicious  circle,  are  decidedly  better.  While,  according  to  the  last 
great  statistical  report  of  Chlumky,  the  mortality  from  1881  to  1885  was 
still  75  per  cent.,  from  1886  to  1890  it  decreased  to  48.4  per  cent.,  and 
from  1890  to  1896  declined  to  36.61  per  cent.;  for  the  past  five  years 
V.  Mikulicz  estimated  his  operative  loss  at  only  28  per  cent,  (in  his  last 
report  v.  Mikulicz  computes  these  fatalities  at  26  per  cent.). 

In  gastroenterostomy,  however,  not  only  the  immediate  results  of  the 
operation  but  the  prolongation  of  life  as  well  as  the  functional  results  must 
also  be  considered.  As  to  the  former,  the  average  results  are  not  very 
satisfactory.  Life  was  prolonged  for  five  or  six  months;  now  and  then 
there  must  have  been  brilliant  exceptions  to  this. 

jSTor  is  the  functional  effect  in  all  cases  satisfactory.     Frequently  the 


2  r.  Mikulicz,  73.  Tersammlung  deutscherNaturforscher  und  Aerzte  in  Hamburg, 
1901.     Referat. 


TREATMENT   OF  CARCINOMATA  259 

pains  and  vomiting  recur,  jaundice,  ascites  and  edema  appear,  and  a 
persistent  anorexia  leads  to  early  loss  of  strength.  Even  in  favorable 
cases,  in  spite  of  an  increase  in  weight,  the  patients  do  not  gain  in  strength, 
and  are  unable  to  follow  their  usual  occupations.  In  other  words,  the 
prolongation  of  life  is  frequently  nothing  more  than  a  prolongation  of 
suffering.  It  is  true  some  strikingly  favorable  results  occur,  but  in  the 
overwhelming  majority  of  cases,  after  a  brief  improvement  a  progressive 
downward  course  is  noted. 

It  follows  from  this  that,  although  the  immediate  results  of  gastro- 
enterostomy are  relatively  beneficial,  for  the  duration  of  life  as  well  as 
for  the  general  bodily  condition  and  functions,  after  gastroenterostomy 
there  is  still  much  to  be  desired. 

Under  these  circumstances  surgeons  as  well  as  physicians  frequently 
raise  the  question  whether  gastroenterostomy  should  not  be  limited  in 
favor  of  total  extirpation.  After  I  had  formulated  this  conclusion  based 
upon  my  own  experience,^  v.  Mikulicz,  in  the  article  cited  above,  and  from 
his  far  greater  experience,  arrived  at  the  same  opinion. 

If  from  this  standpoint  we  make  a  strict  choice,  the  number  of  cases 
suitable  for  resection  will  not  be  great,  perhaps  will  even  be  less  than 
before,  but  the  patient  will  have  the  benefit  of  not  only  an  apparent  but, 
an  actual  result  which  may  in  some  cases  prolong  life  for  many  years. 

At  the  present  time,  our  conclusions  amount  to  this,  that  in  cases  in 
which  total  extirpation  cannot  be  performed  we  should  under  special  cir- 
cumstances advise  gastroenterostomy;  for  example,  when  there  are  very 
marked  disturbances  (pain,  vomiting),  a  fair  degree  of  strength,  and  when 
the  use  of  internal  remedies  has  been  futile.  Occasionally,  at  the  urgent 
desire  of  the  patient  and  his  relatives,  to  whom,  for  personal  reasons,  even 
a  brief  prolongation  of  life  is  a  boon,  we  are  constrained  to  consent.  When 
the  question  of  total  extirpation  arises,  and  the  surgeon  considers  the 
patient's  strength  sufficient,  this  operation  should  be  performed.  Often 
enough,  in  such  cases,  we  will  be  convinced  of  the  futility  of  total  extirpa- 
tion and  content  ourselves  with  gastroenterostomy,  but  now  and  then  the 
constellation  of  conditions  appears  so  favorable  that  radical  procedures 
are  undertaken. 

We  now  turn  to  carcinoma  of  the  intestines,  and  in  the  case  of  carci- 
noma of  the  small  intestine  the  laws  and  indications  are  the  same  as 
those  which  have  just  been  described.  The  higher  the  situation  of  the 
carcinoma  the  more  difficult  is  its  total  removal,  as  the  duodenum  nor- 
mally is  so  fixed  that  the  total  extirpation  of  a  tumor  is  not  only  extremely 
difficult  and  attended  therefore  with  great  loss  of  time  but  is  combined 
with  great  danger  for  the  patient.  Lower  dowTi,  as  is  proven  by  a  few 
successful  sarcoma  operations,  complete  success  has  been  attained.     But 

^  Boas,  "  Diagnostik  und  Therapie  der  Magenkrankheiten,"  II,  4,  Auuage,  p.  222. 


260  GASTRIC  AND  INTESTINAL  CARCINOMATA 

the  decision  as  to  the  most  suitable  time  for  operation  meets  with  many 
obstacles. 

The  conditions  are  more  favorable  in  carcinomata  of  the  large  intes- 
tine and  rectum.  Whenever  possible  the  radical  method  is  here  to  be 
preferred  to  the  palliative.  Generally  speaking,  the  conditions  for  total 
extirpation  in  the  previously  discussed  carcinoma  varieties  are  decidedly 
better  than  in  carcinoma  of  the  stomach ;  for,  as  we  have  stated,  metastases 
usually  occur  late,  the  tumor  being  for  a  long  time  movable,  and  less 
technical  difficulty  is  encountered  at  the  operation. 

In  spite  of  this  the  results  fall  far  below  our  expectations.  According 
to  Wolffler-Schloffer,  up  to  the  year  1896  the  mortality  in  resections  of 
carcinoma  of  the  large  intestine  still  amounted  to  50  per  cent.  Yet  the 
prognosis  in  regard  to  prolongation  of  life  appears  to  be  decidedly  better 
than  in  high-seated  carcinomata.  Cases  are  on  record  of  cure  lasting 
seventeen  years  (Martini-Gussenbauer),  of  ten  years  (Czerny,  a  case  of 
sarcoma),  of  eight  and  nine  years  (Korte),  etc.  I  have  a  patient  who  had 
carcinoma  of  the  cecum  (adenocarcinoma)  and  whose  recovery  has  lasted 
over  five  years. 

Nevertheless,  up  to  the  present  time  such  recoveries  are  rare.  Most 
cases,  even  after  a  radical  operation,  perish  in  the  next  two  years. 

In  case  a  radical  operation  cannot  be  performed  two  palliative  methods 
of  treatment  remain:  Entero-anastomosis  and  anus  prseter  naturam  (colos- 
tomy). Unquestionably  the  first  method  is  preferable  to  the  other  for 
obvious  reasons.  It  also  gives  relatively  good  results — according  to 
Wolffler-Schloffer  the  mortality  is  20  per  cent. — and  prolongs  life  from  a 
year  to  a  year  and  a  half.  But  here  we  must  bear  in  mind  not  only  that 
the  patients  live,  but  how  they  live.  Although  there  are  very  favorable 
functional  results,  I  have  repeatedly  observed,  soon  after  the  entero- 
anastomosis,  renewed  attacks  of  severe  colic,  marked  loss  of  weight  which 
had  at  first  been  increased,  edema,  and  ascites. 

In  conclusion,  colostomy  will  only  come  into  question  when,  on  ac- 
count of  the  general  condition,  an  immediate  operation  is  necessary,  there- 
fore cither  when  the  strength  is  markedly  reduced  in  the  early  stages  of 
obstruction,  or  where  debility  has  more  fully  developed.  These  conditions 
will  usually  be  found  associated.  The  indications  for  colostomy  are  closely 
related  to  the  situation  of  the  carcinoma.  For  example,  in  carcinoma 
of  the  cecum  the  production  of  a  fistula  of  the  ileum  is  a  questionable 
proceeding,  both  from  a  cosmetic  and  a  nutritive  standpoint.  The  true 
domain  of  colostomy  is  found  in  carcinoma  of  the  sigmoid  flexure  and  of 
the  rectum,  for  here  the  feces  have  acquired  a  consistence  which  makes  it 
possible  readily  to  remove  them. 

We  now  turn  to  the  operative  treatment  of  carcinoma  of  the  rectum. 
According  to  the  seat,  the  development,  the  movability  of  the  tumor,  and 
the  presence  of  metastases,  the  following  procedures  must  be  considered: 


TREATMENT   OF  CARCINOMATA  261 

Extirpation  of  the  tumor,  curettage,  and  the  production  of  an  artificial 
anus. 

The  ideal  method  is,  naturally,  the  radical  removal  of  the  tumor 
(amputatio  recti  or  resectio  recti),  but,  only  when  the  tumor  is  sufficiently 
movable,  and  when  there  are  no  metastases  of  distant  organs,  especially 
of  the  liver,  is  this  possible.  Enlargement  of  regional  lymph-glands,  how- 
ever, forms  no  contra-indication  to  total  extirpation.  Since  the  perform- 
ance of  resection  of  the  sacrum  by  Kraske  (1883)  high-seated  carcinomata 
of  the  rectum  have  also  been  radically  removed. 

The  results  of  these  operations  at  the  hands  of  different  surgeons  are 
far  asunder,  but  in  the  last  ten  years  they  have  become  decidedly  more 
favorable.  According  to  Czerny's  comprehensive  statistics  of  the  Heidel- 
berg Clinic,  which  have  the  advantage  of  originating  with  him  and  which 
cover  a  long  period  of  time,  152  rectal  carcinomata  were  observed  in  the 
years  from  1878  to  1891  and  109  radical  operations  were  performed. 
Among  83  cases  which  were  operated  upon  by  the  perineal  method  3  died, 
=  3.6  per  cent. ;  of  66  according  to  the  sacral  method,  9  perished,  giving 
13.64  per  cent.  The  total  mortality  of  10  deaths  in  109  cases  is  9.1  per 
cent.  Of  99  in  whom  radical  operation  was  performed  followed  by  a 
cure,  21  lived  two  years  and  more  after  the  operation,  15,  three  years 
and  longer,  13,  four  years  and  longer,  8,  five  years  and  longer;  among 
these  one  case  lived  for  18  years,  one  case  for  16  years,  four  cases  re- 
spectively thirteen  years  and  nine  months,  eleven  years  and  six  months, 
eight  years  and  nine  months,  and  six  years  and  nine  months.  The  fre- 
quency of  relapse  after  extirpation  is  calculated  differently  by  different 
authors.  The  figures  vary  between  41.6  and  73,3  per  cent.  Czemy  main- 
tains that  20  to  25  per  cent,  of  those  in  whom  radical  operation  is  per- 
formed continue  free  from  relapses  for  two  years,  and  the  majority  of 
them  are  permanently  cured.  The  sacral  method  in  particular  diminishes 
the  danger  of  relapse,  as  the  lymph-glands  situated  in  the  excavatio  sacralis 
are  likewise  removed. 

The  functional  results  vary  according  to  whether  the  sphincter  is  re- 
tained or  removed.  In  the  former  case,  the  functional  results,  quoad 
continentiani  recti,  are  very  satisfactory.  In  the  latter,  the  condition  of 
the  patient  is  most  unpleasant,  as  he  can  retain  neither  gas  nor  fluid 
feces,  and  it  is  therefore  necessary  by  diet  and  drugs  to  make  the  feces 
compact. 

Where  a  radical  operation  is  impossible,  as  is  unfortunately  often  the 
case,  there  are  two  methods,  curetting  and  the  production  of  an  artificial 
anus — the  one  direct,  the  other  indirect — by  which  we  diminish  or  arrest 
the  symptoms  of  stenosis.  The  curetting  which  may  be  performed  with 
instruments,  or,  still  better,  with  the  hands,  is  best  adapted  to  deep-seated 
carcinomata  with  special  implication  of  the  posterior  wall  of  the  rectum. 
When  the  tumor  is  high-seated  it  is  best  not  to  use  this  method  as,  under 


262  GASTRIC  AND  INTESTINAL  CARCINOMATA 

some  circumstances,  more  harm  than  good  is  done.  The  same  is  true  of 
deep-seated  carcinomata  in  the  anterior  wall  of  the  rectum. 

The  most  suitable  and,  relatively,  the  least  dangerous  measure  for  the 
removal  of  the  symptoms  of  stenosis  is  unquestionably  colostomy.  This 
method  most  certainly  relieves  the  irritation  of  the  tumor,  and  cases  are 
on  record  of  prolongation  of  life  for  two  or  three  years  after  the  produc- 
tion of  an  artificial  anus. 

In  regard  to  the  indications  for  colostomy  the  opinions  of  physicians 
and  surgeons  are  wide  asunder.  While  colostomy  is  frequently  employed 
in  England  and  France,  in  Germany,  like  all  fistulous  operations,  it  appears 
to  liave  lost  favor  in  the  last  few  years.  We  may  here  speak  of  a  relative 
and  an  absolute  indication  for  its  performance.  The  indication  is  relative 
if,  while  a  fair  intestinal  passage  remains,  the  patient  steadily  loses  in 
weight  and  strength,  is  tormented  by  pain,  and  passes  much  pus  and  blood. 
In  such  cases  we  are  decidedly  in  favor  of  operation,  provided  internal 
remedies  have  proven  ineffectual.  As  long  as  evacuations  at  all  sufficient 
are  brought  about  by  mild  dietetic  measures  or  by  purgatives,  we  do  not 
advise  colostomy.  With  a  suitable  diet  I  have  kept  well  advanced  cases 
of  carcinoma  of  the  rectum  alive  just  as  long  as  by  the  production  of  an 
artificial  anus. 

Colostomy  is  absolutely  indicated  when  complete  intestinal  occlusion 
occurs  or  is  threatened.  In  this  case  it  is  best  not  to  wait  so  long  that 
the  patient's  strength  is  diminished  by  vomiting,  pain,  and  high-graded 
mcteorism.  The  functional  results  of  colostomy  are  satisfactory,  provided 
we  are  careful  to  produce  compact  feces  and  the  fistulous  opening  is  kept 
well  closed  with  a  hernia  bandage.  We  must  consider,  too,  that  many 
])ationts  naturally  find  the  daily  manipulation  of  their  intestines  and  of 
the  dejecta  exceedingly  repugnant.  It  is,  therefore,  the  duty  of  the  physi- 
cian and  the  surgeon,  in  order  to  prevent  subsequent  regret,  to  explain 
to  the  patient  in  no  uncertain  manner  before  the  operation  the  light  and 
shade  aspects  of  the  anus  praeternaturalis. 


DISPLACEMENTS    OF   THE    ABDOMINAL 
VISCERA    AND    OF   THE    HEART 

By  F.  HIRSCHFELD,  Berun. 

INTRODUCTION 

Until  about  twenty  years  ago  a  displacement  of  the  viscera  was  gen- 
erally regarded  as  a  rarity.  It  is  true  that  at  the  beginning  of  the  nine- 
teenth century  celebrated  clinicians  such  as  Esquirol  had  devoted  much 
consideration  to  displacements  of  the  abdominal  viscera,  and  had  even 
recognized  the  connection  between  displacement  of  the  colon  and  the  devel- 
opment of  mental  disease;  but,  toward  the  middle  of  the  century,  these 
views  were  no  longer  considered  tenable,  as  appears  from  the  works  of 
Griesinger,  Wunderlich,  Canstatt  and  others.  Displacement  of  the  colon 
was  looked  upon  as  unimportant,  that  of  the  stomach  could  not  be  de- 
tected by  the  ordinary  clinical  methods  of  the  day,  and  only  that  of  the 
kidneys  was  considered,  this,  however,  being  regarded  as  a  rare  occurrence 
since  it  was  only  occasionally  noted  by  anatomists.  The  reason  for  this 
may  be  found  in  the  technic  of  autopsies,  as  well  as  in  the  fact  that  in 
most  cadavers  the  organs  have  regained  their  normal  position  by  the  bodily 
rest  which  usually  precedes  death.  It  is  true  that  in  isolated  reports 
abnormal  movability  was  occasionally  pointed  out,  but  general  attention 
was  directed  to  this  only  about  in  1880,  in  Germany,  by  the  labors  of 
Landau,  Leube,  Ewald,  L.  Kuttner,  Litten  and  Meinert,  and  in  France 
by  Glenard,  Fereol  and  Cuilleret.  In  1890,  Virchow  demonstrated  that  a 
change  in  the  position  of  the  abdominal  viscera,  and  particularly  of  the 
intestines,  could  be  detected  in  the  majority  of  persons.  Glenard  did  much 
to  promote  the  recognition  of  these  changes  in  position  as  a  pathologic 
condition  by  creating  the  name,  enteroptosis.  His  investigations,  however, 
soon  led  him  to  a  path  on  which  he  could  no  longer  be  followed.  His  orig- 
inal view  that  enteroptosis  is  a  sharply  characterized  substantive  disease 
(entite  morbide)  was  not  at  once  generally  accepted,  but  in  the  main  was 
considered  justifiable.  It  was  admitted  that  in  many  persons  a  moderate 
degree  of  downward  displacement  of  the  stomach,  a  unilateral  movability 
of  the  kidney,  and  a  displacement  of  the  colon  could  be  demonstrated, 

263 


264     DISPLACEMENTS  OF  THE  ABDOMINAL   VISCERA  AND  HEART 

and  (he  embodiment  of  these  phenomena  in  one  clinical  picture  appeared 
all  the  more  warranted  since  they  presented  themselves  in  nervous,  weak 
females,  usually  anemic,  therefore  in  persons  who  in  their  external  appear- 
ance already  presented  the  same  t3rpe.  Glenard  believed  that  downward 
displacement  of  the  colon,  particularly  of  the  right  portion  of  the  trans- 
verse colon,  was  chiefly  responsible  for  the  production  of  these  disturbances. 
On  the  other  hand,  in  the  development  of  displacement  of  these  organs, 
he  was  but  little  inclined  to  take  into  consideration  mechanical  conditions, 
flaccidity  of  the  abdominal  walls,  the  disappearance  of  fat  in  the  abdom- 
inal spaces,  the  influence  of  external  pressure  from  lacing,  etc.  The  im- 
portance of  these  factors  in  the  etiology  of  enteroptosis  was  especially 
demonstrated  by  Landau,  Meinert,  and  Dennig,  and  was  proven  by  the 
fact  that  in  many  persons,  and  under  certain  conditions,  a  loosening  of 
the  attachments  and  the  descent  of  one  or  more  organs  was  possible.  The 
anatomical  prior  condition  may  be  favorable  to  a  displacement  in  one 
case,  still  more  so  in  another,  but  it  is  difficult  to  regard  this  weakness 
of  the  ligaments  as  the  foundation  of  a  disease,  particularly  as  it  occurs 
in  most  persons  without  producing  symptoms.  Thus  we  see  floating  kidney 
appear  in  one  person  by  the  development  of  asthma  and  emphysema, 
because  of  the  disappearance  of  fat  in  the  abdominal  cavity,  and,  perhaps, 
because  the  flaccidity  of  the  abdominal  walls  which  increases  with  age 
diminishes  pressure  in  the  abdomen,  and  thus  the  firm  position  of  the 
kidneys  is  so  far  weakened  that  under  the  influence  of  shock  to  the 
abdominal  cavity  (as  in  prolonged  paroxysms  of  coughing)  they  finally 
descend ;  in  other  cases,  however,  we  note  particularly  how  the  heart  is 
limited  in  its  movability  by  the  formation  of  empyema  in  the  lungs,  and 
sul)se(iuently  the  phenomenon  of  "displaced  heart"  disappears.  Only  the 
minute  consideration  of  all  the  mechanical  conditions  will  enable  us  to 
understand  clearly  the  genesis  of  these  changes  in  position  and  their 
influence  upon  the  functions  of  the  various  organs. 

By  some  clinicians,  such  as  Stiller  and  Obrastzow,  enteroptosis  or 
splanchnoptosis  is  to  a  certain  extent  regarded  as  the  sign  of  degeneration. 
The  ini])erfect  cartilaginous  attachment  of  the  tenth  rib  to  the  thorax 
(cosla  decima  fluctuans),  frequently  found  in  such  persons,  is  looked  upon 
as  pidof.  A  certain  justification  must  be  admitted  for  this  view,  since, 
undoubtedly,  a  displacement  of  the  abdominal  viscera  is  found  in  a  greater 
percentage  of  persons  predisposed  to  nervous  affections  than  in  the  nor- 
mally strong.  On  the  other  hand,  we  must  bear  in  mind  that  in  nervous 
]H'rs()ns  a  lessened  muscular  activity,  a  weaker  muscular  structure,  and 
])i-oba!)ly  a  more  flaccid  ligamentous  apparatus,  are  generally  to  be  expected. 
Therefore,  that  a  displacement  of  the  internal  organs  may  readily  occur 
does  not  ap]war  remarkable,  and  this  circumstance  naturally  explains  the 
greater  distribution  of  enteroptosis  among  the  nervous.  Whether,  in  addi- 
tion, a  certain,  and  perhaps  also  a  hereditary,  predisposition  can  be  as- 


DISPLACEMENT   OF  THE  STOMACH   (GASTROPTOSIS)  265 

sumed  is  extremely  difficult  to  decide.  Very  likely  a  feeble  ligamentous 
apparatus  in  the  internal  organs  and  certain  peculiarities  in  the  structure 
of  the  same  may  be  hereditary,  as  well  as  a  special  predisposition  of  the 
bony  skeleton;  but,  for  the  development  of  enteroptosis,  perhaps,  just  as 
in  the  development  of  kyphoscoliosis  of  the  vertebral  column,  a  number 
of  external  influences  are  necessary.  Therefore,  we  do  not  agree  with 
Glenard  who,  in  accepting  the  French  views  regarding  I'arthritisme,  pro- 
pounds a  theory  according  to  which  most  diseases  are  related  to  enterop- 
tosis, and  a  disturbance  in  the  activity  of  the  liver  which  is  not  described 
(I'hepatisme)  is  the  most  significant  symptom.^ 

Although  certain  uniform  factors  are  decisive  in  the  development 
and  treatment  of  the  various  displacements  of  the  organs,  it  appears 
to  be  most  necessary  for  the  correct  understanding  of  the  subject  un- 
der discussion  to  describe  the  displacement  of  each  individual  organ 
separately. 

Most  important  are  the  displacements  of  the  stomach  and  the  kidneys. 
Displacements  of  the  spleen  and  of  the  liver  are  generally  rare,  those  of 
the  colon  and  heart  more  frequent  but  of  less  clinical  importance. 


DISPLACEMENT   OF   THE    STOMACH    (GASTROPTOSIS) 

Reports  vary  as  to  the  frequency  of  gastroptosis.  According  to  Meinert,^ 
in  Dresden  the  majority  of  women  have  a  displacement  of  the  stomach 
while,  by  estimation,  only  about  5  per  cent,  of  men  show  an  alteration 
in  the  position  of  this  organ.  Similar  proportions  have  been  reported 
by  Dennig  ^  in  the  population  of  Wiirttemberg.  From  his  figures  it  is 
very  evident  in  which  years  of  life  gastroptosis  is  specially  prone  to 
appear. 

Among  3,000  persons  who  presented  themselves  at  a  Stuttgart  Poly- 
clinic on  account  of  various  ailments  not  connected  with  disease  of  the 
stomach, 

in  29.7  per  cent,  of  the  men, 
in  75.4  per  cent,  of  the  women, 

a  displacement  of  the  stomach  was  determined. 


iThe  views  of  Glenard,  except  those  in  his  earlier  publications  (Lyon  medical, 
1885  et  1887),  are  found  in  his  comprehensive  work:  "  Les  ptoses  viscerales.  Diag- 
nostic et  nosographie."  Paris,  1899,  962  pages.  Compare  also  Le  progres  m§dical, 
1899,  I,  page  320 ;  1900,  I,  page  225 ;   1902,  I,  No.  2. 

2  Meinert,  Sammlung  klin.  Yortrdge.  N.  F.,  Nr.  115  u.  116,  Leipzig,  1895;  Cen- 
tralblatt  f.  innere  Med.,  1895,  Nr.  43  und  ebenda,  1896,  Nr.  13  u.  14. 

3  A.  Dennig,  Wurttemhergisches  med.  Correspondenzhl.,  1903,  Nr.  18. 


266     DISPLACEMENTS   OF  THE  ABDOMINAL   VISCERA  AND   HEART 
In  regard  to  age,  gastroptosis  was  present 


In  Mbn. 

In  Women. 

Pro»"  1 4.-9,0 

^ears 

of  age  in 

Per  cent. 
16 
27 
26 
28 
37 
29 
38 
34 
34 
32 

Per  cent. 

21-25 
26-30 
31-35 
36-40 
41-45 
46-50 
51-55 
56-60 
61-70 

62 

79 

81 

92 

96 

92 

85 

97 

100 

It  was  determined  in  girls 

from  10-15  years,  in  20  per  cent., 
"      16-20      "        "   57        " 

From  this  it  can  be  distinctly  seen  that  gastroptosis  is  much  more 
frequent  in  females  than  in  males.  This  displacement  probably  occurs 
even  at  the  age  of  puberty  as  a  consequence  of  wearing  a  corset,  and 
under  the  influence  of  pregnancy  in  the  following  decades  flaccidity  of 
the  abdominal  walls  becomes  more  common  until,  finally,  almost  all  elderly 
women  show  gastroptosis.  According  to  Dennig  the  same  deleterious  in- 
fluence as  that  of  the  corset  is  ascribed  to  a  habit  very  common  among 
the  female  rural  population  of  Wiirttemberg  of  tying  the  skirts  around 
tlie  waist  and  drawing  the  strings  very  tight.  When  the  hips  have  not 
as  yet  attained  the  growth  characteristic  in  woman,  tightness  about  the 
waist  is  especially  desired  to  prevent  the  skirt  from  slipping  down.  Sus- 
])ension  of  the  clothes  from  the  shoulder,  as  is  the  rule  with  children, 
is  seldom  seen  in  girls  over  fifteen  years  of  age. 

The  correctness  of  these  conclusions  is  proven  by  the  results  of  investi- 
gations in  males.  Here  the  injurious  effects  of  wearing  a  belt  to  fasten 
tlie  trousers  instead  of  suspenders  from  the  shoulder  is  distinctly  recog- 
nized, for  of  172  men  with  marked  gastroptosis,  73  wore  narrow  belts 
around  the  waist,  while  among  406  men  with  a  normal  position  of  the 
sto)iuu'li  only  l(i  used  the  belt;  the  remainder  wore  suspenders. 

In  children,  as  a  rule,  the  stomach  lies  in  a  horizontal  position.  Meinert 
declares  it  to  be  true  that  every  child  is  bom  with  a  vertically  lying 
stomach,  the  pylorus  of  which  is  therefore  deeply  situated,  but  that  after 
a  few  weeks  this  position  is  changed.  The  lower  curvature  of  the  stomach 
forms  an  almost  horizontal  line  above  the  umbilicus. 

'J'lie  conspicuously  frequent  occurrence  of  gastroptosis  in  Saxony,  which 
was  first  pointed  out  by  Meinert,  has  given  rise  to  much  speculation. 
Some  investigators  reject  the  entire  theory,   and  believe  that  the  large 


DISPLACEMENT  OP  THE  STOMACH   (GASTROPTOSIS)  267 

amounts  of  gases  developed  from  the  carbonic  acid  employed  for  distend- 
ing the  stomach  abnormally  displace  this  organ,  and  probably  also  give 
no  well-defined  idea  of  the  size  of  the  stomach  so  inflated.  According  to 
Meinert,  in  the  above  investigations 

8  grams  of  sodium  bicarbonate, 
6     "      of  tartaric  acid, 

were  employed;  this  was  dissolved  in  a  little  water  and  taken  at  once  or 
in  divided  doses  rapidly  succeeding  each  other.  Gastroptosis  was  assumed 
whenever  the  pylorus  could  not  be  recognized  at  the  scrobiculus  cordis,  or 
was  situated  more  deeply;  the  greater  and  lesser  curvatures  of  the  stomach 
must  have  descended  at  the  same  time. 

As  large  doses  of  this  mixture  will  produce  nearly  3  liters  of  carbonic 
acid,  the  criticism  is  justifiable  that  the  normal  stomach  which,  as  a  rule, 
has  merely  a  capacity  of  about  1^  liters,  is  immoderately  distended  and 
perhaps  also  is  drawn  somewhat  downward.  Dennig  employed  a  large 
double  bellows  with  which  he  inflated  the  stomach  after  introducing  the 
stomach-tube.  With  this  method,  as  I  have  fully  convinced  myself,  par- 
ticularly with  tense  belly  walls,  it  is  necessary  to  exert  considerable  pressure 
if  the  boundaries  of  the  stomach  are  to  be  sharply  defined.  We  must, 
however,  remember  that  neither  in  powerful  men  nor  in  children  does 
this  downward  displacement  of  the  distended  stomach  ever  take  place. 
We  are  thus  forced  to  conclude  that  this  property  of  the  stomach  or,  rather, 
of  the  pylorus,  to  descend  upon  immoderate  inflation,  is  a  pathologic  devia- 
tion, and  to  a  certain  extent  indicates  a  predisposition  to  gastroptosis. 

In  the  description  of  the  development  of  gastroptosis  from  the  influ- 
ence of  gastric  catarrh,  general  weakness  of  the  stomach,  etc.,  I  shall 
attempt  to  show  that,  to  a  certain  extent,  the  same  process  takes  place 
as  in  the  downward  displacement  of  the  organ  artificially  inflated  by 
carbonic  acid  gas. 

The  purely  mechanical  course  may  best  be  understood  by  some  illus- 
trations.^ 

In  Fig.  11  we  see  a  stomach  in  its  normal  position.  The  pylorus  is 
situated  at  a  point  almost  directly  behind  the  right  arch  of  the  ribs, 
where  this  is  crossed  by  the  tip  of  the  ensiform  process  upon  a  horizontal 
plane  (Meinert).  The  axis  of  the  stomach  more  nearly  approaches  the 
horizontal  than  the  vertical.  The  pyloric  portion  of  the  stomach  is  in  the 
main  situated  in  the  scrobiculus  cordis. 

In  Fig.  12  we  see  the  so-called  vertical  position  of  the  large  normal 

1  These  illustrations  have  been  taken  from  the  "  Diagnostic  Lexicon  "  of  A.  Bum 
and  Schnirer,  Vienna.  1884,  III.  p.  111.  Presentation  of  gastric  examination  by 
Rosenheim.  My  description  of  the  individual  figures  differs  somewhat  from  that 
given  by  Rosenheim. 


268     DISPLACEMENTS   OF  THE   ABDOMINAL   VISCERA  AND   HEART 

stomach  when  inflated.  The  pylorus  can  no  longer  be  detected  in  the  pit 
of  the  stomach.  The  greater  curvature  is  decidedly  lower  than  the  umbili- 
cus. The  axis  of  the  stomach  is  in  a  vertical  rather  than  a  horizontal 
position. 

Fig.  13  shows  a  somewhat  later  stage.    The  greater  curvature  has  de- 
scended lower.    The  cardia  may  be  recognized  in  about  the  same  area  as 


Fig.  1 1 . — Normal  situation  of  the  stomach ;  dotted  line,  .....,,  shows  the  margin  of  the  liver. 

in  tlie  normal  stomach.  Especially  noteworthy  is  the  great  bulging  of  the 
pyloric  portion  of  the  stomach  downward  and  to  the  right.  As  the  muscles 
of  the  stomach  which  chiefly  propel  the  chyle  are  situated  around  the 
pylorus,  an  enlargement  of  the  stomach  to  the  right,  which  may  be  dis- 
tinctly demonstrated  by  percussion,  clearly  denotes  a  weakness  of  the 
muscular  apparatus  and  beginning  insufficiency  of  the  same,^  although 
gastric  dulness  appears,  in  the  main,  to  be  but  slightly  increased. 

In  Fig.  14  we  see  a  decidedly  enlarged  stomach.  Such  a  condition 
may  have  been  caused  by  gastroptosis  and  subsequent  insufficiency  as  well 
as  by  a  mere  descent  from  gastrectasis.  A  decision  cannot  be  based  alone 
upon  these  pictures;  for  this  purpose  the  consideration  of  all  the  points 
necessary  in  an  examination  is  called  for. 

'  Rosenheim,  "  Krankheiten  der  Speiserohre  und  des  Magens,"  I.  Aufl.  1891 ;  Leo, 
Deutsch.  med.  Wochenschr.  1896;  xmd  W.  Michaelis,  Zeitschr.  f.  klin.  Med., 
XXXIV. 


DISPLACEMENT   OF  THE   STOMACH   (GASTROPTOSIS) 


269 


A  somewhat  different  condition  is  shown  by  Fig.  15,  which  is  taken 
from  Bollinger's  book.^ 

This  illustration  of  Bollinger,  first  of  all,  shows  distinctly  how  the 
vertical  position  of  the  stomach  with  constriction  of  its  pyloric  portion 
occurs  from  the  external  pressure  of  tight  lacing,  just  as  this  acts  upon 
the  liver.  A  vertical  position  of  the  stomach  without  dilatation  is  fre- 
quently not  considered  pathologic  by  the  anatomist,  and  therefore  we  often 
see  illustrations  of  a  vertical  stomach  in  books  upon  normal  topographic 
anatomy. 

How  do  the  effects  of  a  downward  displacement  of  the  pylorus,  of  gas- 
troptosis,  become  noticeable  during  life? 

In  a  normal  person  this  occurs  by  downward  pressure  on  the  liver  and 
pylorus  in  consequence  of  tight  lacing  around  the  waist,  and,  except  for 
slight  discomfort  which,  perhaps,  is  only  due  to  pressure  upon  the  skin, 
the  activity  of  these  organs  is  usually  but  slightly  affected.     It  is  true 


Fig.  12. — Gastroptosis  of  the  first  degree. 

the  passage  of  the  chyle  from  the  stomach  into  the  duodenum  is  probably 
impeded,  but  we  know  that  the  smooth  muscles  of  the  intestine  rapidly 
hypertrophy  after  the  addition  of  obstructions  in  the  intestinal  canal,  and 
thus  by  increased  labor  bring  about  compensation.    The  majority  of  healthy 

1  O.  Bollinger,  "  Atlas  und  Grundriss  der  pathologischen  Anatomie,"  I.,  page  193, 
2.  Aufl.  Munchen,  1901. 


270     DISPLACEMENTS   OF  THE  ABDOMINAL  VISCERA  AND  HEART 

young  girls,  therefore,  notice  no  immediate,  injurious  effect  from  the 
wearing  of  a  constricting  corset  which  simultaneously  presses  down  the 
liver  and  the  pylorus.     It  is  different,  however,  if  the  stomach  of  the 


Fig.  13. — Gastroptosis  of  the  second  degree. 

person  in  question  has  previously  shown  a  tendency  to  disturbance,  or  if 
a  general  weakness  of  the  system  exists. 

These  disturbances  most  frequently  occur  in  young,  anemic,  poorly 
nourished,  growing  girls.  Under  these '  circumstances,  the  stomach  cannot 
so  readily  compensate  the  obstruction  to  the  propulsion  of  chyle  by  the 
unfavorable  position.  Decided  insufficiency  readily  takes  place.  The  symp- 
toms of  the  patient  all  distinctly  point  to  the  fact  that  the  corset  is  the 
disturber  of  the  peace,  for,  after  discarding  it,  decided  amelioration  is 
noted.  Gradually  the  gastric  catarrh  disappears,  and,  on  resuming  the 
corset,  the  patient  readily  becomes  accustomed  to  her  instrument  of  torture. 

In  these  cases,  therefore,  a  slight  gastroptosis  persists  which  usually 
cannot  be  determined  by  the  ordinary  clinical  methods  of  examination, 
unless  it  be  by  decided  inflation  of  the  stomach.  As  a  rule,  symptoms 
appear  only  when  an  error  in  diet  produces  an  acute  gastric  catarrh. 
While  the  consequences  of  such  a  gastric  disturbance  in  patients  with  a 
normal  stomach  soon  disappear  under  suitable  treatment,  in  those  with 
a  latent  gastroptosis  a  high-graded  insufficiency  of  the  stomach  occasion- 
ally develops.    A  loud,  splashing  sound  most  distinctly  reveals  the  enlarge- 


DISPLACEMENT   OF  THE  STOMACH   (GASTROPTOSIS)  271 

ment  of  the  stomach.  The  greater  the  distention  of  the  stomach  in  the 
course  of  the  affection,  the  more  difficult,  naturally,  is  the  propulsion  of 
chyle  into  the  duodenum.  The  affection,  therefore,  spontaneously  forms 
a  vicious  circle.  An  immoderate  dilatation  of  the  stomach  is  also  promoted 
when  the  belly  wall  is  very  flaccid.  Even  in  young  girls  who  are  unac- 
customed to  bodily  labor,  the  muscles  exerted  in  the  abdominal  press 
form  only  a  flaccid,  thin  wall.  The  activity  of  the  abdominal  muscles 
is  still  further  impaired  in  women  by  successive  labors,  the  consequent  pen- 
dulous abdomen  described  by  Landau  ^  becoming  particularly  noticeable. 

The  persistence  of  gastric  catarrh  or  gastric  insufficiency  in  gastrop- 
tosis,  however,  leads  to  other  dangers.  Being  insufficiently  nourished  the 
organism  is  forced  by  metabolism  to  the  combustion  of  its  body  substance, 
the  fat  in  the  abdomen  and  the  mesentery  being  first  utilized  for  this 
purpose.    Here  we  note  the  well  known  fact  that  in  an  antifat  treatment 


Fig.  14. — Gastroptosis  of  the  third  degree. 

a  decrease  in  the  circumference  of  the  waist  is  most  perceptible.  The  loss 
of  fat  accumulated  in  the  abdominal  cavity  makes  itself  felt  in  the  same 
way  as  a  weakening  of  the  abdominal  walls.  The  position  and  attach- 
ment of  the  organs  are  no  longer  secured  by  simultaneous  pressure,  but 
these  depend  upon  the  suspensory  ligaments  which  may  readily  yield.     In 


19 


1  Landau,  Terhandl.  der  Berl.  med.  Gesellschaft,  1890. 


272     DISPLACEMENTS   OF  THE   ABDOMINAL   VISCERA  AND  HEART 

severe  diseases,  such  as  gall-stone  colic,  gastric  ulcer,  or  gastric  cancer, 
this  dilatation  of  the  prolapsed  stomach  becomes  noticeable  much  more 
frequently  than  after  simple  gastric  catarrh.  Its  manner  of  development 
is  interesting,  and  is  as  follows:  I  have  repeatedly  heard  young  persons 
who  liave  recovered  from  an  appendicitis  operation  state  that  in  the  first 


Fig.  15. — Constriction  of  the  right  lobe  of  the  liver  and  of  the  pylorus. 


few  days  after  they  had  left  their  beds  they  observed  an  increase  in  the 
t'ircu inference  of  the  abdomen,  which  was  confirmed  by  the  objective  ex- 
iiiiiination  of  the  physician.  In  these  cases  there  was  no  abdominal  hernia, 
l)ut  an  enlargement  and  displacement  of  the  stomach  was  evident  without 
any  syinptoiii  of  gastric  disease.  This  was  explained  by  the  marked  dis- 
appeaianee  of  fatty  tissue  in  the  abdominal  cavity,  since  the  persons  in 


DISPLACEMENT  OF  THE  STOMACH   (GASTROPTOSIS)  273 

question  had  lost  from  11  to  16^  lbs.  in  weight.  A  few  days  after  getting 
out  of  bed,  and  being  in  an  upright  position,  they  were  well  enough  to 
take  large  quantities  of  food,  and  this  had  caused  the  over-burdened  and 
distended  stomach  with  all  of  the  other  viscera  to  descend. 

That  occasionally  a  decided  displacement  of  the  stomach  may  be  de- 
termined in  kyphoscoliosis  is  readily  comprehended.  In  these  cases,  also, 
the  prolapse  usually  occurs  without  producing  any  disturbance  in  gastric 
activity   ( Fleiner  ^ ) . 

Lordosis  of  the  vertebral  column,  which  sometimes  develops  to  a  de- 
cided degree  in  women  predisposed  to  it  if  they  wear  high  heels,  produces 
a  condition  in  which  the  pressure  of  the  viscera  dilates  the  abdominal  walls 
downward  and  anteriorly,  and  the  internal  organs  themselves  drop  (Csery, 
Koninyi,  and  Meltzing^). 

In  some  diseases,  for  instance,  tuberculosis,  the  effect  of  mechanical 
shock  makes  itself  felt  in  the  abdominal  cavity.  The  paroxysmal  shock 
to  the  thorax  and  abdominal  wall  produced  by  cough  must  assist  this 
process,  particularly  when  the  factors  we  have  mentioned  which  favor  the 
descent  of  the  stomach  have  already  been  active. 

From  these  descriptions  it  is  obvious  that  gastroptosis  may  be  looked 
upon  as  a  disease  in  only  a  small  number  of  cases  when,  from  any  com- 
plication, the  compensation  is  lacking  which  would  otherwise  be  produced 
by  increased  activity  of  the  muscular  structure  of  the  pylorus.  In  regard 
to  the  frequency  of  these  disturbances,  no  absolute  general  rules  can  be 
laid  down. 

Gastroptosis  and  enteroptosis  are  most  frequently  met  with  in  patients 
suffering  from  gastric  disease.  Thus  Einhorn  ^  reports  that  within  a  few 
months  he  found  9  cases  among  141  male  patients  with  gastric  disease, 
and  among  92  women  he  found  these  changes  32  times.  It  is  true  that 
the  more  vigilantly  we  search  for  changes  in  position,  the  more  frequently 
we  will  diagnosticate  them  in  a  greater  or  less  degree.  Often  the  appear- 
ance of  hysteria  or  neurasthenia  leads  us  to  suspect  gastroptosis.  It  may 
then  be  doubtful  which  affection  existed  first. 

SYMPTOMS 

Symptoms  of  gastroptosis  may  be  entirely  absent.  In  young  girls  who 
press  the  pylorus  down  by  wearing  a  corset,  possibly  because  of  the  in- 
creased difficulty  with  which  the  chyle  is  propelled  into  the  duodenum, 
eructations  will  often  occur,  and  the  peculiar  rumbling  or  gurgling  fre- 
quently heard  in  women  who  lace  very  tight  is  declared  by  Fleiner  to  be 


^Fleiner,  Miinch.  med.  Wochcnschr.   1895.  Nr.  42-44. 

'Kordnyi,  Berl.  kl.  Wochenschr.,   1890.  Nr.  31;   Meltzing,  Tolkmann'sche  Vortr. 
1896;  Cscry.  Wiener  med.  Wochetischr.,  1901.  Nr.  28. 

•if.  Einhorn,  "Die  Krankheiten  des  Magens,"  Berlin,  1898,  page  270. 


274     DISPLACEMENTS   OF  THE   ABDOMINAL   VISCERA  AND   HEART 

a  murmur  of  stenosis  due  to  compression  of  the  stomach.  In  most  cases, 
however,  as  has  been  stated,  symptoms  are  either  absent,  or  these  mild 
signs  are  regarded  by  healthy  persons  as  due  to  a  disturbance  of  gastric 
movement.  In  weak,  anemic  persons  with  a  tendency  to  chlorosis  the 
constriction  of  the  stomach  may  exert  such  a  deleterious  effect  that  not 
only  the  signs  of  gastric  catarrh  but  also  manifold  nervous  disturbances 
may  present  themselves.  The  symptoms  due  to  gastroptosis  are  then  closely 
intermingled  with  those  of  chlorosis,  of  general  debility,  ahd  of  nervous- 
ness, but  are,  in  the  main,  attributed  to  chlorosis;  they  may  continue  for 
weeks,  months,  or  even  for  years.  Quite  properly  Meinert  attributes  the 
old  axiom,  founded  upon  experience,  that  marriage  is  the  remedy  for 
chlorosis  to  the  fact  that  when  pregnancy  occurs  the  growing  uterus  forces 
the  distended  stomach  upward  again. 

The  symptoms  which  subsequently  arise,  provided  no  intercurrent  dis- 
ease suddenly  produce  marked  insufficiency  of  gastric  activity,  as  in  the 
manner  I  have  described,  resemble  those  which  generally  appear  in  per- 
sons suffering  from  gastric  catarrh.  A  conspicuous  symptom  in  such 
])atients  is  the  great  weakness  and  debility  which  cannot  be  accounted 
for  by  any  preceding  error  in  diet.  In  the  horizontal  position,  especially 
in  the  right  lateral,  the  symptoms  ameliorate,  for  then  the  propulsion  of 
food  goes  on  under  the  most  favorable  mechanical  conditions.  Vomiting 
is  rarely  mentioned  in  the  history,  but  is  most  frequent  at  the  onset,  and 
very  rare  in  the  later  course.  Incessant  vomiting  throughout  the  entire 
])eriod  of  the  disease  might  therefore  be  utilized  as  excluding  gastroptosis. 

The  patients  almost  invariably  complain  of  marked  constipation,  for 
which  various  causes  are  assigned.  In  the  first  place,  a  displacement  of 
the  colon,  particularly  of  the  mesocolon  in  which  the  thin,  fluid  feces 
first  become  more  compact,  may  cause  kinking  and,  naturally,  a  retardation 
of  the  feces.  However,  too  much  stress  is  not  to  be  laid  upon  this  cir- 
cumstance, since,  after  the  removal  of  other  causes,  and  in  spite  of  the 
persistently  abnormal  course  of  the  colon,  regular  fecal  discharges  almost 
always  take  place.  It  is  significant  that  these  women — and  with  such 
we  usually  deal  in  gastroptosis — generally  prefer  easily  digested  food  which 
leaves  but  little  residue  in  the  intestine.  We  know  from  physiology  that 
with  food  consisting  chiefly  of  meat  and  wheat  bread  the  fecal  mass  in 
twenty- four  hours  amounts  to  only  100  to  130  grams  of  moist,  and  from 
>?()  to  30  grams  of  dry,  substance,  while  with  a  diet  rich  in  cellulose,  there- 
fore with  the  ingestion  of  much  rye  bread,  the  feces  amount  to  400  to  600 
grams  of  moist,  and  60  to  80  grams  of  dry,  substance.  As  the  intake  of 
food  in  gastric  affections  is  generally  even  less,  and  accordingly  there  is  less 
icsidue,  a  fecal  evacuation  every  two  or  three  days  appears  quite  natural. 
Moreover,  a  pendulous  abdomen  decidedly  decreases  the  force  of  the  ab- 
(loiniiial  press,  so  that  small  fecal  masses  formed  from  easily  digested  food 
are  only  evacuated  by  great  effort.     Finally,  in  my  experience,  the  lack 


DISPLACEMENT   OF  THE   STOMACH   (GASTROPTOSIS)  275 

of  muscular  exercise  on  the  part  of  most  women  adds  much  to  torpidity 
of  the  bowels,  which  therefore  cannot  be  looked  upon  as  entirely  the 
consequence  of  gastroptosis,  coloptosis  or  enteroptosis. 

Among  the  objective  symptoms,  a  loud  splashing  sound  in  the  umbili- 
cal region  is  noted  by  the  physician.  This  sign  is  so  characteristic  that 
when  absent  in  repeated  examinations  one  or  two  hours  after  the  ingestion 
of  fluid,  insufficiency  of  the  displaced  stomach  may  be  denied.  The  im- 
portance of  the  succussion  sound  in  judging  of  the  gastric  activity  has 
lately  been  the  subject  of  much  controversy.  Although  I  am  willing  to 
admit  that  this  symptom  may  occasionally  be  observed  in  thin,  healthy 
persons,  nevertheless  I  coincide  with  Stiller  and  Kuttner  ^  in  the  view 
that,  under  these  circumstances,  the  gastric  wall  is  incapable  of  contract- 
ing strongly  enough  about  its  contents.  In  gastroptosis  the  splashing 
sound  is  usually  detected  around  the  umbilicus,  often,  however,  below  this 
region. 

Among  other  signs  epigastric  pulsation,  which  is  emphasized  by  Gle- 
nard,  must  be  considered.  It  is  not  of  the  same  diagnostic  import  as  the 
succussion  sound,  for,  in  the  first  place,  when  the  abdominal  walls  are 
thin  and  the  pylorus  is  situated  in  the  scrobiculus  cordis,  the  pulsation 
of  the  vessels  may  sometimes  be  felt  through  the  gastric  walls,  and  sec- 
ondly, when  the  abdominal  walls  are  rich  in  adipose  tissue,  pulsation  is 
unrecognizable  notwithstanding  the  existence  of  gastroptosis. 

Another  symptom,  a  feeling  as  of  the  pressure  of  a  girdle  in  the  gastric 
region,  the  "  corde  colique,"  leaves  us  completely  in  doubt.  Glenard  be- 
lieves this  band  to  be  the  colon,  while,  according  to  Ewald,  the  area  of 
resistance,  which,  however,  can  rarely  be  felt,  is  to  be  looked  upon  as 
the  pancreas.  This  fact  is  not  generally  known ;  it  is,  however,  occasionally 
of  great  practical  value,  for,  otherwise,  upon  palpation  in  this  region,  and 
when  there  is  a  disturbance  of  gastric  activity,  we  might  mistake  this 
resistance  for  a  neoplasm.  I  know  of  a  case  in  which  such  an  error  led 
to  a  laparotomy  being  performed — a  state  of  things  naturally  not  very 
desirable,  yet  not  so  serious  as  the  inverse  assumption  that  a  neoplasm 
is  only  the  head  of  the  pancreas. 

The  most  signal  proof  of  gastroptosis,  or  that  the  disturbances  present 
are  chiefly  due  to  displacement  of  the  stomach,  is  furnished  us  by  the 
movability  of  other  abdominal  organs,  particularly  of  the  kidneys.  In  how 
far  it  is  possible  to  palpate  the  kidneys  will  be  discussed  later.  In  almost 
every  marked  case  of  gastroptosis  it  is  possible  distinctly  to  palpate  the 
kidneys,  at  least  the  right  one,  upon  the  posterior  wall  of  the  abdomen. 
Often  one  or  both  kidneys  are  movable  in  the  abdominal  cavity,  or  they 
are  shown  to  be  fixed  in  certain  areas. 

1  Berliner  klin.  Wochenschr.,  1901,  Nr.  50. 


276     DISPLACEMENTS   OF  THE   ABDOMINAL   VISCERA  AND   HEART 

DIAGNOSIS 

Naturally  the  diagnosis  is  assisted  when  the  walls  are  very  flaccid. 
In  the  majority  of  eases  of  gastroptosis  the  distention  of  the  stomach  is 
so  marked  that  the  findings  appear  to  be  entirely  out  of  proportion  to  the 
symptoms,  which  have  usually  existed  but  a  short  time.  In  gastrectasis 
which  develops  in  consequence  of  some  other  gastric  affection,  derangement 
of  the  activity  of  the  stomach  has  gradually  become  marked.  Finally,  we 
must  remember  that  a  displacement  may  have  occurred  secondarily  from 
the  cicatrix  of  an  ulcer  or  a  neoplasm  which  had  narrowed  the  stomach, 
and  that  dilatation  had  subsequently  occurred.  In  practice,  therefore, 
llio  proof  of  a  displacement  is  naturally  much  less  significant  than  the 
recognition  of  some  other  obstruction  to  the  propulsion  of  the  ingesta 
through  the  pylorus.  For  this  reason,  in  the  examination  of  a  patient 
suffering  from  gastric  disease,  I  must  advise  against  a  great  inflation  of 
the  stomach,  provided  we  desire  only  to  determine  gastroptosis  or  the 
tendency  to  displacement.  In  my  experience,  only  in  hysterical,  very 
nervous  persons,  or  in  those  debilitated  from  disease  of  some  other  organ, 
trill  gastroptosis  cause  a  decided  disturbance  in  nutrition.  On  the  con- 
trary, examination  should  reveal  the  cause  of  the  compensatory  disturb- 
ance in  the  activity  of  the  displaced  stomach.  According  to  the  age,  the 
stw.  and  the  general  appearance  of  the  patient,  we  must  search  for  gastric 
nicer,  for  malignant  disease  of  the  gastrointestinal  canal,  for  cholelithiasis, 
or  for  pulmonary  tuberculosis. 

TREATMENT 

In  the  treatment,  prophylaxis  plays  the  first  role.  By  prohibiting 
lacing  the  chief  cause  of  the  development  of  gastroptosis,  as  well  as  dis- 
placement of  other  organs,  will  be  removed.  Probably  every  woman  will 
assure  the  physician  that  she  does  not  lace  too  tight,  although  an  exam- 
ination of  the  skin  will  reveal  distinct  lines  about  the  waist  due  to  the 
constricting  corset.  In  regard  to  these  views  there  is  little  unanimity 
Ix'tween  physicians  and  their  women  patients.  A  corset  of  stiff  material 
worn  by  those  anemic  women,  weak  in  muscle,  who  form  the  majority  of 
tlu'  well-to-do  classes,  may  have  the  advantage  that  it  gives  a  certain 
support  to  the  weak  vertebral  column  which  is  lacking  in  strength  of 
muscle  and  will  remedy  defects  in  the  carriage  of  the  body.  But,  as  a 
rule,  the  physician  must  insist  that  the  corset  be  not  worn  too  tight,  nor 
tlie  skirts  suspended  from  the  waist.  This  danger  is  greatest  in  girls 
from  fourteen  to  sixteen  years  of  age  whose  hips  have  not  yet  sufficiently 
developed.  The  skirts  must  be  suspended  from  the  shoulders  like  the  trou- 
s(M-s  of  men,  and  a  belt  must  not  be  worn.  It  is  well  known  that  the 
"  dress  reform,"  which  has  already  become  somewhat  general  in  Germany, 
is  directed  toward  this  purpose.     Unfortunately,  stout  women  refuse  to 


DISPLACEMENT   OF  THE  STOMACH   (GASTROPTOSIS)  277 

abandon  the  corset,  because  without  it  the  waist  appears  to  them  to  be 
too  large,  and  the  bust  is  not  sufficiently  supported.  It  is  to  be  hoped, 
although  it  is  by  no  means  certain,  that  in  this  respect  common  sense 
will  finally  prevail  over  vanity  and  the  present  standards  of  beauty. 

On  account  of  the  tendency  of  the  vertebral  column  to  marked  lordosis, 
the  wearing  of  high-heeled  shoes  should  be  prohibited,  the  height  of  the 
heel  being  limited  to  2  or  3  cm. 

The  formation  of  a  pendulous  abdomen  in  consequence  of  childbirth 
may  be  prevented  by  maintaining  the  recumbent  posture  as  long  as  possible 
after  labor,  and  on  rising  from  bed  the  flaccid  abdominal  walls  should  be 
firmly  supported  by  a  well-fitting  bandage. 

The  most  effectual  means  to  prevent  the  displacement  of  organs  prob- 
ably lies  in  the  education  of  the  female  from  infancy  as  to  the  value  of 
physical  exercise.  With  this  we  might  hope  that  the  abdominal,  as  well 
as  all  the  other  muscles  of  the  body,  would  attain  their  fullest  develop- 
ment, and  that  the  wearing  of  sensible  clothing  by  the  majority  of  women 
would  prevent  many  other  disabilities  of  civilized  people. 

If  a  displacement  of  the  stomach  has  already  occurred,  yet  no  symp- 
toms are  present,  treatment  may  appear  to  be  superfluous.  Nevertheless, 
in  such  cases  I  must  advise  prophylactic  interference  and  the  interdiction 
of  tight  lacing,  especially  if  occasional  symptoms,  such  as  loud  gurgling 
in  the  intestines,  have  already  been  noted.  If  there  are  distinct  signs  of 
insufficiency  of  the  stomach,  a  binder  which  supports  the  lower  parts 
of  the  abdomen  is  serviceable.  An  abdominal  bandage  lately  advised  by 
Ostertag  ^  is  especially  valuable  for  this  purpose.  In  women  the  symp- 
toms sometimes  disappear  immediately  on  its  use. 

In  advising  an  abdominal  binder  it  must  be  borne  in  mind  that  it 
would  be  the  height  of  folly  to  forbid,  on  the  one  hand,  the  constricting 
corset,  and  then,  for  the  opposite  effect,  to  recommend  an  abdominal 
bandage  which  compresses  the  organs  from  the  waist  downward. 

According  to  the  statements  of  Landau  and  Bardenheuer,  there  are 
stays  supplied  by  instrument  makers  which  exert  no  special  pressure  about 
the  waist,  and  to  this  the  abdominal  bandage  for  the  lower  parts  of  the 
abdomen  is  already  attached.  I  advise  these  corsets  in  antifat  cures 
even  if  there  is  no  gastroptosis,  since  in  hyponutrition,  as  already  re- 
marked, fat  disappears  from  the  abdominal  cavity  with  comparative  rapid- 
ity and,  therefore,  the  condition  for  displacement  of  organs  is  already 
present.  Bial  ^  has  lately  proven  by  the  illumination  of  the  organ  that 
a  prolapsed  stomach  cannot  be  supported  by  a  bandage.  He  also  relates 
I  his  experiences,  according  to  which  the  desired  result  may  be  attained 
by  suitable  hydrotherapeutic  and  dietetic  measures.     Nevertheless  I  advise 

'  Ostertag,  Monatsschr.  f.  Geburtsh.  ii.  Gyn.,  XV. 
'Bial,  Vcrh.  d.  Congr.  f.  innere  Med.,  1897,  p.  521. 


278      DISPLACEMENTS  OF  THE  ABDOMINAL  VISCERA   AND   HEART 

the  employment  of  these  abdominal  supporters.  In  the  first  place,  in 
women  the  weakened  abdominal  wall  is  strengthened,  and  thereby  the 
danger  of  a  marked  displacement  of  the  abdominal  organs  is  averted. 
Moreover,  it  is  quite  clear  to  me  that  not  only  does  the  motor  activity 
of  the  stomach  improve,  but  the  action  of  the  bowels  is  decidedly  facili- 
tated. The  descent  of  the  diaphragm,  which  by  the  abdominal  press  forces 
tlie  abdominal  viscera  downward,  encounters  a  stronger  resistance  in  the 
abdominal  bandage  than  in  the  flaccid  belly  walls,  which,  when  strong 
pressure  is  exerted,  invariably  become  more  distended. 

Dietetic  rules  form  an  important  part  of  the  treatment.  From  a 
purely  mechanical  standpoint  the  difficulty  of  propelling  the  ingesta  from 
tlio  stomach  is  at  once  obvious,  v.  Mering  ^  has  lately  pointed  out  that  in 
tlie  riglit  lateral  position  the  stomach  is  most  rapidly  emptied,  and,  under 
the  conditions  here  discussed,  we  should  utilize  this  fact.  In  debilitated 
persons,  a  rest  of  one  or  two  hours  in  the  right  lateral  position  after  the 
principal  meal  should  certainly  be  advised. 

Furthermore,  it  is  unwise  to  permit  too  copious  meals.  At  least  while 
active  symptoms  are  present,  several  small  meals  must  take  the  place  of 
the  cliief  meal.  Oertel  and  Schweninger's  advice  to  the  obese  not  to  drink 
while  eating,  which  they  erroneously  regarded  as  an  important  law,  is, 
on  the  contrary,  well  adapted  to  gastric  patients,  and  particularly  to  those 
sufTering  from  gastroptosis. 

Under  some  circumstances  we  may  attempt  to  hasten  the  evacuation 
of  the  stomach  by  massage.  In  most  cases  I  believe  this  effect  is  to  be 
attributed  to  autosuggestion.  Nevertheless,  I  have  several  times  seen 
such  favorable  results  that  I  frequently  advise  it,  and  the  more  so  since 
it  may  be  readily  practised  by  the  patients  upon  themselves.  The  hand 
rests  upon  the  left  arch  of  the  ribs,  and  about  this  point  rotary  motions 
are  made  from  the  left  below  to  the  right  upward.  Massage  by  another 
person  I  do  not  advise,  because,  particularly  with  movable  kidneys,  there 
is  danger  that  these  may  be  irritated — a  danger  which  cannot  be  excluded. 

I  am,  therefore,  decidedly  opposed  to  the  advice  given  by  some  authors 
to  treat  gastroptosis  by  a  course  of  massage  of  from  six  to  eight  weeks, 
in  which  the  massage  is  given  one  or  two  hours  before  eating.  This  will 
not  bring  about  a  true  cure  of  gastroptosis,  and  a  temporary  insufficiency 
of  the  musculature  of  the  stomach  may  more  certainly  be  made  to  disap- 
pear by  other  means. 

In  the  choice  of  food  the  same  rules  are  operative  which  are  applicable 
to  all  patients  suffering  from  gastric  disease.  When  there  is  marked  dis- 
turbance of  gastric  digestion  small  quantities  of  milk  may  first  be  per- 
mitted, and  are  very  serviceable  as  easily  digested,  rich,  nutritive  products. 
II    is  not  advisable  to  give  more  than  one  liter  of  milk  in  the  course  of 

*  V.  Mering,  Therapie  der  Oegenwart,  1902,  Heft  5. 


DISPLACEMENT   OF  THE  STOMACH   (GASTROPTOSIS)  279 

the  day;  more  than  this  will  over-burden  the  stomach.  If  there  is  repug- 
nance to  milk,  cream  may  be  given,  more  or  less  fatty  according  to  the 
severity  of  the  condition,  and  some  tea.  Zwieback,  wheat  bread,  lean  meat, 
eggs,  green  vegetables  are  the  foods  which  next  come  into  question.  We 
must  be  careful  with  those  foods  which  readily  generate  fermentation  and 
gas  in  the  stomach,  therefore  those  especially  rich  in  sugar.  Naturally, 
the  individual  taste  and  the  experience  of  special  patients  must  here  be 
taken  into  consideration.  In  regulating  the  bowels  we  must  always  con- 
sider whether  a  food  shows  a  strong  tendency  to  generate  gas.  In  consti- 
pation we  are  generally  inclined  to  advise  foods  rich  in  cellulose,  conse- 
quently bread  rich  in  gluten.  The  cellulose  of  gluten  at  first  mechanically 
stimulates  the  intestine,  subsequently  it  undergoes  decomposition  in  the 
intestine  by  the  activity  of  bacteria,  and  thus  volatile  acids  and  gases  are 
formed.  In  gastroptosis,  on  account  of  the  pendulous  belly  which  usually 
coexists,  gas  production  is  probably  already  present  and  very  disagreeable 
to  the  patient,  so  that,  under  these  circumstances,  the  physician  must  be 
cautious.  Here  fruit,  stewed  fruit,  and  acid  fruit  wine,  buttermilk  or 
milk  sugar  lemonade  are  frequently  preferable  to  the  coarser  varieties  of 
rye  bread. 

As  in  all  displacements  of  organs  we  must  consider  in  each  individual 
case  whether  it  is  wise  to  attempt  a  "  fattening  cure  "  by  profuse  nourish- 
ment, so  that  the  fat  which  has  disappeared  from  the  abdominal  cavity 
may  again  accumulate  there.  I  believe  that  this  question  should  generally 
be  answered  in  the  affirmative.  Patients  with  an  affection  of  the  stomach 
are  usually  so  debilitated  that  even  a  gain  in  weight  of  a  few  pounds  is 
worth  our  efforts,  because  this  furnishes  the  best  proof  of  the  retardation 
of  the  pathologic  phenomena.  In  all  cases  of  hypernutrition  prolonged  rest 
is  absolutely  necessary,  for  we  must  never  forget  that  the  displaced  stomach, 
even  more  than  the  normal  stomach,  is  burdened  by  the  ingested  food. 
The  more  food,  therefore,  the  patient  eats,  the  less  should  the  stomach 
labor  under  unfavorable  mechanical  conditions.  As  already  stated,  it  is 
not  enough  that  the  patient  assume  the  lateral  position  for  some  time 
after  eating,  but  for  the  whole  day,  uninterruptedly,  or  at  least  for  the 
greater  part  of  the  day,  he  should  remain  in  bed  or  upon  a  lounge.  The 
too  free  consumption  of  milk — over  three  liters  daily,  according  to  the 
advice  of  Weir  Mitchell — as  was  formerly  and  is  even  now  the  general 
rule,  can  only  aggravate  the  insufficiency  of  the  displaced  organ  by  over- 
burdening the  stomach.  On  the  other  hand,  easily  digested  fats,  such  as 
cream,  butter,  bacon,  or  some  carbohydrates,  such  as  milk  sugar  and  man- 
nite,  should  be  employed.  Alcohol  ^  can  rarely  be  dispensed  with  in  the 
form  of  brandy,  good  wine,  or  even  as  beer.     But  only  slight  quantities 


'  Compare  F.  Hirschfeld,  "  Die  Ueberernahrung  und  die  Untererniihrung,"  Frank- 
furt, 1897,  p.  43  u.  f. 


280     DISPLACEMENTS   OF  THE  ABDOMINAL  VISCERA   AND   HEART 

of  the  last  named  stimulant  should  be  allowed,  and  never  more  than  200 
CO.  at  a  meal.  Brandy  may  be  advantageously  given  with  milk,  or  even 
with  cream  provided  it  be  not  too  fat.  Not  only  the  property  of  alcohol 
as  a  nutrient,  but  also  its  stimulating  effect  upon  the  gastric  activity,  is 
especially  desirable   (G.  Klemperer). 

In  gastroptosis  I  have  made  but  little  use  of  drugs  to  improve  the  nutri- 
tion. Sodium  bicarbonate  or  magnesia,  about  as  much  as  will  cover  the 
tip  of  a  knife,  frequently  lessens  the  gastric  symptoms.  Hydrochloric 
acid,  as  a  rule,  unquestionably  has  a  deleterious  effect.  A  favorable  influ- 
ence is  usually  obtained  by  the  employment  of  bitters;  and  I  have  fre- 
q\iently  used  the  following  prescription: 

I^   Tinct.   Cinchona  comp 20.0 

Tinct.  Nucis  Vomica? 5.0 

30  drops  in  water  or  brandy  three  or  four  times  daily. 

In  gastroptosis  a  mineral  spring  treatment  is  naturally  not  advisable. 
Even  in  Carlsbad,  particularly  in  young,  nervous  persons,  such  treatment 
of  these  cases  is  often  ineffectual.  A  residence  in  a  place  of  high  altitude 
is  more  beneficial,  and  care  must  be  taken,  especially  at  first,  to  avoid 
too  great  bodily  exertion,  or  to  see,  at  least,  that  it  corresponds  with  the 
strength  of  the  patient.  In  nervous  patients  it  is  easily  understood  that 
rest  in  a  sanatorium,  or  a  residence  with  surroundings  of  beautiful  scenery, 
will  have  a  favorable  effect.  Sea  baths,  also,  on  account  of  their  stimula- 
tion of  the  appetite,  are  worthy  of  consideration  in  some  cases,  but  the 
physician  should  always  be  consulted  in  these  instances.  In  Germany, 
bathing  in  the  Baltic  Sea  is  generally  more  beneficial  to  such  patients 
than  in  the  North  Sea. 

Finally,  in  gastroptosis,  as  in  so  many  other  diseases,  hydrotherapy 
may  be  employed,  and  is  particularly  adapted  to  the  many  nervous  symp- 
toms which  develop  in  connection  with  all  gastric  affections. 

Buxhaum  ^  and  Winternitz  advise  quick,  cool  Sitz  baths,  while  others 
(Matthes,  Boas^)  have  seen  favorable  results  from  a  needle  douche  which 
may  ho  used  either  cold  or,  like  the  so-called  Scotch  douche,  cool  and  warm 
alternately.  In  this  treatment,  other  measures  may  occasionally  precede 
tlie  local  douche,  as  a  lukewarm  full  bath,  or  general  friction  of  the 
entire  body. 

For  tlie  sake  of  completeness  I  shall  only  mention  that  electrical  treat- 
ment of  the  stomach,  the  faradic  as  well  as  the  galvanic  current,  is  occa- 
sionally employed  in  gastroptosis.     I  saw  favorable  results  in  a  case  in 


'  liu.rbaum,  "Festschrift  fur  Winternitz,"  1892. 

-Miitthrs.  "  Klinische  Hydrotherapie,"  Jena,  1900,  p.  326;  Boas,  Internat.  klin. 

h'lOKl-sclinu.  1894,  Nr.  6. 


DISPLACEMENT  OF  THE   KIDNEYS  281 

which  almost  all  other  remedies  had  proven  ineffectual.  The  patient  was 
a  lady,  exceedingly  nervous,  who  complained  of  spasmodic  pain  several 
hours  after  taking  food. 

In  the  treatment  of  all  cases  of  gastroptosis  the  following  must  be 
remembered : 

We  may  relieve  and  improve  a  state  of  insufficiency  of  the  gastric 
musculature  which  develops  in  consequence  of  an  unfavorable  position  of 
the  stomach,  and  brings  about  severe  nutritive  disturbance  in  the  patient. 
The  low  position  of  the  pylorus,  however,  remains,  and,  as  is  the  case  with 
a  damaged  cardiac  valve,  only  hypertrophy  of  the  cardiac  muscle  produces 
compensation;  in  the  same  way  greater  labor  is  demanded  of  the  muscu- 
lature of  the  pylorus  on  account  of  its  unfavorable  effect  upon  the  pro- 
pulsion of  the  chyle.  The  efforts  of  the  physician  must  be  directed,  on 
the  one  hand,  to  removing  the  disturbance  of  compensation  which  has 
occurred,  and  he  must  subsequently  try  to  prevent  such  a  condition.  This 
part  of  his  work  is  practical  and  of  the  utmost  importance.  An  attempt 
should  also  be  made  to  strengthen  the  abdominal  walls  and,  in  so  far  as 
possible,  to  prevent  the  patient  from  over-burdening  his  stomach.  In  how 
far  this  may  be  done  in  the  individual  case  by  giving  minute  directions  in 
regard  to  the  food  can  be  ascertained  only  by  careful  observation. 

The  surgical  treatment  of  gastroptosis  rarely  comes  into  question,  be- 
cause the  continuance  of  the  symptoms,  notwithstanding  careful  treat- 
ment, must  probably  be  attributed  to  a  disturbance  of  the  nervous  system. 
Duret  and  Eowsing  have  proposed  to  attach  the  gastric  wall  to  the  anterior 
parietal  peritoneum.  Bier  ^  advises  us  to  shorten  the  gastrohepatic  liga- 
ment by  folding  and  stitching  it,  and  in  four  cases  he  had  favorable  results 
by  this  means.  The  previous  nutritive  condition,  which  was  very  poor, 
the  cachexia  of  gastroptosis,  and  the  nervous  symptoms  were  said  to  be 
relieved  by  this  treatment. 

DISPLACEMENT   OF   THE    KIDNEYS-WANDERING   KIDNEY— 

NEPHROPTOSIS 

While  displacement  of  the  stomach  almost  invariably  develops  after 
puberty,  displacement  of  the  kidneys  is  often  observed  in  children.  This 
anomaly  was  even  noted  in  a  nursling.^ 

A  male  nursling,  a  few  days  after  birth,  was  attacked  by  serious  vomiting  and 
symptoms  of  collapse.  Physical  examination  revealed  a  small  oval  tumor  at  the 
right  arch  of  the  ribs  which  could  be  moved  over  the  entire  abdomen.  The  other 
kidney  was  also  movable,  but  not  to  the  same  extent.  The  attacks  recurred  in  the 
next  few  days,  spasms  simultaneously  taking  place.    There  was  marked  constipation. 

^  Bier,  Zeitschr.  f.  Chirurgie,  1901. 
*Rees  Phillips,  The  Lancet,  1903,  p.  731. 


282     DISPLACEMENTS   OF  THE   ABDOMINAL  VISCERA  AND   HEART 

A  case  of  this  kind  shows  that  displacement  of  the  kidneys  may  be 
congenital.  In  by  far  the  great  majority  of  cases,  however,  it  develops 
gradually,  as  is  evident  from  the  following  statistics  of  L.  Kuttner.^ 

The  age  in  326  cases  was  as  follows: 


1-10 

10-20 

20-30 

30-40 

40-50 

50-60 

60-70  years. 

6 

32 

82 

123 

49 

26 

8 

The  right  kidney  is  most  frequently  displaced.  According  to  Ewald 
and  Kiittner,  we  may  assume  that  the  right  kidney  is  seven  or  eight  times 
more  frequently  displaced  than  the  left  kidney.  Often  the  position  of 
both  kidneys  is  changed,  and  in  the  majority  of  cases  greater  movability 
may  bo  determined  in  the  right  than  in  the  left.  E.  Hahn  ^  attributes  this 
to  the  firm  attachment  of  the  left  kidney  to  the  descending  colon  (which  is 
little  inclined  to  displacement)  and  to  the  pancreas  and  the  spleen,  while 
the  right  kidney  possesses  but  one  point  of  fastening,  the  hepatorenal 
ligament.  The  sexes  are  affected  by  this  anomaly  in  about  the  proportion 
of  7  or  8  to  1 ;  among  97  cases  of  nephroptosis  Landau  ^  found  10  to 
occur  in  nien  and  87  in  women.  Hahn,  it  is  true,  assumed  that  floating 
kidney  was  20  times  more  frequent  in  women  than  in  men. 

In  regard  to  the  absolute  proportion  of  cases  showing  change  of  posi- 
tion it  is  difficult  to  give  a  positive  opinion.  From  investigations  in  the 
living  subject,  Ewald  and  Kuttner  assume  15  per  cent.,  and  with  this  the 
reports  of  anatomists  coincide.  In  the  reports  of  the  seventh  decade  of 
the  preceding  century,  among  the  autopsies  of  the  pathological  institutes 
of  Berlin,  Vienna  and  Kiel,  movability  of  the  kidney  was  found  in  only 
0.1 :  0.4  per  cent.,  but  the  more  recent  investigations  of  Fischer-Benzon, 
in  Kiel,  show  from  17  to  23  per  cent. 

According  to  the  degree  of  movability  of  the  kidney  we  differentiate 
various  grades.  Under  physiologic  conditions,  the  kidneys  move  slightly 
from  their  position  with  each  respiration,  descending  on  inspiration,  and 
rising  on  expiration.  Some  clinicians,  such  as  Israel,  Litten,  Lennhof 
and  Becher,  maintain  that  this  movability  may  be  determined  by  palpation 
even  during  life,  while  the  majority  of  authors  deny  this.  At  all  events, 
therefore,  in  the  normal  person  this  movability  must  be  very  slight,  and  in 
the  majority  of  healthy  adults  the  kidney  cannot  be  palpated  from  the 
abdomen.  In  the  minority  this  is  to  some  extent  possible,  but  only  the 
lower  third  of  the  organ  can  be  felt.     Of  course,  thin,  flaccid  abdominal 

'  L.  Kuttner,  Berl.  klin.  Wochenschr.,  1890,  p.  364;  compare  in  the  same  journal 
Ksviild's  lecture  before  the  Berlin  Medical  Society,  March,  1890,  and  the  discussion 
in  connection  with  it.  (Virchow,  Litten,  Landau,  P.  Guttmann,  Senator,  Israel 
and  others.) 

'  h:.  Hiilin.  Zritftrhr.  f.  Vhininjie,  LXVII,  p.  356  et  seq. 

'  L.  Landau,  "  Die  Wanderniere,"  Berlin,  1881. 


DISPLACEMENT   OF  THE   KIDNEYS  283 

walls  will  extraordinarily  facilitate  the  examination.  Becher  and  Lenn- 
hof  ^  point  to  a  special  structure  of  the  body  which  lends  itself  to  palpa- 
tion. Although  tall  persons  usually  form  the  bulk  of  this  group,  a  definite 
bodily  proportion  is  decisive,  and  this  may  be  found  in  individual  persons 
and  in  various  races  under  different  conditions.  The  greater  the  distance 
from  the  manubrium  sterni  to  the  symphysis  pubis,  the  greater  the  portion 
of  the  kidney  susceptible  to  palpation.  If  the  slight  physiologic  movabil- 
ity  of  the  kidney  is  increased,  it  is  possible  during  palpation  of  the  abdo- 
men not  only  to  feel  a  small  portion  of  the  kidney  but  two-thirds,  or 
even  the  complete  extent,  of  the  organ;  under  the  influence  of  the  respira- 
tory movements  the  displacement  becomes  particularly  prominent.  In  a 
later  stage  of  abnormal  movability,  the  kidney  can  no  longer  be  recognized 
in  its  normal  position  upon  the  posterior  wall  of  the  abdominal  cavity,  but 
may  be  felt  in  some  other  area  of  the  abdomen,  and  thence  it  may  either 
be  readily  moved  or  it  becomes  adherent  to  this  region  so  that  it  can  only 
be  displaced  in  connection  with  other  abdominal  viscera. 

ETIOLOGY 

A  primal  cause  of  abnormal  movability  is  probably  a  congenital  pre- 
disposition. In  the  normal  person  the  kidneys  are  usually  situated  in  a 
groove  in  the  posterior  abdominal  wall,  anterior  to  and  alongside  the  trans- 
verse processes  of  the  vertebrae,  and  extending  from  about  the  height  of 
the  twelfth  cervical  to  the  third  lumbar  vertebra.  Two  Eussian  investi- 
gators, Wolkow  and  Delitzin,^  have  especially  called  attention  to  the  im- 
portance of  the  formation  of  this  paravertebral  niche  for  holding  the 
kidney.  If  this  niche  is  markedly  flattened,  the  kidney,  naturally,  will 
much  more  readily  slip  out.  Besides  this  congenital  flatness  of  the  groove, 
which  is  readily  seen,  scoliosis  of  the  vertebral  column  adds  to  the  condi- 
tion. We  must  also  consider  that  in  intra-uterine  life  the  kidneys  are 
low  down  in  the  abdominal  cavity  in  the  sacral  hollow  of  the  pelvis. 
Gradually  they  move  up  higher.  This  shows  at  once  that  the  kidneys 
are  not  supplied  with  very  tense  suspensory  ligaments;  they  are  partially 
held  by  their  ligamentous  apparatus,  but  are  also  supported  by  the  peri- 
toneal layers  and  the  fatty  capsule;  on  the  other  hand,  the  kidneys  main- 
tain their  position  by  the  pressure  of  all  the  abdominal  viscera.  Accord- 
ingly, by  a  sundering  of  various  links,  this  girdle  which  supports  them  may 
become  slack  or  broken.  A  flattening  of  the  niche  simultaneously  with  a 
loosening  of  the  ligamentous  apparatus  seldom  causes  a  displacement  of 
the  kidney.     Rigid  abdominal  walls,  such  as  are  found  in  most  young, 

*  W.  Becher  und  R.  Lennhof,  Deutsche  med.  Wochenschr.,  1898,  Nr.  32,  und  Verh. 
(1.  XVIII.  Conor,  f.  inn.  Med.,  p.  476. 

*  Wolkow  und  Delitzin,  "  Die  Wanderniere,"  Berlin,  1899;  compare  also  M. 
Zondek,  "  Die  Topographie  der  Niere,"  Berlin,  1903. 


284     DISPLACEMENTS   OF  THE  ABDOMINAL  VISCERA   AND   HEART 

robust  persons,  usually  hold  the  abdominal  organs  in  their  natural  position. 
This  explains  the  rarity  of  floating  kidney  in  persons  under  twenty  years 
of  age.  When,  from  any  circumstance,  pressure  in  the  abdomen  is  less- 
oned, this  favorable  influence  is  lacking.  Lacing  is  the  most  frequent 
among  the  deleterious  factors  which  must  here  be  considered,  because  the 
liver  is  thereby  pressed  do\vnward,  and  the  right  kidney,  which  is  inti- 
mately connected  with  the  liver,  also  has  pressure  exerted  upon  it.  This 
explains  the  fact  that  the  right  kidney  shows  abnormal  displacement  so 
much  more  frequently  than  the  left.  We,  however,  are  under  the  im- 
pression that  lacing  is  here  not  so  predisposing  as  is  the  case  in  gastrop- 
tosis.  Repeated  pregnancies  which  markedly  diminish  the  support  of  the 
ai)doininal  wall  mostly  have  a  decided  effect  in  that  a  portion  of  the  abdom- 
inal contents,  usually  the  intestines,  bulge  forward  and  downward,  so  that 
lateral   pressure  upon  the  kidneys  is  diminished. 

The  greatest  decrease  in  pressure  occurs  when  the  abdominal  cavity 
suddenly  becomes  smaller,  as  after  the  operative  removal  of  large  tumors. 
I'lidei-  such  circumstances,  Israel  noted  that,  before  his  very  eyes,  the 
kidneys  l)ecame  abnormally  movable. 

A  gradual  decrease  in  pressure  may  also  be  expected  when  from  general 
emaciation  considerable  adipose  tissue  disappears  from  the  abdominal 
cavity.  Other  deleterious  effects  may  also  be  operative,  such  as  shock  to 
the  abdominal  wall.  Thus  I  would  explain  the  wandering  kidney  which 
I  several  times  saw  develop  in  emaciated  patients  in  the  course  of  pulmo- 
nary disease.  In  emphysema  and  asthma  floating  kidney  may  easily  be 
])roduced,  because,  from  the  emphysematously  distended  lung,  pressure  is 
exerted  upon  the  diaphragm,  and  then  referred  to  the  liver  and  the  right 
kidney.  Repeated  shock  to  the  abdominal  wall  from  paroxysms  of  cough 
uuiy  gradually  loosen  the  kidneys.  In  one  case  of  wandering  kidney  caus- 
ing abdominal  symptoms  the  patient  attributed  it  to  prolonged  laughter, 
in  a  similar  manner  straining  during  a  difficult  fecal  evacuation,  or  in  lift- 
ing a  heavy  load,  may  be  the  cause.  Under  such  circumstances  traumatic 
origin  of  wandering  kidney  is  quite  possible,  while  in  a  normal,  well-fastened 
kidney  this  theory  is  scarcely  plausible. 

Just  as  the  stomach  may  subsequently  be  displaced  by  a  neoplasm 
wliieb  adds  to  its  weight  and  dilates  it,  so  may  this  condition  result  in 
tbe  kidney  from  hydronephrosis  or  pyonephrosis.  Such  cases,  of  course, 
are  not  wandering  kidneys  in  the  usual  acceptation  of  the  term. 

SYMPTOMS 

Symptoms  of  wandering  kidney  may  be  entirely  absent.  The  patients, 
in  this  instance,  are  usually  strong,  plethoric  persons  otherwise  quite  well, 
whose  kidneys,  one  or  both,  have  descended  into  the  abdomen  without 
eausing  any  symptoms.     Occasionally  abnormal  sensations  are  noted  which 


DISPLACEMENT   OF  THE   KIDNEYS  285 

incidentally  make  known  to  the  person  in  question  that  he  has  a  movable 
kidney.  Some  patients  report  after  unusual  exertion  a  sensation  of  rum- 
bling or  one  like  the  gliding  about  of  a  heavy  substance.  It  is  difficult 
to  decide  whether  these  reports  depend  merely  upon  auto-suggestion,  or 
to  what  extent  indefinable  sensations,  due  to  the  influence  of  already  ex- 
istent factors,  may  subsequently  be  explained.  It  is  still  more  difficult 
to  assign  vague  nervous  symptoms,  whatever  their  nature,  to  nephrop- 
tosis. While  we  cannot  doubt  that  all  varieties  of  nervous  symptoms  may 
appear  in  persons  whose  kidneys  are  normally  attached,  yet,  when  people 
are  predisposed  to  nervous  affections,  we  are  justified  in  assuming  a  mov- 
able kidney  to  be  the  cause  of  various  painful  sensations  such  as  sciatica, 
intercostal  neuralgia,  or  similar  affections.  Sensitiveness  in  the  region  of 
the  iliac  fossa  may  be  attributed  to  the  kidney.  In  any  case  the  physician 
is  wise  not  at  once  to  communicate  the  fact  that  during  an  examination 
he  has  accidentally  discovered  a  wandering  kidney.  The  precautions  yet 
to  be  considered,  such  as  wearing  a  bandage,  refraining  from  lacing,  etc., 
can  also  be  insisted  upon  when  we  speak  to  the  patient  merely  of  "  a 
predisposition  to  wandering  kidney,"  and  the  first  duty  is  to  prevent  the 
production  of  a  floating  kidney. 

Symptoms  on  the  part  of  the  stomach  are  most  frequently  noticed,  and 
these  usually  simulate  a  chronic  gastric  catarrh;  acute  attacks,  designated 
as  gastric  spasm,  are  very  rare.  As  a  rule,  we  note  loss  of  appetite,  eruc- 
tations, and  pressure  in  the  gastric  region,  less  frequently  vomiting.  We 
know  from  numerous  observations  that  in  diseases  of  other  organs,  and 
particularly  in  those  of  the  abdomen,  the  stomach  is  likely  to  become 
implicated,  A  heavily  coated  tongue  is  almost  invariably  present  in  dis- 
ease of  the  gall-bladder,  of  the  urinary  bladder,  and  in  inflammation  of  the 
renal  pelvis,  and  the  appetite  is  always  decreased.  It  must  be  borne  in 
mind  that  nephroptosis  is  often  combined  with  gastroptosis.  These  pa- 
tients are  usually  pale  and  weak  young  persons  in  whom  gastric  difficulties 
are  prominent;  stout,  elderly  women,  even  when  a  pendulous  abdomen  has 
developed,  are  more  rarely  affected.  According  to  statistics,  the  implica- 
tion of  the  stomach  in  nephroptosis  is  about  as  follows: 

In  89  cases  of  movable  kidney  Kuttner  found  the  position  of  the 
stomach  normal  in  only  10,  that  is,  the  greater  curvature  of  the  stomach 
was  situated  normally  in  the  median  line  between  the  umbilicus  and  the 
ensiform  process. 

In  79  cases  the  greater  curvature  was  3  to  4  cm.  below  the  navel, 
occasionally  even  lower  than  this;  in  15  of  these  cases,  by  inflation  of  the 
abdomen  with  air  by  means  of  a  double  bellows,  a  true  prolapse  of  the 
stomach  could  be  observed. 

Dyspeptic  symptoms  were  present  in  70  of  these  persons,  hence  this 
symptom  may  be  designated  as  the  most  important  and  most  common  in 
floating  kidney. 


286     DISPLACEMENTS  OF  THE  ABDOMINAL  VISCERA  AND  HEART 

A  peculiarity  of  the  gastric  symptoms  in  nephroptosis  is  their  increase 
after  muscular  exertion  and  their  disappearance,  or  at  least  improvement, 
after  prolonged  rest.  As  a  rule,  the  majority  of  these  female  patients 
suffer  most  during  the  menstrual  period. 

In  nephroptosis,  just  as  in  gastroptosis,  constipation  is  important  and 
is  duo  to  the  same  causes — weakness  of  the  abdominal  walls,  insufficient 
nourishment  or  food  poor  in  residue,  often  kinking  of  the  colon,  etc. 

Symptoms  on  the  part  of  the  kidneys  are  rare.  It  might  readily  be 
supposed,  and  would  seem  likely,  that  torsion  and  kinking  of  the  ureters 
would  occur  frequently.  As  a  matter  of  fact  such  an  accident  is  very  rare. 
Dittl,  Landau,  Lindner  and  others  have,  it  is  true,  described  attacks  which 
resembled  renal  colic  and  which  were  mistaken  for  this.  Occasionally  it 
was  believed  that  spasmodic  contraction  of  the  ureter  could  be  felt  through 
the  abdominal  walls.  Some  patients  are  attacked  so  suddenly  with  sensa- 
tions of  nausea,  vomiting,  and  severe  pain  in  the  renal  region,  the  ureters 
and  the  bladder,  that  the  physician  must  assume  severe  peritoneal  irrita- 
tion, for  the  pulse  also  is  small  and  increased,  the  skin  is  cool,  cold  sweat 
appears,  etc.  But  such  intermediate  attacks  which  probably  depend  upon 
kinking  of  the  ureter  or  of  the  vessels,  or  torsion  of  the  renal  nerves, 
are  rare;  I  have  only  once  seen  a  case  of  the  kind.  Albuminuria  and 
hematuria  are  infrequent,  as  are  also  so-called  intermittent  hydronephro- 
sis, pyonephrosis,  and  pyelitis.  Up  to  the  present  time  but  little  attention 
has  been  given  to  the  latter  complication,  therefore  I  shall  briefly  relate 
my  own  experience  in  regard  to  it.  [These  attacks  are  the  so-called 
"  Dittl's  crises."] 

Pyelitis  as  a  Complication  of  Hydronephrosis. — The  patients,  usually 
women  about  forty  years  of  age,  who  for  ten  or  even  twenty  years  have 
had  no  symptoms  of  their  wandering  kidney,  are  suddenly  attacked  with 
acute  pains  in  the  abdomen.  The  pains,  as  shown  by  palpation  of  the 
abdomen,  are  chiefly  located  in  the  displaced  kidney,  and  radiate  along 
the  course  of  the  ureter  to  the  region  of  the  bladder.  Strangury  fre- 
quently occurs.  There  is  fever  from  100.4°  to  102.2°  F.  which  is  re- 
mittent in  type.  The  urine  is  turbid,  usually  of  acid  reaction,  and  micro- 
scopically is  composed  almost  exclusively  of  pus  corpuscles.  Chemical 
examination,  of  course,  reveals  albumin,  but  decided  amounts  (up  to  5  per 
1,000)  are  also  found  in  the  filtered  urine  or  in  the  clear  urine  after 
sedimentation  has  occurred. 

After  one  or  two  weeks  the  inflammatory  symptoms  subside.  The 
tem])orature  becomes  normal,  but  the  pulse  for  some  time  continues  to 
be  accelerated.  The  sensitiveness  of  the  kidney  gradually  passes  away. 
Tlie  albumin  decreases  so  rapidly  that  after  two  or  three  weeks  none  can 
bo  detected  in  a  clear  layer  of  urine;  but  the  excretion  of  pus  and  the 
turbidity  of  the  urine  due  to  this  may  continue  for  months  and,  occasion- 
ally, even  for  years.     For  a  long  time  the  patients  are  able  to  take  but 


DISPLACEMENT  OF  THE   KIDNEYS  287 

little  exercise  and  must  avoid  all  exertion.  Prolonged  sitting  is  impossible. 
A  slight  tenderness  of  the  urinary  organs  upon  pressure  continues  to  exist 
for  some  time,  and  makes  the  wearing  of  bandages  or  corsets  irksome. 
Slow  recovery  from  pyelitis  and  floating  kidney  is  characteristic. 

In  the  treatment  warm  drinks,  warm  baths,  hot  poultices,  etc.,  are 
most  effective;  among  drugs  salol,  urotropin,  uva  ursi  and  the  like. 

In  one  case,  eight  days  after  a  very  movable  right  kidney  had  become 
affected  I  saw  the  left  kidney  also  attacked,  this,  so  far  as  could  be  ascer- 
tained, being  in  its  normal  situation.  The  fever,  which  had  declined, 
again  rose,  and  all  of  the  s3Tnptoms  returned. 

The  sudden  appearance  of  pyelitis  without  other  s3nnptoms  may  be 
attributed  to  an  acute  infection;  but  the  nature  of  the  infection  is  not 
clear.  If  gonorrhea  or  cystitis  have  not  previously  been  present,  it  is 
very  likely  due  to  an  emigration  of  bacteria  from  the  intestine  (Posner). 
But  such  complications  are  rare,  for  Kuttner  saw  only  4  among  his  89 
cases,  and  among  93  cases  operated  upon  by  Kiister  ^  only  two  displaced 
kidneys  showed  the  development  of  pathologic  processes. 


DIAGNOSIS 

The  diagnosis  of  floating  kidney  is  in  some  cases  very  easy.  Even 
upon  superficial  palpation  of  the  abdomen,  we  feel  an  organ  of  the  size 
and  consistence  of  the  kidney  which  either  moves  about  or  is  fixed  in 
some  area.  In  the  majority  of  cases  the  organ  is  situated  upon  the  right 
side  of  the  body,  which  confirms  the  opinion  that  the  right  kidney  is  by 
far  the  most  frequently  displaced.  The  diagnosis  becomes  difficult  when 
the  kidneys  still  retain  their  position  in  the  posterior  abdominal  wall. 
Bimanual  examination  then  becomes  necessary.  As  already  stated,  only 
in  those  persons  who  are  tall  and  thin  is  it  possible  to  feel  a  portion  of  the 
normally  situated  kidney,  that  is,  about  one-third  of  the  organ,  and  this 
is  most  readily  perceptible  in  the  deeper  situated  right  kidney.  To  over- 
come the  marked  tension  of  the  abdominal  walls  which  is  often  present, 
Becher  and  Lennhof  advise  an  occasional  examination  in  a  warm  bath. 
A  simpler  method  which  I  found  serviceable  was  the  employment  of  a 
moist,  hot  poultice  about  the  abdomen.^ 

For  the  examination,  the  patient  is  placed  in  a  horizontal  position,  the 
legs  are  flexed  somewhat,  and  abducted  and  rotated  outwardly  to  ensure 
a  comfortable  position,  then  one  hand  is  placed  upon  the  back  at  the 

*  P.  Gets,  "  18  Jahre  Nierenchirurgie,"  Marburg,  1900. 

'  The  relaxation  of  the  tension  of  the  abdominal  walls  is  naturally  also  of  value 
in  the  consideration  of  other  pathologic  processes.  For  diagnostic  purposes  in  peri- 
typhlitis, the  occasional  employment  of  the  hydropathic  poultice  to  determine  the 
presence  and  extension  of  the  exudate  is  especially  useful.  The  enlarged  appendix 
can  then  occasionally  be  palpated. 
20 


288     DISPLACEMENTS   OF  THE   ABDOMINAL   VISCERA   AND  HEART 

heio-ht  of  the  eleventh  or  twelfth  rib  while  the  other  gradually  makes 
deep  pressure  from  above  downward.  An  accumulation  of  fat,  as  well 
as  marked  tension  of  the  abdominal  walls,  renders  this  examination  dif- 
ficult, and  even  with  abvmdant  practice  it  often  gives  a  doubtful  result. 
If  upon  respiration  the  kidney  seems  to  be  movable  we  may  draw  the  con- 
clusion that  it  has  descended  somewhat,  since,  under  normal  circumstances, 
this  movability  is  hardly  perceptible.  Another  method  of  examination, 
percussion,  often  leaves  us  absolutely  in  the  dark. 

Renal  Dystopia. — In  considering  the  findings,  we  must  first  answer  the 
question:  Is  not  the  displacement  a  congenital  change,  a  so-called  renal 
dystopia?  Miillerheim  ^  has  recently  taught  us  by  his  special  investiga- 
tions that  this  renal  dystopia  depends  upon  an  embryonal  inhibitive  for- 
mation, and  is  by  no  means  rare,  for  he  succeeded  in  finding  200  cases 
reported  in  literature.  The  characteristics  of  renal  dystopia  are,  as  a 
rule,  the  change  in  form,  the  fixation  of  the  position,  the  abnormal  vascu- 
lar su])ply,  and  the  shortness  of  the  ureters.  Some  of  these  character- 
istics, such  as  the  abnormal  vascular  supply,  cannot  be  recognized  during 
the  life  of  the  patient.  More  significance  is  to  be  attached  to  the  change 
in  form  detected  by  palpation.  Frequently  the  kidneys  still  show  fetal 
lobulation,  or  they  have  coalesced  and  formed  the  so-called  horseshoe 
kidney.  Sometimes,  the  dystopic  kidney  lies  in  the  pelvis.  If,  however, 
the  assumption  of  a  congenitally  displaced  kidney  is  already  likely  from 
the  fixation,  the  proof  may  be  found,  according  to  Miillerheim,  by  meas- 
uring the  ureters.  Normally,  these  have  a  length  of  about  25  cm.,  but 
in  a  dystopic  kidney  there  is  often  a  difference  of  10  cm.  Unfortunately 
to  take  these  measures  is  a  very  complicated  procedure;  it  can  only  be 
done  by  catheterization  of  the  ureters,  and,  with  a  tortuous  ureter,  this 
is  often  deceptive. 

The  diagnosis  "  floating  kidney  "  naturally  receives  some  support  from 
the  appearance  of  the  person  in  question.  In  a  patient  with  a  tendency 
to  anemia  there  must  also  be  either  a  pendulous  abdomen  or  a  somewhat 
flaccid  abdominal  wall.  A  certain  degree  of  "nervousness"  or  hysteria 
is  significant  of  this  affection.  The  presence  of  Stiller's  sign,  abnormal 
movability  or  deficient  chondrification  of  the  tenth  rib,  gives  a  view  of 
this  kind  an  objective  basis.  The  presence  of  kyphoscoliosis  strengthens 
the  diagnosis  of  wandering  kidney.  Naturally,  we  must  remember  that 
many  women  show  a  moderate  degree  of  kyphoscoliosis.  In  men,  and  in 
a  left-sided  floating  kidney,  the  greatest  care  in  the  diagnosis  is  presup- 
posed. The  fact  that  in  floating  kidney  the  stomach  rarely  is  normal  in 
positicm  and  size  may  also  be  utilized  in  the  diagnosis.  Finally,  an  ex- 
amination of  the  patient  in  various  positions  of  the  body  (upon  the  side 

^  R.  Miillerheim,  Verhandl.  der  Medicm.  Oesellschaft  in  Berlin,  November,  1892; 
see  also  its  ensuing  discussion. 


DISPLACEMENT   OF  THE   KIDNEYS  289 

and  upon  the  back)  must  be  made,  the  alteration  in  position  of  the  movable 
organ  must  be  followed  and  investigated,  and  we  must  observe  whether 
it  is  connected  with  other  organs.  According  to  J.  Israel,*  the  proof  that 
the  kidneys  are  out  of  their  normal  positions  is  alone  decisive,  since  con- 
striction of  the  right  lobe  of  the  liver,^  carcinomatous  and  tubercular 
tumors  of  the  ascending  colon  and  of  the  flexure  of  the  colon,  carcinomata 
of  the  pylorus,  small  ovarian  tumors  with  long  pedicles,  and  enlarged 
gall-bladder  have  been  mistaken  for  floating  kidney. 

(For  confusion  with  wandering  spleen  see  page  293.) 


TREATMENT 

The  treatment  of  floating  kidney  must  be  limited  in  most  cases  to  the 
application  of  a  suitable  bandage,  to  preventing  the  formation  of  a  pendu- 
lous belly,  and,  in  case  this  is  already  present,  preventing  its  further 
enlargement.  It  is  easy  to  understand  that  the  s3maptoms  of  wandering 
kidney  are  not  so  readily  removed  by  a  bandage  as  those  of  gastroptosis. 
If  pyelitis  has  preceded,  such  a  bandage  is  often  intolerable  to  the  patient. 

Occasionally  a  corset  specially  designed  is  useful,  yet  often  this  fails 
to  have  any  effect.  Then  we  are  compelled  to  resort  to  strips  of  adhesive 
plaster.     Rose  ^  advises  the  following : 

"  Three  strips  as  wide  as  the  hand  and  of  varying  length  are  used,  the 
longest  being  applied  firmly  around  the  belly;  the  entire  abdominal  mass 
is  firmly  pressed  upward  from  below,  and  the  two  ends  of  the  adhesive 
strip  are  brought  together  at  or  over  the  vertebral  column.  The  crest 
of  the  ilium  should  remain  free,  but  the  plaster  must  be  applied  imme- 
diately above,  and  adjacent  to,  this  bone.  The  propping  of  the  abdominal 
wall  is  strengthened  by  the  application  of  two  additional  lateral  strips 
which  also  meet  at  the  vertebral  column,  running  upward  and  backward 
from  Poupart's  ligament." 

If  these  bandages  do  not  at  once  relieve  the  discomfort  of  the  patient, 
we  should  insist  upon  a  few  weeks  of  rest  in  bed. 

Plentifvd  nourishment  and  prolonged  bodily  rest  will,  as  a  rule,  re- 
move the  symptoms  which  appear  in  very  nervous  patients  who  suffer 
from  floating  kidney.  By  this  treatment  fat  will  perhaps  be  deposited  in 
the  belly  and  the  capsules  of  the  kidneys,  and  thus  a  cause  of  abnormal 
movability  will  be  removed.  The  nervous  symptoms,  too,  are  usually  re- 
lieved by  a  rest  cure  in  suitable  environment  and  by  the  employment  of 
hydrotherapeutic  measures.     But,  in  the  end,  the  results  do  not  entirely 


*</.  Israel,  "  Chirurgische  Klinik  der  Nierenkrankheiten."     Berlin,  1901,  p.  20. 
'Penzoldt,  Miinchener  med.  Wochenschr.,  1903,  Nr.   10. 

'Rose,  Zeitschr.  f.  prakt.  Aerzte,  Sept.,  1901 ;  quoted  from  B.  Presch,  "  Die  physi- 
kalisch-diatetische  Therapie  in  der  arztlichen  Praxis."     Wiirzburg,   1903,  p.  170. 


290     DISPLACEMENTS   OF  THE  ABDOMINAL   VISCERA  AND   HEART 

correspond  with  our  hopes.  After  a  short  time,  the  old  complaints  of  a 
wandering  kidney  are  again  heard. 

The  inefficacy  of  treatment  indicates  that  operation  for  the  removal 
of  the  symptoms  should  he  considered.  The  excision  of  the  kidney  has 
been  proposed  and  carried  out,  but,  fortunately,  this  is  no  longer  advised 
1)V  any  surgeon.  The  knowledge  that  when  one  kidney  is  very  movable 
the  other  organ  often  shows  the  same  disability,  although  to  a  less  extent, 
sliould  have  prevented  such  a  method  of  procedure.  Even  when  the  opera- 
tion of  suture,  yet  to  be  touched  upon,  would  be  useless,  extirpation  must 
he  rejected,  for,  no  matter  how  great  the  nervous  symptoms,  the  most 
important  disease  is  in  the  nervous  system,  so  that,  as  a  rule,  the  removal 
of  the  kidney  brings  no  permanent  improvement.  The  dangers  of  this 
operation  may  best  be  seen  from  E.  Hahn's  ^  report  of  42  extirpations  for 
wandering  kidney,  with  the  result  that  11  patients  succumbed  to  sepsis, 
peritonitis  and  uremia. 

Tlie  operation  usually  employed  at  the  present  time  is  suture  of  the 
kidney  to  the  abdominal  wall  (nephrorrhaphy) ,  introduced  by  E.  Hahn. 
The  kidney  is  exposed  by  excision  in  the  lumbar  region,  the  fatty  capsule 
is  partly  removed  and  fastened  to  the  muscles  by  a  few  stitches  through 
the  capsula  propria  and  the  substance  of  the  kidney.  According  to  Israel, 
under  some  circumstances,  the  repetition  of  nephrorrhaphy,  perhaps  by 
another  method,  may  be  necessary.  Objections  have  been  raised  to  this 
ojieration.  In  the  first  place,  Hahn  himself  emphasizes  that  it  is  not 
(|uite  devoid  of  danger.  The  mortality  is  said  to  be  from  2  to  3  per  cent. 
Furtliermore,  the  cure  is  often  not  permanent,  the  difficulties  being,  in 
fact,  not  alone  due  to  the  kidneys,  but  also  to  a  simultaneously  present 
j^astroptosis,  and  symptoms  referable  to  the  stomach  and  to  the  nervous 
system  are  combined.  According  to  the  reports  of  various  surgeons,  the 
cures  may  be  estimated  at  50  to  60  per  cent.  From  this  the  conclusion 
is  obvious  that  the  operation  is  advisable  only  in  such  cases  of  floating 
kidney  as  present  also  renal  symptoms,  therefore,  symptoms  of  constric- 
tion, of  hydronephrosis  or  pyonephrosis,  or  a  stubborn,  distressing  pyelitis. 
This,  as  has  been  stated,  is  only  the  case  in  a  minority  of  the  patients. 

DISPLACEMENT   OF   THE   LIVER— WANDERING   LIVER 
(HEPATOPTOSIS) 

Displacement  of  the  liver  is  comparatively  rare,  provided  we  mean 
the  complete  descent  of  this  organ  from  its  usual  position.  Slight  de- 
trices  of  displacement,  however,  are  comparatively  frequent,  as  has  been 
>h(>\vii  wlicn  tlie  abdominal  cavity  has  been  opened  during  life.  Kehr, 
therefore,  maintains  that  a  somewhat  movable  liver  is  found  in  all  women 

•  E.  Hahn,  Zeitschr.  f.  Chirurgie,  LXVII,  p.  363. 


DISPLACEMENT   OF  THE   LIVER 


291 


who  have  borne  children.  When  the  liver  descends  into  the  lower  abdom- 
inal cavity,  we  naturally  first  attribute  it  to  an  abnormal  weakness  of  the 
suspensory  ligaments,  and,  secondly,  repeated  pregnancies  which  weaken 
the  abdominal  walls  are  frequently  held  responsible.  Thus  Landqu  ^  found 
a  very  marked  displacement  of  the  liver  into  the  lower  abdominal  cavity 
in  a  woman,  aged  38,  who  in  three 
years  had  passed  through  four  preg- 
nancies. 

Cantani  ^  was  the  first  to  describe 
such  a  change  of  position,  and  other 
cases  were  subsequently  reported  by 
various  authors.  In  1885,  Landau 
published  a  comprehensive  mono- 
graph, "  Ueber  Wanderleber  und 
Hangebauch,"  in  which  these  altera- 
tions in  the  position  of  the  liver  are 
accurately  described  as  well  as  their 
mechanical  effect  upon  the  position 
of  the  abdominal  organs. 

Among  31  cases  of  floating  liver 
which  Landau  collected  from  litera- 
ture, 27  occurred  in  women  and  4 
in  men;  14  of  these  cases  were  his  own  patients,  and  he  expressly  points 
out  that  most  authors  underestimate  the  frequency  of  wandering  liver 
because  the  liver  is  rarely  examined  while  the  patient  is  in  the  erect 
posture.     The  age  of  the  person  affected  is  usually  over  forty  years. 

Hepatoptosis  is  recognized  by  the  absence  of  liver  dulness  in  the  usual 
area,  and  by  the  discovery  of  a  movable  tumor  of  the  size  and  consistence 
of  the  liver  in  the  lower  abdominal  cavity;  movability  generally  occurs 
when  the  body  changes  its  position.  In  many  cases,  displacement  of 
other  organs  can  also  be  determined;  Landau,  for  instance,  among  his 
14  cases  of  wandering  liver  found  a  floating  kidney  in  4. 

The  position  of  the  liver  is  best  shown  by  the  accompanying  illustrations 
taken  from  Landau's  book. 

Confusion  with  cancer  of  the  stomach,  tumors  of  the  omentum,  and 
ovarian  cysts  may  occur  if  we  do  not  bear  in  mind  displacement  of  the 
liver,  and  thus  fail  to  trace  the  boundaries  of  the  liver  in  the  right  hypo- 
chondrium. 


Fig.  16. — Displacement  of  the  liver. 


'L.  Landau,  "Die  Wanderleber  und  der  Hangebauch  der  Frauen,"  Berlin,  1885, 
comprehensive  compilation  of  the  literature. 
*  Cantani,  Schmidt'sche  Jahrbiicher,  CXLI. 


292     DISPLACEMENTS  OF  THE  ABDOMINAL  VISCERA  AND   HEART 


SYMPTOMS 

Symptoms  of  wandering  liver  are  usually  manifest,  for  the  organ  is 
so  large  that,  when  in  an  unusual  position,  its  pressure  upon  other  organs 
could  not  be  unnoticed.  A  sensation  of  fulness,  rumbling  in  the  abdomen, 
ill-definod  pains  which  sometimes  extend  over  the  entire  abdomen,^  to  the 
cbost,  to  the  small  of  the  back,  and  to  the  right  shoulder  are,  according  to 
Landau,  the  most  frequent  signs.  As  in  displacement  of  other  organs, 
the  patients  complain  most  after  exertion ;  on  prolonged  rest  in  the  recum- 
bent posture  the  symptoms  disap- 
pear. Some  patients  are  annoyed 
by  the  pulsation  of  the  abdominal 
aorta  and  other  large  abdominal 
vessels  which  is  distinctly  felt. 
Sometimes  it  is  impossible  to  trace 
an  intimate  connection  between  the 
nervous  symptoms  and  the  abdo- 
men. Disturbances  of  gastric  di- 
gestion and  of  bowel  action  are 
often  noted,  as  in  displacement  of 
all  other  abdominal  organs. 

TREATMENT 

The  treatment  generally  con- 
sists in  applying  a  binder  to  sup- 
port the  pendulous  abdomen.  Schott  ^  has  constructed  a  shield  resembling 
the  human  hand  to  hold  the  liver  in  its  normal  position,  but,  like  all  other 
apparatus  to  support  the  abdomen,  the  results  are  not  very  satisfactory. 


Fig.  17. — Displacement  of  the  liver. 


DISPLACEMENT    OF   THE    SPLEEN— WANDERING   SPLEEN 

A  displacement  of  the  unenlarged,  normal  spleen  is  very  rare.  Glenard 
reports  that  he  found  it  only  twice  in  160  cases  of  enteroptosis.  The  loca- 
tion of  the  spleen  near  the  diaphragm  is  such  that  in  all  pathologic  proc- 
esses which  dilate  the  left  thoracic  cavity  it  is  forced  downward,  and 
tlicrchy  is  more  readily  reached  by  the  palpating  finger;  but  there  is  no 
•ricatcr  permanent  movability  than  in  the  normal  organ.  A  displacement 
(if  the  sjileen  is  also  observed  when  it  becomes  enlarged  by  pathologic 
Iiroccsscs  (by  uncompensated  valvular  lesions,  hepatic  cirrhosis,  malaria, 
leukemia).  But,  even  in  this  case,  the  movability  is  usually  not  great. 
Finally,  those  cases  remain  in  which  extreme  movability  of  the  spleen  is 


'  Schott,  "  D.  Medicinalzeitg."     1882,  Nr.  21  und  22. 


DISPLACEMENT   OF  THE  SPLEEN  293 

noted  in  some  area  of  the  abdominal  cavity,  most  frequently  in  the  left 
iliac  fossa.  The  cause  of  this  displacement  is  unknown.  Flaccidity  of  the 
abdominal  walls  or  shock  naturally  favors  its  occurrence;  but  only  in 
a  very  slight  number  of  persons,  and  these  mostly  women,  are  the  ligaments 
of  the  spleen  so  feebly  developed  as  to  permit  a  marked  displacement. 

DIAGNOSIS 

In  the  diagnosis,  a  differentiation  must  be  made  between  wandering 
spleen  and  the  far  more  frequent  floating  kidney.  The  spleen  frequently 
shows  upon  its  anterior  border  one  or  more  incisures  which  are  lacking 
in  the  kidney.  The  entire  configuration  of  the  spleen  is  different  from 
that  of  the  kidney.  It  must  be  remembered,  too,  that  the  right  kidney  is 
most  likely  to  be  displaced,  and  this  is  generally  detected,  although  not 
always,  upon  the  right  side  of  the  abdomen.  When  the  spleen  is  absent 
from  its  normal  area  on  percussion  the  diagnosis  is  certain,  but  this  is 
a  proof  naturally  very  difficult  to  obtain  in  the  obese  and  in  very  old 
persons.  The  kidneys  should  either  be  palpable  in  their  normal  position, 
or  their  absence  decided  upon.  In  conclusion,  they  may  be  confounded 
with  very  movable  ovarian  cysts  having  long  pedicles. 

SYMPTOMS 

Symptoms  of  wandering  spleen  may  be  entirely  absent;  occasionally 
there  are  pains  of  very  indefinite  nature.  The  turning  of  the  pedicle 
and  consequent  compression  of  the  splenic  vessels  may  cause  atrophy  or 
even  gangrene  in  the  surroundings  of  the  organ  or  in  the  stomach.  In 
one  case  the  spleen  steadily  decreases  in  size,  the  disturbances  gradually 
disappear,  and  recovery  takes  place;  in  another,  peritoneal  processes  may 
develop.  But  these  are  probably  great  rarities,  always  current  in  medical 
literature.^ 

TREATMENT 

In  the  treatment,  the  employment  of  an  abdominal  bandage  must 
first  be  considered;  then,  by  the  administration  of  arsenic,  quinin,  and 
iodin,  we  must  attempt  to  decrease  the  size  of  the  spleen;  finally,  the 
nervous  symptoms  should  be  combated  by  hydrotherapy. 

Among  surgical  measures,  fixation  of  the'  spleen,  splenopexy,  which 
was  first  proposed  by  Kydygier  ^   is  prominent.     Litten  ^   quite  properly 


'  It  is  quite  remarkable  how  few  reports  there  are  in  the  literature  of  the  last 
few  decades  regarding  wandering  spleen,  which  is  a  proof  of  the  rarity  of  the  aflfec- 
tion,  for  the  obverse  conclusion  that  everything  relating  to  this  condition  has  been 
ascertained,  and  that,  therefore,  further  reports  would  be  superfluous,  is  unjustifiable. 

^Rydygier,  Verhandl.  der  deutschen  Gesellschaft  f.   Chirurgie,  Berlin,   1895. 

» Litten,  "  Die  Krankheiten  der  Milz,"  Wien,  1898,  p.  37. 


294     DISPLACEMENTS  OF  THE  ABDOMINAL  VISCERA  AND   HEART 

raises  to  this  the  objection  that  permanent  fastening  of  an  organ  which 
to  so  great  an  extent  takes  part  in  the  respiratory  excursus  of  the  dia- 
phragm can  hardly  be  expected.  When  the  spleen  is  decidedly  enlarged, 
however,  its  total  removal  may  be  considered.  It  is  self-evident  that  this 
is  by  no  means  a  simple  operation  ^  and  that  it  should  never  be  advised 
when  nervous  symptoms  only  are  present. 


DISPLACEMENT    OF   THE    COLON    (COLOPTOSIS) 

In  1853  Virchow  -  called  attention  to  the  fact  that  displacement  of 
the  colon  was  of  frequent  occurrence,  and  attributed  this  to  local  chronic 
peritonitis  and  to  acute,  infectious,  intestinal  diseases,  especially  dysen- 
tery. Displacement  of  the  colon  is  due  to  the  same  causes  as  general 
splaiit'hnojjtosis,  to  a  weakness  of  the  ligamentous  apparatus  and  a  de- 
cidedly ])en(lulous  abdomen.  The  greatest  deviation  in  course  is  shown 
l)y  the  transverse  colon,  particularly  by  the  right  flexure,  which  occasion- 
ally forms  a  sharp  angle  whose  vertex  is  situated  below  the  umbilicus, 
the  entire  large  intestine  resembling  in  shape  the  letter  M.  Under  these 
circumstances,  particularly  in  aged  persons,  portions  of  the  intestine 
jiacked  with  feces  are  felt  in  the  right  iliac  fossa,  a  finding  which  led 
me  to  regard  perityphlitis  as  the  consequence  of  fecal  stasis,  whereas  we 
iKnv  know  with  certainty  that  the  feces  above  the  ileo-cecal  valve  are  still 
fluid  in  composition,  the  solidification  chiefiy  taking  place  in  the  trans- 
verse colon. 

Displacement  of  the  colon  may  be  proven  by  inflation  from  the  rectum. 
Such  a  process,  however,  is  usually  superfluous,  because  valueless  in  treat- 
ment. For  although  displacement  of  the  colon  may  hinder  the  propulsion 
f)f  the  intestinal  contents,  as  has  been  stated,  an  obstruction  in  the  intes- 
tinal canal  is  easily  compensated  for  by  a  greater  activity  producing  hyper- 
tro])liy  of  the  smooth  musculature  of  the  intestine.  The  causes  of  consti- 
]iati(in  may  be  readily  found  in  weakness  of  the  abdominal  muscles,  in 
the  composition  of  the  food  which  leaves  too  little  residue,  and  often  also  in 
irastrie  disturbances.  Nervous  symptoms  may  usually  be  attributed  to  a 
•rencral  splanchnoptosis  and  to  neurasthenia  rather  than  to  coloptosis.' 

The  most  effective  treatment  in  displacement  of  the  colon  as  well  as 
any  other  ])art  of  the  intestines  consists  in  the  application  of  a  well-fitting 
ahdoniinal  l)inder,  and  the  regulation  of  the  diet  and  the  entire  mode  of 
life,  in  the  manner  already  described. 

Just  as  in  gastroptosis.  Bier  attempted  the  surgical  treatment  of  colop- 

'^  Com  pare  Tvlpius,  Beitrdge  zur  klin.  Chirurgie,  XI,  1894;  Kirchhoff,  Therapeut. 
Moniitsh..   1898. 

2  Virchoir's  Archiv,  V,  1853. 

3  Blocker,  Zeitschr.  f.  Chirurgie,  LVI. 


DISPLACEMENT   OF  THE   HEART 


295 


tosis.  In  a  patient  who  suffered  from  constipation  accompanied  by  pain 
in  the  left  side  of  the  abdomen,  the  mesocolon  of  the  transverse  colon, 
which  was  extremely  tortuous,  was  straightened  by  silk  sutures. 

From  the  description  just  given,  which  shows  that  the  symptoms  de- 
pend only  in  small  part  upon  displacement  of  the  colon,  it  is  evident  that 
such  surgical  treatment  is  not  advisable. 


DISPLACEMENT   OF   THE   HEART— WANDERING    HEART 
COR   MOBILE  1 

Under  physiologic  conditions  the  heart  is  held  in  position  by  the  aorta 
and  the  pulmonary  artery  which  are  firmly  adherent  to  the  pericardium, 
and  also  by  its  attachment  to  the  diaphragm  in  the  thorax;  it  is  still 
further  supported  by  the  large 
veins  which  empty  into  the 
heart.  As  is  shown  by  the  illus- 
tration (Fig.  18),  taken  from 
Determann's  ^  work,  the  heart 
is  attached  at  such  points  on 
its  right  and  upper  side  as 
will  permit  to  the  apex  of  the 
heart  the  greatest  possible 
movability  in  conformity  with 
the  movements  of  the  thorax, 
and  this  position  is  most  dis- 
tinctly revealed  by  the  apex 
beat.  As  is  the  case  with  the 
abdominal  organs,  the  heart 
is  also  maintained  in  position  by  the  pressure  of  the  adjacent  organs. 
Thus  the  lungs  completely  surround  the  heart  and  exert  pressure  which, 
in  the  case  of  pleural  effusion  or  any  other  process  which  decreases  the 
space  in  the  thorax,  may  increase  to  such  an  extent  as  to  force  the  heart 
away  from  its  normal  position.  The  heart  is  also  held  in  place  by  its 
attachment  to  the  diaphragm,  and  particularly  to  the  central  tendon,  by 
means  of  which  every  variation  in  pressure  within  the  abdominal  cavity 
is  transmitted  to  the  heart  (see  Fig.  19,  taken  from  C.  Toldt's  =*  Anatom- 
ical Atlas). 


-Pericardium    with    vessels. 
Henke.) 


(After 


1  The  term  employed  by  some  authors,  cardioptosis,  does  not  appear  to  me  to  be 
happily  chosen,  in  which  opinion  A.  Hoffmann  coincides,  since  it  is  too  suggestive  of 
a  low  position  of  the  cardia,  therefore  of  a  portion  of  the  stomach. 

^  Determann,  Deutsche  med.  Wochenschr.,  1900,  Nr.  5;  compare  also  the  discus- 
sion following  this. 

3  C.  Toldt,  Anatom.  Atlas,  III,  Aufl.,  IV,  Liefer.,  p.  482,  Berlin  und  Wien.,  1903. 


296     DISPLACEMENTS  OF  THE  ABDOMINAL   VISCERA  AND   HEART 

To  a  certain  degree  every  heart  is  movable;  this  has  been  known  to 
clinicians  ever  since  the  introduction  of  percussion.  It  has  also  been 
known  tliat  the  heart  could  be  displaced  1  or  2  cm.  to  the  left,  and,  to  a 
somewhat  slighter  extent,  also  to  the  right.  But  the  investigations  of 
Kumpff,  Determann,  A.  Hoffmann,  Cherchewski,i  L.  Braun,  Leusser  and 
others  liave  given  us  more  accurate  information.  Determann,  in  particu- 
lar, deserves  great  credit  for  having  widened  our  knowledge  of  this  process 
hv  a  large  number  of  researches,  in  which  the  results  of  percussion  were 
subjected  to  a  subsequent  test  by  X-rays.  These  results,  later  confirmed 
by  other  investigations,  are  as  follows: 

In  a  normal  person  in  the  left  lateral  position  displacement  of  the 
heart  takes  place,  upon  the  average  2  to  3  cm.  to  the  left,  and  in  the 
right  lateral  position  about  1  cm.  A  displacement  is  rarely  absent,  but 
occasionally  it  may  be  very  slight.  In  some  healthy  persons,  however,  this 
displacement  is  decided,  and  amounts  to  6  cm.  to  the  left  and  4  cm.  to 
the  right.  Generally,  these  extreme  degrees  of  displacement  are  found 
in  middle-aged  persons  who  are  poorly  nourished  and  have  a  weak  mus- 
cular system,  in  whom,  therefore,  an  abnormally  great  displacement  of 
the  abdominal  organs  is  also  most  frequently  found.  This  coincides  with 
the  opinion  that  in  women  the  heart  is  generally  much  more  movable 
than  in  Tuen.  In  the  newborn,  cardiac  displacement  is  almost  unknown, 
and  in  children  it  is  very  slight.  A  deviation  from  the  normal  state  of 
the  abdominal  viscera  is  found  when,  in  the  aged,  the  movability  of  the 
heart  does  not  increase  but  decreases,  probably  because,  by  augmentation 
of  the  emphysema,  the  pressure  exerted  by  the  lungs  upon  the  heart  be- 
comes greater.  But  the  pressure  from  the  abdominal  cavity  influences  the 
movability  of  the  heart  still  more  than  pressure  from  the  lungs.  During 
pregnancy  the  heart  is  forced  upward,  and  rests  upon  the  diaphragm  in 
such  a  way  that  hypertrophy  is  simulated;  yet  the  heart  is  but  slightly 
movaljle.  Soon  after  labor,  however,  the  highest  grades  of  cardiac  displace- 
ment may  be  noted,  as  a  rule,  to  the  left  and  upward,  so  that  the  apex 
l)eat  appears  near  the  axillary  cavity.  A  similar  influence  is  exerted  by 
all  other  ])rocesses  in  the  abdomen,  such  as  ascites,  meteorism,  by  a  pendu- 
lous belly,  or  enteroptosis. 

Emaciation,  as  a  rule,  intensifies  the  movalbility.  In  the  first  place, 
the  layers  of  fat  normally  surrounding  the  heart  and  which  reach  their 
greatest  development  (Gerhardt)   in  the  obese  occasionally  disappear;  the 

^  Chercheicski,  Gaz.  med.  de  Paris,  1887,  No.  53;  Rumpff,  Verhandl.  d.  VI.  Con- 
firrsscs  f.  innere  Med.,  1888;  Deutsche  med.  Wochenschr.,  1902,  Nr.  31,  und  1903, 
Xr.  3:  .1.  Hoffmann,  also,  1900,  Nr.  19;  L.  Braun,  "  Ueber  Herzbewegung  und  Herz- 
stoss,"  Jena,  1898  u.  Centralbl.  f.  innere  Med.,  1902,  Nr.  35;  Leusser,  Miinchener 
med.  Wochrnschrift,  1902,  Nr.  26;  Pick,  Wiener  klin.  Wochenschr.,  1889,  p.  747; 
.1.  Schmidt,  Deutsche  med.  Wochenschr.,  1901,  Nr.  16.  I  have  also  made  investiga- 
tions in  a  small  number  of  cases. 


Venous  angle 


Trachea 
Innominate  nrterj- 


Internal  jugular  vein 


Arch  of  the  aorta 


Subclavian  vein 


Coracoid  process 


Superior  medias- 
tinal or  cardiac 
1 y  m  ph  a  t  i  c 
glands 

Ascending  aorta 


Superior  vena 
cava 

Semilunar  or  sig- 
moid valves  of 
the  aorta 

Mitral  or  bicus- 
pid valve 

Right  lung 

Orifice  of  the 
coronary  sinus 


Eustachian  valve 


Branches  of  the 
hepatic  veins 

Phrenocostal  or 
diaphragmatico- 
costal  supple- 
mental   pleural 


Branches  of  the 
portal  vein  with 
Glisson's  cap- 
sule 


GaU-bladder 


Hepatic    flexure 
of  the  colon 


"~"  Clavicle 


.—  Body  or  shaft 
of  the  first  rib 

— '  Mediastinal 
pleura 

— ■•'  Costal  pleura 


Left  lung 

Pulmonary 
artery 

•Pericardial 
cavity 

Pericardium 

W  XiU Pleural  cavity 

_ILti<_»  »  luett  ventricle 

Apex  of  the 
heart 

[mm Diaphragm 

II... 
'lira Left  lobe  of  the 

liver 

Body  or  shaft 
of  the  seventh 
rib 

Spleen  (inferior 
extremity) 

Body  of   the 
stomach 


Transverse 
colon 


Pyloric  portion  of  the  stomach 


Duodenum  Pylorus 

(superior  portion  or  first  part) 


Fig.   19. — Frontal  section  through  the  trunk. 


298     DISPLACEMENTS   OF  THE  ABDOMINAL  VISCERA  AND  HEART 

abdominal  fat  is  largely  decreased  also  in  hyponutrition.  This,  therefore, 
favors  a  loosening  of  the  viscera  from  their  attachments,  a  downward 
displacoinent  of  the  diaphragm,  and,  thereby,  leads  to  a  decrease  of  pres- 
sure in  tiie  thorax. 

IMovability  of  the  abdominal  organs  and  of  the  heart  is  also  observed 
in  eldorosis,  Hoffmann  considers  this  the  explanation  of  the  passive 
dilatation  after  exertion  so  frequently  reported  by  some  investigators 
(])r()bal)ly  from  erroneous  observations),  but  he  is  probably  incorrect.  For 
as  we  know  that  the  chlorotic  has  a  flaccid  muscular  system,  and  that 
under  these  circumstances  a  displaced  stomach  readily  dilates,  so  the  same 
may  be  assumed  of  the  heart.  In  this  case  we  would  have  a  complication 
of  abnormal  displacement  and  dilatation. 

We  have  little  definite  knowledge  of  the  pathologic  processes  which 
are  influenced  by  the  amount  of  space  in  the  thorax  and  abdominal  cavity. 
Some  clinicians  (Curschmann,  Braun,  and  Cherchewski)  maintain,  from 
their  exj)erience,  that  arterio-sclerosis  particularly  involving  the  aorta  in- 
creases movability,  while  Determann  was  unable  to  confirm  this. 

It  is  easily  understood  that  just  as  a  neoplasm  burdens  the  stomach, 
or  livdroneplirosis  produces  a  tendency  to  displacement,  so  the  same 
conditions  arise  in  a  hypertrophied  heart.  An  enlargement  of  the  left 
ventricle  may  become  so  extensive  that  dilatation  of  the  right  ventricle 
escapes  observation  (Frankel).  IndividuLl  influences  play  a  great  role, 
and  often  a  hypertrophied  heart  shows  no  displacement. 

As  a  rule,  displacement  is  readily  proven  by  palpation  and  percussion. 

SYMPTOMS 

As  to  the  symptoms,  there  is  no  unanimity  among  clinicians.  Some, 
such  as  Rumpff  and  Leusser,  incline  to  the  view  that  certain  symptoms 
distinctly  indicate  cardiac  displacement,  wandering  heart.  Persons  with 
marked  displaeenient  of  the  heart  cannot  sleep  for  any  length  of  time 
upon  the  left  side  without  distress  arising.  Symptoms  become  noticeable, 
such  as  ])alpitation,  oppression,  difficulty  in  respiration,  attacks  of  syncope, 
fear,  irrcffularity  of  the  pulse,  etc.  Other  clinicians,  such  as  Braun  and 
K'omlierir.  deny  this,  and  quite  properly  emphasize  that  many  persons  have 
a  ^neater  or  less  displacement  of  the  heart  without  any  symptoms.  More- 
over, tlie  persons  who  usually  suffer  from  wandering  heart  are  exceedingly 
nervous,  and  often  complications  are  present,  such  as  alcoholism,  cardiac 
Msthenia.  etc.,  to  which  the  symptoms  are  attributed;  this  makes  an  opinion 
exceedingly  difficult. 

In  tlie  main,  I  agree  vdth  the  latter  view,  and  in  this  connection  I 
wish  to  reiterate  what  I  have  said  regarding  floating  kidney.  A  healthy 
person  will  usually  feel  no  discomfort  from  the  displacement  of  a  kidney 
or  of  tlie  heart,  although  it  cannot  be  denied  that  displacement  of  these 


DISPLACEMENT   OF  THE   HEART  299 

organs,  when  made  known  to  him,  and  particularly  at  the  onset,  may 
give  rise  to  symptoms.  The  rarity  of  cardiac  symptoms  in  healthy  women 
after  labor,  during  which  the  heart  is  especially  prone  to  be  displaced, 
favors  this  view.  Moreover,  I  recently  saw  a  marked  displacement  of  the 
heart  during  an  obesity  cure,  while,  simultaneously,  the  symptoms  refer- 
able to  it  disappeared.  The  case  was  that  of  a  woman,  aged  32,  having 
a  height  of  1.7  meters,  and  weighing  98  kilograms;  the  obesity  had 
particularly  increased  during  the  last  few  years.  The  heart  at  first  re- 
vealed normal  dulness,  the  pulse  ^during  rest  in  the  sitting  posture  was 
from  80  to  88,  but  upon  the  slightest  exertion  it  rose  to  130,  and  at  the 
same  time  decided  dyspnea  appeared.  Questioning  elicited  the  report  that, 
for  many  years,  the  patient  had  slept  only  upon  her  back  or  in  the  right 
lateral  position.  I  instituted  a  moderate  hyponutrition,  and  assured  the 
lady  that  after  the  loss  of  16^  to  22  pounds  she  would  be  able  to  sleep  upon 
the  left  side.  When,  after  six  weeks,  she  had  lost  20  pounds,  quite  a 
decided  displacement  of  the  heart  to  the  left  could  be  determined,  about 
4  to  5  cm.,  which  had  not  previously  been  noticeable.  Of  course,  I  did 
not  tell  her  this.  General  bodily  activity,  as  well  as  that  of  the  heart, 
had  increased,  the  pulse  during  rest  did  not  exceed  80,  and  even  upon 
exertion  dyspnea  did  not  so  rapidly  appear.  Above  all,  the  lady  assured 
me  that  she  could  now  sleep  the  entire  night  upon  her  left  side  without 
any  inconvenience. 

Here,  therefore,  the  antifat  cure  produced  such  an  improvement  in  the 
circulation  that  possible  abnormal  sensations  due  to  displacement  of  the 
heart  were  unnoticed  by  the  patient. 

In  this  respect  erroneous  opinions  may  easily  be  formed  because  under- 
nutrition is  not  well  borne  by  nervous  patients.  In  men  who  work  under 
mental  strain,  and  in  women  who  have  many  household  cares,  it  is  apt 
to  produce  nervous  disturbances,  while,  after  they  are  relieved  from  their 
burdens  and  pressing  duties,  and  are  sent  away  to  a  pleasant  environment, 
most  of  them  bear  a  loss  in  weight  of  from  11  to  16|  pounds  without  the 
consequent  displacement  of  the  heart  having  any  unpleasant  effect. 

Upon  the  basis  of  these  views,  the  removal  of  the  symptoms  of  wander- 
ing heart  by  plentiful  nutrition  might  be  supposed  the  correct  treatment. 
But,  generally  speaking,  this  is  not  the  case.  We  must  not  forget  that 
in  some  persons  blood  formation  is  immoderately  increased  by  plentiful 
nutrition,  and  thus  higher  blood  pressure  arises.  We  do  not  know  under 
what  circumstances  cardiac  hypertrophy  occurs,  but  it  must  all  the  more 
be  reckoned  with  since  the  development  of  this  affection  usually  escapes 
observation.  It  is  quite  likely  that  disturbances  regarded  as  "  cardiac 
neuroses  "  mark  its  onset,  usually  designated  cardiac  hypertrophy  follow- 
ing "  luxury  consumption."  In  practice,  even  after  minute  investigation 
of  the  heart,  we  may  sometimes  doubt  whether  certain  symptoms  are  due 
to  an  increased  displacement  or  to   a  beginning  hypertrophy.      Only   in 


300     DISPLACEMENTS  OF  THE  ABDOMINAL   VISCERA   AND   HEART 

tliin,  debilitated  individuals  does  hypernutrition  appear  to  be  justified. 
Tbo  efforts  of  the  physician  must  be  chiefly  directed  to  combating  the 
nervous  symptoms  by  means  of  rest,  a  proper  regulation  of  the  muscular 
activity,  plentiful  amounts  of  fresh  air,  and,  perhaps,  also  the  employment 
of  hydrotherapeutic  measures.  In  some  cases  the  binder  advised  by  Abee 
in  Xauheim,  a  so-called  heart  brace  or  heart  bandage,  may  be  advised. 
The  chief  value  of  the  apparatus  is,  however,  merely  suggestive;  at  all 
events,  unlike  the  advantage  from  the  employment  of  the  binder  in  dis- 
placement of  the  abdominal  organs,  it  js  impossible  to  explain  by  purely 
meclianical  laws  the  benefits  from  its  use. 


DISEASES  OF  THE   PANCREAS 


elf   '^i'   OtTlfUl^A' 


SYMPTOMATOLOGY    OF    THE    DISEASES    OF 
THE    PANCREAS 

By  L.  OSER,  Vienna 

HISTORY 

Although  physiology  and  experimental  pathology  were  busy  in  the 
last  third  of  the  preceding  century  with  a  study  of  the  pancreas  which 
has  led  to  a  better  understanding  of  the  various  vital  functions  of  this 
organ,  practical  medicine  has  utilized  this  knowledge  to  but  very  slight 
extent. 

Hospitals  and  medical  colleges,  especially  the  departments  of  surgery, 
have  devoted  increasing  attention  to  the  pancreas  within  the  last  few  years, 
and  it  has  come  to  pass  that,  in  making  a  diagno^s  of  digestive  disturb- 
ances from  certain  alterations  of  metabolism,  the  pancreas  also  has  been 
considered,  yet  in  the  popular  current  of  professional  life,  diseases  of  the 
pancreas  have  been  almost  ignored. 

Regrettable  as  this  apparent  apathy  is,  its  cause  is  easily  understood 
when  sought  for.  Chief  among  the  reasons  is  the  fact  that,  until  recently, 
this  indifference  was  manifest  also  in  the  schools,  in  the  clinics,  and  in  the 
laboratories.  Even  to-day,  adequate  attention  is  not  devoted  to  the  pan- 
creas, as  is  evident  when  we  consider  the  manifold  and  complicated  ques- 
tions brought  up  for  consideration,  questions  which  often  relate  to  ele- 
mentary but  most  significant  processes.  Even  pathologic  anatomy  has 
added  little  to  our  knowledge  of  the  pancreas;  at  autopsies,  the  pancreas 
frequently  is  not  considered  at  all,  or  but  superficially  investigated,  and 
a  cursory  examination  of  this  organ  is  usually  without  value.  It  is  true 
the  difficulties  are  great.  An  apparently  normal  pancreas  will,  upon 
careful  microscopic  investigation,  frequently  show  changes  which  are  ex- 
ceedingly difficult  to  interpret  correctly  for  the  reason  that  the  organ, 
during  the  death  agony  and,  perhaps,  also  for  some  time  after  death, 
undergoes  change  from  continued  self-digestion,  and  this  may  very  readily 
be  mistaken  for  a  pathologic  alteration  which  had  occurred  during  life. 

In  the  last  few  years  a  decided  change  for  the  better  has  taken  place, 
as  is  shown  by  the  increasingly  rich  literature.  Since  the  important  re- 
searches of  V.  Mering  and  Minkowski,  which  point  with  certainty  to  the 
connection  between  diabetes  and  the  pancreas,  an  active  interest  in  this 
21  303 


304  DISEASES  OF  THE  PANCREAS 

organ  has  been  awakened  and,  owing  to  the  victorious  advance  of  surgery, 
following  the  initiative  of  Gussenbauer,  the  pancreas  has  become  the 
border-land  between  internal  medicine  and  surgery,  and  incontrovertible 
proof  has  been  furnished  of  the  great  practical  importance  of  this  organ. 

The  pancreas  to-day,  on  account  of  individual  causative  observations, 
is  not  only  the  subject  of  discussion  in  inaugural  dissertations,  but  promi- 
nent exponents  of  theoretical  and  practical  medicine  in  different  countries 
have  devoted  their  best  endeavors  to  the  development  of  a  positive  founda- 
tion for  the  study  of  diseases  of  the  pancreas.  Naturally  we  are  still  far 
from  the  goal — but  a  few  important  facts  have  been  ascertained,  which  are 
not  only  interesting  to  the  practical  physician,  but  the  knowledge  of  these 
he  cannot  and  dare  not  ignore  in  his  professional  work.  This  is  our 
justification  for  calling  close  attention  to  the  present  status  of  clinical 
knowledge  concerning  diseases  of  the  pancreas. 

This  article  will  be  devoted  to  a  description  of  the  symptoms  by  which 
we  are  enabled  to  make  a  diagnosis  of  disease  of  the  pancreas. 

ANATOMY  AND    PHYSIOLOGY 

Before  entering  upon  my  actual  theme,  I  desire  to  emphasize  a  few 
points  in  the  anatomy  ^and  physiology  of  the  pancreas  which  have  a  direct 
bearing  on  our  subject.  First  in  importance,  the  gland,  as  a  rule,  has 
two  duds,  a  fact  which  is  not  always  borne  in  mind,  even  by  physiologists, 
since  in  the  animal  usually  experimented  upon — the  dog — two  ducts  are 
invariably  present.  The  tying  of  one  duct,  or  the  introduction  of  a  can- 
nula into  one  duct,  may  lead  to  error.  In  the  dog — as  recently  reported 
by  Helly — these  ducts  are  always  distinctly  separated,  which  in  man  is 
the  exception.  Helly,  under  the  direction  of  Zuckerkandl,  has  recently 
studied  this  subject  thoroughly.  He  examined  50  cases,  and  among  these 
he  only  once  found  the  ductus  Santorini  and  no  ductus  Wirsungianus ;  in 
all  of  the  other  cases  he  found  the  ductus  Santorini  connected  with  the 
ductus  Wirsungianus,  or  the  duct  existed  alone,  the  latter  condition  being 
much  the  rarer.  Of  the  50  cases,  Santorini's  duct  had  free  passage  into 
the  intestine  in  40  cases,  and  was  obliterated  in  10. 

The  relations  between  the  pancreas  and  the  ductus  choledochus  are  of 
the  utmost  practical  importance;  the  latter  enters  a  groove  upon  the  side 
of  the  gland,  bends  toward  the  duodenum,  and,  as  Zuckerkandl  reports, 
embeds  itself,  but  soon  terminates  in  a  canal.  Helly,  in  his  investigation 
of  70  cases,  confirmed  these  reports  of  Zuckerkandl.  He  found  that  the 
terminal  portion  of  the  ductus  choledochus  is  always  closely  connected 
with  the  head  of  the  pancreas  to  the  extent  of  from  2  to  7  cm. 

Pawlow  made  some  interesting  experiments  in  regard  to  innervation. 
According  to  this  author,  the  vagus  is  the  secretory  nerve  of  the  pancreas, 
l)ut  tliis  nerve  also  carries  fibers  which  have  an  inhibitive  secretory  func- 


ANATOMY  AND  PHYSIOLOGY  305 

tion;  in  the  sympathetic  Pawlow  also  determines  secretory  and  vaso- 
constrictory  fibers.  More  recent  investigations  by  Wertheimer  and  Lepage 
have  demonstrated  that,  after  the  severing  of  all  nerve  centers,  secretion 
does  not  cease ;  that,  therefore,  there  must  also  be  an  automatic  nerve  appa- 
ratus present  in  the  gland.  These  investigations  permit  us  to  conclude 
with  certainty  that  in  pathologic  cases  disturbances  in  secretion  may  also 
be  caused  by  disturbances  of  innervation. 

The  incessant  labors  of  physiologists  in  the  last  few  decades  have  fre- 
quently demonstrated  the  great  importance  of  the  physiological  functions 
of  the  pancreas.  Undoubtedly  the  pancreas  is  one  of  the  most  important 
organs  of  the  body;  in  digestion  and  in  metabolism  perhaps  the  most 
important.  The  pancreatic  juice  is  the  only  glandular  secretion  which  is 
capable  of  converting  all  substances  that  can  be  at  all  digested  into  that 
form  which  is  necessary  for  their  complete  utilization  as  food.  It  is 
more  active  than  any  other  ferment  (trypsin)  in  the  splitting  of  the 
albumin  bodies;  it  emulsifies  and  splits  the  fats  so  that  they  are  capable 
of  absorption  (steapsin) ;  it  transforms  the  carbohydrates  into  sugar  (pan- 
creatic diastase)  and  also  possesses  a  milk-coagulating  ferment.  The  secre- 
tions of  the  other  digestive  glands  also  possess  these  properties,  but  they 
are  not  combined  in  the  secretion  of  any  single  organ.  The  specific  property 
of  the  pancreas,  which  belongs  to  it  alone,  is  the  splitting  up  of  fat.  In 
the  intestine,  it  is  true,  a  certain  degree  of  fat-splitting  is  possible,  but  only 
by  bacteria.  The  enormous  importance  of  the  pancreatic  juice  in  digestion 
has  been  decisively  proven  by  animal  experiments,  to  which  we  shall  later 
revert.  But  its  digestive  function  is,  however,  not  the  only  activity  of 
the  gland.  It  also  performs  an  important  part  in  the  human  economy 
by  the  transformation  and  preparation  of  sugar.  We  attribute  this  func- 
tion to  the  internal  secretion,  the  conclusive,  experimental  proofs  of  which 
we  shall  later  discuss  minutely. 

This  sketch  indicates  the  great  importance  of  the  pancreas  in  the  human 
economy.  Disease  of  this  organ  must,  naturally,  produce  severe  disturb- 
ances, and  we  might  suppose  that,  in  consequence,  such  marked  symptoms 
would  appear  that  the  recognition  of  a  disturbance  in  function  would 
present  no  difficulty,  but  the  contrary  is  the  case.  How  can  this  fact 
be  explained?  The  most  significant  reason  is  this — that  only  very  ex- 
tensive or  complete  destruction  of  the  organ  and  the  occlusion  of  both 
ducts  will  cause  characteristic  symptoms.  In  partial  disease,  or  the  occlu- 
sion of  ojie  duct,  as  we  shall  see,  the  internal  as  well  as  the  digestive 
function  may  remain  intact,  and  the  normal  remainder  of  the  gland, 
although  with  only  one  duct,  and  perhaps  vicariously,  may  compensate 
for  the  functions  of  the  neighboring  organs.  Total  or  very  extensive  dis- 
ease is  certainly  much  rarer  than  partial,  and  the  latter  usually  gives  rise 
only  to  doubtful  symptoms  which  are  but  uncertain  points  of  support  for 


306  DISEASES  OF  THE  PANCREAS 

its  recognition.  The  symptoms  are  interesting,  because,  as  a  rule,  it  is 
not  only  the  pancreas  that  is  diseased,  but  a  simultaneous  disease  of  the 
noiiThboring  organs  may  be  the  cause,  or  consequence,  of  disease  of  the 
l)ancreas,  and  its  physical  signs  be  much  more  distinctly  and  obviously 
a]iparent  than  those  of  the  diseased  pancreas.  If,  for  example,  chronic 
jiancreatitis  develops  in  the  course  of  gall-stone  disease,  cholelithiasis  forms 
the  most  prominent  symptom,  and  the  signs  of  disease  of  the  pancreas 
may  be  completely  disguised. 

I'he  symptoms  of  absence   of  function,  therefore,  are  of  paramount 
importance  in  diagnosis,  and  to  these  we  shall  devote  our  attention. 


SYMPTOMS 

First  among  these  are  diabetes  and  alimentary  glycosuria. 

Autopsy  findings  long  ago  directed  attention  to  the  relation  between 
I  he  ])aiK'reas  and  diabetes.  The  oldest,  most  reliable  report  was  in  1788 
1)V  Cowlcv,  wlio,  in  a  diabetic,  foimd  numerous  calculi  in  the  substance 
of  the  pancreas.  Chopart  later  made  a  similar  observation.  Bright,  in 
l.S,S3,  saw,  in  a  diabetic,  aged  19,  a  hard,  nodular  tumor  at  the  head  of 
the  pancreas  wliile  the  gland  itself  was  atrophic.  Since  that  time,  similar 
cases  have  been  frequently  mentioned  in  literature. 

Tlie  frequent  coincidence  of  diabetes  and  disease  of  the  pancreas  caused 
Frerichs,  Seegen,  and  Friedreich  to  assume  a  causal  connection  between  the 
clinical  and  anatomical  findings;  but  it  was  still  questionable  whether 
disease  of  the  pancreas  was  the  cause  or  the  consequence  of  diabetes. 
Froncli  authors — above  all,  Bouchardat — took  a  more  decided  stand;  they 
])roi)(is('d  a  clinical  type,  diabete  maigre,  and  looked  for  its  foundation  in 
a  disease  of  the  pancreas.  This  assumption  was  enticing,  and  was  also 
frequently  confirmed  by  conclusive  reports  of  cases;  nevertheless,  it  re- 
mained but  a  hypothesis  until  by  animal  experiment  v.  Mering  and  Min- 
kowski finally  furnished  the  incontestable  proof  that  by  removing  or  de- 
stroying the  pancreas  in  a  dog  severe  diabetes  occurred.  A  radical  change 
in  opinion  was  the  result,  and  it  is  now  believed  beyond  all  doubt  that 
(lial)etes  in  man  is  caused  by  disease  of  the  pancreas.  The  results  obtained 
by  those  authors  were  soon  confirmed  by  many  others,  and  in  an  entire 
scries  of  animals  diabetes  was  produced  by  extirpating  the  pancreas.  But 
diabetes  occurred  only  by  removal  of  the  entire  gland,  or,  at  least,  of  its 
(jrcater  portion;  partial  extirpation  gave  varying  results.  If  one-fifth  to 
one- fourth  of  the  gland  were  allowed  to  remain,  v.  Mering  and  Minkowski 
frequently  found  no  glycosuria.  But  severe  diabetes  might  also  be  pro- 
duced. This  depended  particularly  upon  the  composition  of  the  portion 
of  tlic  gland  remaining.  If  this  was  subsequently  destroyed  by  consecu- 
tive inflammation  or  atrophy,  diabetes  developed;  cases  of  diabetes  of 
medium  severity,  or  only  a  transitory  or  more  or  less  permanent  alimentary 


I 


SYMPTOMS  307 

glycosuria  arose;  or,  as  already  mentioned,  in  the  great  majority  of  cases 
no  form  of  sugar  excretion  took  place.  Sandmeyer  found,  in  a  patient 
in  whom  severe  diabetes  developed  13^  months  after  partial  extirpation 
of  the  pancreas,  that  diabetes  persisted  for  eight  months  and  until  death 
occurred.  In  the  experiments  in  partial  extirpation  conducted  by  Katz 
and  myself,  it  was  impossible  to  produce  severe  diabetes,  but  only  transU 
tory  and  alimentary  glycosuria;  in  some  cases,  sugar  was  absent  from  the 
urine. 

Minkowski  definitely  proved  that  the  cause  of  diabetes  in  extirpation 
of  the  pancreas  could  be  found  neither  in  a  lesion  of  the  nerves  nor  in 
injuries,  and  that  it  could  not  be  attributed  to  the  absence  of  the  pan- 
creatic secretion. 

This  was  demonstrated  in  an  indisputable  manner  by  the  transplanta- 
tion of  portions  of  the  pancreas  under  the  abdominal  skin,  first  by  Min- 
kowski and  later  by  Hedon,  A  portion  of  the  pancreas  may  be  detached 
and,  without  injuring  the  vessels  which  supply  it,  may  be  transplanted 
under  the  skin  of  the  abdomen.  If  the  portion  remaining  in  the  abdominal 
cavity  is  removed,  no  glycosuria  occurs,  not  even  the  alimentary  form ;  if 
the  section  underneath  the  abdominal  skin  is  subsequently  removed,  severe 
diabetes  is  produced.  If  the  transplanted  portion  is  badly  nourished,  mild 
diabetes  may  occur.  If  complete  atrophy  takes  place  in  the  grafted  por- 
tion, severe  diabetes  develops.  The  mere  tying  of  the  ducts  never  leads 
to  diabetes,  except  when  such  a  change  due  to  these  processes  subsequently 
occurs  in  the  glandular  substance  that  it  is  completely  destroyed. 

It  is  absolutely  true  that  removal  of  the  pancreas  in  quite  a  number  of 
animals  has  produced  diabetes.  Besides  its  digestive  function,  the  pan- 
creas unquestionably  has  another  which  is  related  to  sugar  metabolism. 
We  do  not  err  when  we  refer  this  function  tb  a  secretion  quite  distinct  from 
the  digestive  juice;  this  is  called  the  internal  secretion,  or,  following 
Hansemann,  the  positive  function.  In  what  manner  this  internal  secre- 
tion exerts  its  activity  is  still  doubtful.  Minkowski,  and  also  most  authors, 
assume  that  the  pancreas  in  the  preparation  of  sugar  also  generates  a  prod- 
uct which  acts  in  the  organs. 

A  series  of  hypotheses  have  been  proposed  in  explanation,  but  no  defi- 
nite proof  of  the  correctness  of  one  or  the  other  is  yet  at  hand. 

The  hypothesis  of  Lepine  is  most  interesting;  he  assumes  a  glycolitic 
ferment  which  is  normally  produced  in  the  pancreas.  This  glycolitic  fer- 
ment reaches  the  lymph,  thence  the  blood,  particularly  the  white  blood- 
corpuscles,  and  carries  on  the  preparation  of  sugar  in  the  tissues.  If  this 
ferment  is  absent,  hyperglycemia  and  diabetes  result.  Lepine  later  modi- 
fied this  hypothesis,  no  longer  referring  the  point  of  attack  of  the  glycolitic 
ferment  to  the  blood  but  to  the  tissues.  In  consequence,  as  Minkowski 
points  out,  the  assumption  of  such  a  ferment  is  no  longer  impossible, 
although  we  have  no  actual  proof. 


308  DISEASES  OF  THE  PANCREAS 

Other  hypotheses,  such  as  those  of  Chauveau  and  Kaufmann,  in  which 
an  increase  of  sugar  formation  in  the  liver  is  assumed  to  be  the  basis, 
and  also  the  views  of  the  brothers  Cavazzani  are  disproven  by  the  experi- 
ments of  Minkowski,  who  demonstrated  that  in  experimental  pancreatic 
diabetes  not  an  increase  of  the  sugar  production,  but  a  decrease  in  its 
consumption,  occurs.  We  only  know,  therefore,  that  the  pancreas  has  a 
function  wliicli  regulates  the  consumption  of  sugar,  but  we  do  not  know 
ilio  nature  of  this  function. 

An  attempt  has  lately  been  made  to  discover  the  region  in  which  this 
internal  secretion  is  found.  Langerhans  in  1869  described  structures  in 
tlie  pancreas  which  differ  from  the  pancreatic  tubules.  These  so-called 
intertubular  cell  clumps  are  also  found  in  man  and  in  various  animals, 
and  have  different  forms.  Recently  the  property  of  furnishing  the  internal 
secretion  has  l)een  ascribed  to  these  intertubular  cell  clumps.  Laguesse 
as  well  as  Diamare  some  years  ago  expressed  the  view  that  these  cell 
clumps  hear  some  relation  to  the  internal  secretion. 

Recently  Walter  Schulze  has  attempted  to  solve  this  question  experi- 
mentally. He  ligated  small  portions  of  the  pancreas  in  guinea  pigs,  and 
studied  the  changes  which  followed.  After  a  few  days  an  atrophic  process 
developed  in  the  glandular  elements  which  continually  increased — even 
after  80  days,  at  which  time  the  tubular  area  was  completely  atrophied, 
being  replaced  by  delicate  connective  tissue;  the  cell  clumps  had  taken 
no  part  in  this  atrophy,  but,  on  the  contrary,  showed  not  the  slightest 
change.  Schulze  concludes  from  this  that  these  cell  clumps  are  substantive 
structures  independent  of  the  glandular  system  of  the  pancreas.  It  is 
true  this  does  not  prove  that  they  have  any  bearing  on  sugar  metabolism. 
It  had  long  been  believed  that  these  structures  were  in  their  nature  different 
from  the  secreting  glandular  elements.  Langerhans  himself  regarded  them 
as  nervous  elements;  other  authors  have  looked  upon  them  as  lymphatic 
tissue.  Some  authorities  believe  them  to  be  embryonal  remains,  and  they 
have  also  been  considered  in  connection  with  the  secretion  of  the  diastatic 
ferment. 

Walter  Schulze's  experiments  are  evidently  of  importance,  but  the 
proof  that  these  structures  do  not  belong  to  the  glandular  system  and  are 
related  to  the  internal  secretion  must  be  furnished  by  further  investigation. 
Szobolew  recently  undertook  to  prove  by  chemical  and  microscopical  in- 
vestigations that  Langerhans's  cell  clumps  have  some  relation  to  sugar 
metabolism,  and  decided  this  to  be  a  fact.  In  two  cases  of  pancreatic  dia- 
Itetos  the  disappearance  of  these  cell  clumps  was  confirmed.  Opie  arrived 
at  the  same  conclusion;  in  11  cases  of  interlobular  pancreatitis  in  which 
foiiii  of  tlic  disease  Langerhans's  cell  clumps  are  visible  only  when  the 
jnoeess  is  very  far  advanced,  he  noted  mild  diabetes  only  once,  and  at  that 
in  a  cast^  in  which  the  sclerosis  had  also  attacked  Langerhans's  cell  clumps. 
In  three  cases  of  interacinous  pancreatitis  in  which  form  also  the  previ- 


SYMPTOMS  309 

ously  mentioned  cell  clumps  were  implicated,  diabetes  was  present  twice, 
and  in  the  fourth  case  of  diabetes  there  was  complete  hyaline  degeneration 
of  Langerhans's  islands. 

If  we  succeed  in  proving  positively  that  these  cell  clumps  are  con- 
cerned in  the  internal  secretion,  important  knowledge  as  to  the  true  cause 
of  pancreatic  diabetes  will  have  been  gained. 

The  demonstration  in  animals  of  an  experimental  pancreatic  diabetes 
enables  us  to  understand  much  more  fully  than  was  previously  possible 
the  numerous  autopsy  reports  in  literature  of  changes  in  the  pancreas  in 
the  diabetes  of  man.  All  doubts  disappear,  and  it  is  certain  that  in  a  large 
number  of  cases  disease  of  the  pancreas  was  the  cause  of  the  diabetes.  At 
the  necropsy  of  diabetics  various  changes  were  found  in  the  pancreas, 
most  frequently  atrophy,  but  often  also  induration,  calculi  formation, 
carcinoma  and  fatty  degeneration.  Doubtless,  some  of  these  changes  in 
the  pancreas  are  not  the  cause  of  diabetes;  in  many  cases  they  are  either 
its  consequences  or  are  in  no  way  related  to  it.  Atrophy  has  often  been 
demonstrated  to  be  the  cause  of  the  marasmus  which  occurs  in  diabetes. 
Hansemann  reports  a  characteristic  form  of  diabetic  atrophy  with  well 
developed  symptoms  of  an  active  process  added  to  the  process  of  the  secre- 
tory cells;  this  belongs  to  the  varieties  of  interstitial  inflammation,  similar 
to  that  in  certain  forms  of  granular  atrophy  of  the  kidneys.  Hansemann 
describes  early  stages  of  these  processes,  and  designates  them  as  anatomical 
individualities  which  must  necessarily  lead  to  diabetes. 

If,  in  many  cases  of  diabetes,  no  changes  are  found  in  the  pancreas, 
not  even  upon  minute  microscopic  examination,  this  is  additional  proof 
that  there  are  other  causes  of  diabetes  than  disease  of  the  pancreas — a 
view  now  generally  accepted.  Lanceraux  in  the  last  Congress  at  Paris 
maintained  the  unity  of  diabetes,  and  of  its  origin  in  disease  of  the  pan- 
creas. He  assumes  that  there  are  anatomical  determinable  changes  or 
functional  disturbances  of  the  pancreas  which  lead  to  diabetes.  Lan- 
ceraux formulates  a  hypothesis  against  which  weighty  objections  may  be 
raised,  and  which  cannot  be  sustained  at  this  present  time. 

A  vulnerable  point  in  the  theory  of  pancreatic  diabetes  in  man  is  the 
fact  that  total  destruction  of  the  pancreas  has  been  found  without  diabetes 
having  existed  during  life,  Hansemann's  hypothesis  does  not  sufficiently 
explain  the  fact  that  in  cases  of  total  destruction  of  the  pancreas  by 
diffuse  carcinoma,  carcinomatously  degenerated  cells  may  perhaps  "furnish 
the  internal  secretion  of  the  pancreas,  as  there  are  also  other  varieties  of 
total  destruction  of  the  pancreas  without  diabetes.  Perhaps  future  inves- 
tigation of  the  anatomical  findings  revealed  in  Walter  Schulze's  experi- 
ments will  clear  up  the  situation.  No  matter  what  the  conclusion  may 
be,  this  loop-hole  cannot  alter  the  fact  that  in  man  diabetes  is  due  to 
the  absence  of  the  pancreatic  function. 

Not  only  permanent  diabetes  but  also  transitory  and  alimentary  glyco- 


310  DISEASES  OF  THE  PANCREAS 

suria  may  be  caused  by  changes  in  the  pancreas;  this  is  shown  by  animal 
experiments,  as  well  as  by  the  facts  demonstrated  in  the  disease  in  man. 
After  various  injuries  of  the  pancreas,  even  although  slight,  transitory 
glycosuria  may  occur.  In  15  out  of  33  cases  of  partial  extirpation,  Min- 
kowski saw  transitory  glycosuria.  Minkowski,  as  well  as  myself,  demon- 
strated alimentary  glycosuria  in  the  previously  mentioned  experiments. 
In  one  of  these  there  was  a  transitory  excretion  of  sugar  after  every 
operation  upon  the  pancreas.  Upon  an  exclusive  meat  diet,  on  the  admin- 
istration of  10  grams  of  grape  sugar  slight  glycosuria  occurred,  and  after 
50  grams  it  was  marked.  In  an  interesting  article  Wille  has  furnished 
proof  that  alimentary  glycosuria  in  man  is  also  connected  with  changes 
in  the  pancreas.  In  800  patients  in  the  Hamburg  General  Hospital,  Willc 
made  feeding  experiments,  administering  100  grams  of  grape  sugar  in 
oacli  case,  and,  with  a  positive  result,  this  was  repeated  once  weekly.  In 
4T  cases  he  found  alimentary  glycosuria.  In  77  of  the  800  cases  an 
autopsy  was  held;  in  15  of  these  alimentary  glycosuria  had  been  recog- 
nized during  life,  and  at  the  autopsy  high-graded  changes  in  the  pancreas 
were  invariably  found.  Ten  doubtful  cases  still  remained  in  which  during 
life  alimentary  glycosuria  had  been  proven,  and  at  the  autopsy  marked 
changes  in  the  pancreas  were  found.  Alteration  in  the  pancreas  was  also 
observed  at  the  autopsy  in  cases  which,  during  life,  had  given  no  evidence 
of  alimentary  glycosuria.  Wille  arrived  at  the  conclusion  that  the  regular 
appearance  of  alimentary  glycosuria  is  an  important  diagnostic  sign  of 
existing  disease  of  the  pancreas,  that  in  a  periodically  appearing  alimentary 
glycosuria  the  suspicion  of  disease  of  the  pancreas  should  not  be  at  once 
rejected,  but  that,  in  the  absence  of  this  symptom,  the  pancreas  cannot  be 
looked  upon  with  certainty  as  normal. 

These  reports  of  Wille  are  noteworthy ;  they  show  that  cases  of  constant 
alimentary  glycosuria  may  be  the  result  of  changes  in  the  pancreas.  But 
the  relatively  small  number  of  positive  reports  prevents  our  proving  with 
certainty  that  this  is  always  the  case.  Alimentary  glycosuria — also  the 
constant  form — is  frequently  found  associated  with  various  diseases,  par- 
ticularly those  of  the  nervous  system.  In  these  numerous  cases  but  few 
autopsy  reports  relating  minutely  to  the  pancreas  are  at  hand,  and  it 
may  be  assumed  that  there  are  cases  of  alimentary  glycosuria  not  caused 
by  changes  in  the  pancreas.  It  may  be  true,  as  in  permanent  diabetes, 
that  constant  alimentary  glycosuria  occurs  without  changes  in  the  pancreas. 
In  spite  of  these  objections,  we  may  maintain,  on  the  basis  of  our  present 
knowledge,  that  the  proof  of  permanent  diabetes  as  well  as  of  constant 
alimentary  glycosuria  justifies  us  in  including  changes  of  the  pancreas  in 
our  diagnostic  calculations. 

A  second  group  of  symptoms  develops  from  the  absence  or  by  the 
destruction  of  the  digestive  function.     We  know  that  the  pancreas  has  a 


SYMPTOMS  311 

fat-emulsifying  and  fat-splitting,  a  proteol3i;ic  and  an  amylolytic,  function. 
Disease  of  the  pancreas  or  its  destruction  must  necessarily  lead  to  disturb- 
ances of  this  kind.  The  fact  is  also  operative  that  a  large  portion  of  the 
gland,  or  almost  all  of  it,  must  be  incapable  of  performing  its  function, 
hence  symptoms  due  to  the  absence  of  function  must  appear.  Add  to  this 
the  circumstance  that,  as  a  rule,  two  ducts  afe  affected,  in  some  animals 
even  more,  and  it -becomes  clear  that  if  only  one  duct  be  occluded,  provided 
that  in  the  other  the  secretion  is  suflBciently  active,  no  digestive  disturbances 
may  follow.  This  explains  why  we  so  rarely  observe  disturbances  of  diges- 
tion as  a  result  of  disease  of  the  pancreas. 

Let  us  first  consider  the  absence,  or  the  disturbance,  of  fat  digestion. 
This  is  shown  either  macroscopically,  or  only  microscopically  or  chemically 
in  the  changed  condition  of  the  feces. 

For  a  long  time  isolated  clinical  observations  have  pointed  out  the 
connection  between  impaired  assimilation  of  fat  and  changes  in  the  pan- 
creas, and  an  attempt  was  made  to  prove  this  experimentally  in  animals. 
Even  Claude  Bernard  was  of  the  opinion  that  pancreatic  juice  splits  the 
neutral  fats,  emulsifies  them,  and  is  therefore  necessary  for  the  absorption 
of  fats.  Among  those  who  differed  with  him  was  Schiff.  Opinions  varied 
until  the  discovery  of  experimental  pancreatic  diabetes  by  v.  Mering  and 
Minkowski,  and  the  digestive  disturbances  following  the  removal  of  the 
pancreas  were  studied.  Although  even  to-day  there  are  diversities  of  opin- 
ion and  many  doubts  concerning  these  points,  nevertheless  the  view  that, 
in  the  absence  of  the  pancreatic  function,  disturbances  arise  in  the  absorp- 
tion of  fat  is  generally  accepted.  Abelmann,  a  pupil  of  Minkowski, 
found  that  with  an  absence  of  the  pancreas  non-emulsified  fat  is  not  ab- 
sorbed at  all,  and  emulsified  fat  only  to  a  slight  extent;  only  in  the  case 
of  cream  was  the  absorption  more  complete.  With  partial  extirpation,  50 
per  cent,  of  emulsified  fats  was  absorbed  and  80  per  cent,  of  milk.  Upon 
the  addition  of  pancreas  to  the  food,  digestion  improved.  Fat-splitting, 
even  with  a  total  absence  of  the  pancreas,  was  undisturbed.  Similar  re- 
ports were  made  by  Sandmeyer,  Cavazzani,  and  Baldi.  Very  different 
results  were  obtained  by  Hedon  and  Ville  who  raised  objections  to  Abel- 
mann's  method  of  research,  and  in  this  they  were  supported  by  Pfliiger. 
Hedon  and  Ville  found  that  after  total  extirpation  of  the  pancreas,  fat 
absorption  continued,  although  to  a  lessened  extent;  in  a  case  of  severe 
diabetes  it  amounted  to  about  18  per  cent. ;  fat-splitting  remained  about 
normal,  principally  free  fatty  acids,  but  also  small  amounts  of  soap.  In 
more  extensive  investigations  Siegfried  Eosenberg  ascertained  that  in  ex- 
perimental, gradual  destruction  of  the  parenchyma  of  the  gland,  fat  ab- 
sorption still  showed  almost  normal  values ;  that,  however,  upon  increasing 
glandular  destruction,  it  is  damaged.  In  regard  to  fat-splitting,  which 
Rosenberg  attributes  mainly  to  bacterial  action,  he  believes  that  the  low 
fat-splitting  figures  found  with  increasing  glandular  destruction  are  due 


312  DISEASES  OF  THE  PANCREAS 

to  the  frequent  evacuations,  and  are  caused  by  the  undigested  material 
which  passes  through  the  intestine. 

In  complete  unanimity  with  the  results  of  animal  experiments,  clinical 
experience  teaches  us  that  frequently,  but  by  no  means  always,  in  disease 
of  the  pancreas,  in  chronic  inflammation,  in  the  case  of  neoplasms,  of 
cysts,  of  stones  in  the  ducte,  and  in  atrophy,  a  deficient  digestion  of  fat 
can  be  proven.  The  first  undoubted  report  is  by  Kiinzmann  in  1820; 
lie  saw  a  profuse  discharge  of  fat  in  the  feces  of  a  man  who  suffered  from 
induration  of  the  pancreas  with  obliteration  of  Wirsung's  duct,  chronic 
jaundice  and  dropsy.  A  report  by  Fles  is  very  interesting.  A  diabetic 
who  had  eaten  considerable  bacon  and  fat  meat  discharged  ounces  of  fat 
in  Ills  feces  that  could  be  separated  from  the  stool.  If  the  patient  took 
with  his  food  an  emulsion  prepared  from  the  pancreas  of  a  calf,  the  fat 
disappeared.  At  tlie  autopsy  high-graded  atrophy  of  the  pancreas  was 
found.  In  a  case  of  carcinoma  of  the  head  of  the  pancreas  observed  by 
me, ,  there  were  present  for  months  uncommonly  copious,  thick,  pappy, 
fecal  discharges  which  were  always  profusely  admixed  with  fat.  In  both 
cases  jaundice  was  absent — a  fact  which  must  be  particularly  emphasized, 
for,  according  to  the  excellent  researches  of  Friedrich  MtiUer,  if  the  bile 
is  absent  from  the  intestine  fatty  stools  are  quite  normal. 

The  forms  of  disturbance  of  fat  digestion  which  are  combined  with 
disease  of  the  pancreas  vary  considerably.  They  are  sometimes  recognized 
macroscopically,  and  are  then  designated  as  true  steatorrhea.  In  this  con- 
dition large  quantities  of  oily  or  fluid,  yellow  and  yellowish-brown,  fatty 
masses  are  discharged  with  the  evacuations,  or  even  independent  of  them. 
In  the  cold  these  become  compact,  resembling  butter,  grease  or  wax;  the 
hardened  fat  may  then  completely  envelop  the  feces  contained  within  it. 
Pribram,  in  a  case  observed  by  him,  closely  analyzed  these  fatty  discharges, 
and  proved  their  similarity  to  the  varieties  of  fat  ingested.  Chemical 
examination  of  the  fatty  masses  which  are  visible  to  the  naked  eye  shows 
neutral  fats  and  fatty  acids. 

In  diseases  of  the  pancreas  the  stools  are  of  the  consistency  of  clay, 
grayish-white,  or  colorless,  occasionally  asbestos-like,  and  the  increased 
amoimt  of  fat  can  only  be  recognized  by  chemical  and  microscopical 
processes.  Unquestionably  there  are  many  transitional  stages  between  true 
steatorrhea  and  the  previously  mentioned  fatty  stools,  so  that  the  difference 
between  the  two  forms  of  dejecta  may  be  assumed  to  be  a  graduated  one. 
The  chemical  investigation  of  these  feces  chiefly  reveals  neutral  fats,  fatty 
acids  and  soaps.  Such  dejecta,  rich  in  fat,  are  found  by  no  means  exclu- 
sively in  diseases  of  the  pancreas,  but  may  also  occur  normally  in  persons 
who  lunc  eaten  such  a  great  amount  of  fat  that  the  intestine  is  incapable 
of  ahsoi'bing  it;  in  the  majority  of  cases,  however,  the  condition  is  observed 
when  l)ile  is  absent  from  the  intestine,  in  certain  diseases  of  the  intestine, 
in  amyloidosis,  in  tuberculosis  of  the  intestine,  in  distributed  atrophy  of 


SYMPTOMS  313 

the  mucoiis  membrane  of  the  small  intestine,  in  caseation  of  the  mesen- 
teric glands,  in  chronic  tubercular  peritonitis,  and  perhaps — to  which  also 
Nothnagel  calls  attention — in  intense  catarrhal  processes.  It  is  evident 
from  this  fact  that  a  high  percentage  of  fat  in  the  stools  does  not  prove 
disease  of  the  pancreas,  and  we  must  first  exclude  all  other  causes  of 
insufficient  fat  absorption  before  we  can  regard  an  affection  of  the  pancreas 
as  the  cause  of  the  disturbed  fat  digestion. 

Miiller,  who  was  positively  unable  to  determine  a  greater  amount  of 
fat  in  the  stool  upon  the  absence  of  pancreatic  juice  from  the  intestine, 
designated  diminished  fat-splitting  as  a  factor  of  disease  of  the  pancreas. 
Miiller  excised  the  pancreas  of  a  dog,  and,  under  antiseptic  precautions, 
placed  it  in  sterilized  milk  in  the  incubator  for  24  hours.  Fatty  acids 
amounting  to  from  42  to  45  per  cent,  were  present.  In  a  control  experi- 
ment in  which  the  pancreatic  ferment  was  destroyed  by  boiling,  no  fat- 
splitting  occurred.  After  Miiller  had  previously  proven  by  experiment 
that  intestinal  bacteria  had  but  a  slight  influence  upon  fat-splitting,  he 
concluded  that  the  important  factor  for  fat-splitting  in  the  intestine  is 
contained  in  the  pancreatic  juice,  and  the  absence  of  the  pancreatic  func- 
tion is  expressed  by  disturbed  fat-splitting.  In  a  series  of  cases  of  pan- 
creatic disease,  Miiller  proved  the  disturbed  fat-splitting  with  certainty, 
his  reports  being  confirmed  by  several  authors,  but  denied  by  others. 

The  question  has  been  most  thoroughly  studied  by  Katz.  He  formu- 
lated an  expeditious  method  which  enables  us  to  determine  the  degree  of 
fat-splitting  in  24  hours.  In  the  examination  of  a  number  of  cases  ob- 
served in  my  hospital,  in  which  during  life  reduced  fat-splitting,  and  at 
the  autopsy  pathologic  changes  in  the  pancreas,  were  determined,  he  came 
to  the  conclusion  that  a  diminution  of  fatty  acids  and  soaps  to  below  70 
per  cent,  of  the  total  amount  of  fat  in  the  fatty  stool  favors  a  diminished 
or  even  completely  arrested  function  of  the  pancreatic  juice;  but  in  nurs- 
lings, and  in  profuse  diarrhea,  this  decrease  had  no  significance.  Other 
authors  have  also  noted  disturbed  fat-splitting  in  pancreatic  disease,  for 
example,  v.  Noorden,  Rosenheim,  Anschiitz. 

Diminished  fat-splitting  in  disturbed  pancreatic  function  may,  there- 
fore, be  considered  as  proven,  and  the  validity  of  this  proof  does  not  suffer 
from  the  fact  that  there  are  undoubted  cases — perhaps  many — in  which 
no  disturbance  of  fat-splitting  can  be  determined ;  even  in  widely  distributed 
disease  of  the  organ,  a  healthy  portion  of  the  gland  may  serve  the  excre- 
tory ducts,  which  may  discharge  a  sufficiency  of  pancreatic  juice  into  the 
intestine. 

Where  a  disturbance  of  fat-splitting  has  been  found  without  disease 
of  the  pancreas  being  determined,  the  circumstances  are  different.  Katz 
specified  that  in  nurslings  and  in  profuse  diarrhea  reduced  fat-splitting 
might  be  found  without  coexisting  disease  of  the  pancreas.  Certainly  in 
all  cases  in  which  an  increased  peristalsis  rapidly  propels  the  contents 


314  DISEASES   OF  THE    PANCREAS 

through  the  intestine,  the  pancreatic  juice,  normal  in  amount,  will  not 
have  sufficient  time  to  split  the  fat  to  such  an  extent  as  is  possible  under 
normal  circumstances. 

Zoja,  who  recently  published  a  comprehensive  study  of  fat  absorption, 
mentions  two  cases  orf  reduced  fat-splitting  without  changes  being  found 
in  the  pancreas  or  in  the  excretory  ducts.  In  one  case  there  was  stenosis 
of  the  large  intestine,  and  in  the  other  carcinoma  of  the  gall-bladder.' 
Zoja  recognizes  in  deranged  fat  digestion  an  important  indication  of  an 
affection  of  the  pancreas,  but,  on  account  of  the  great  number  of  reported 
cases  he  arrived  at  the  conclusion  that  the  disturbed  fat-splitting  is  not 
the  most  important  symptom,  but  the  small  amount  of  soaps  which  he 
invariably  demonstrated  in  diseases  of  the  pancreas.  Deucher  had  pre- 
viously called  attention  to  the  importance  of  this  factor.  The  demonstra- 
tion in  the  feces  of  a  decided  quantity  of  neutral  fats,  or  of  a  great  amount 
of  fatty  acids,  particularly,  however,  of  a  deficiency  in  soaps,  according  to 
Zoja.  points  with  great  likelihood,  if  not  with  positive  certainty,  to  the 
absence  of  pancreatic  juice  from  the  intestine.  The  main  stress  is  placed 
by  Zoja  upon  the  lessened  quantity  of  soaps.  The  greater  the  percentage 
of  soajis,  the  more  certainly  may  an  occlusion  of  the  pancreatic  ducts  be 
excluded ;  the  less  the  quantity  of  soaps  in  proportion  to  the  neutral  fats 
and  fally  acids,  the  more  readily  may  occlusion  of  the  pancreatic  duct 
be  assumed.  The  less  the  amount  of  pancreatic  juice  which  flows  into  the 
intestine,  the  slighter  is  the  amount  of  alkali,  and,  therefore,  also  the 
smaller  the  amount  of  soaps.  In  this  reasoning  Zoja  finds  no  difference 
between  the  animal  experiment  and  observation  in  man,  which  has  also 
been  emphasized  from  the  standpoint  of  fat-splitting,  since  Abelmann,  as 
well  as  Rosenberg,  found  smaller  amounts  of  soaps. 

We  cannot  enter  here  upon  a  criticism  of  the  work  of  Zoja.  I  shall 
only  mention  that  Abelmann  reported  the  frequent  finding  of  quantities 
of  soaps  which  reached  the  normal.  Miiller  previously  objected  to  this 
niolhod  of  determining  soaps  and  the  combined  fatty  acids,  and  designates 
the  jiroportion  of  free  fatty  acids  to  the  soaps  in  the  feces  as  an  inconstant 
one  wliich  depends  upon  accidental  conditions.  I  must  also  state  that  in 
a  case  of  Zoja's  of  recognized  pancreatic  affection,  normal  values  for  soaps 
were  found.  The  relative  value  of  the  factor  emphasized  by  Zoja,  the 
lessened  soap  figures  in  proportion  to  the  large  amount  of  neutral  acids  and 
fatty  acids,  cannot  be  denied;  but  more  complete  investigations  are  neces- 
sary finally  to  solve  the  important  question  of  the  diagnosis  of  diseases 
of  llio  jiancroas.  We  can  only  state  positively  that  disturbed  fat  digestion 
is  ail  important  symptom  in  pancreatic  disease.  An  increased  amount  of 
fal  in  I  he  stools  is  alone  not  a  basis  for  the  assumption  of  a  pancreatic 
alTcction.  If  uo  jaundice  exists,  and  no  disease  of  the  intestine  is  present, 
if  increased  peristalsis  by  which  the  ingesta  are  rapidly  propelled  through 
(lie  intestine  does  not  explain  the  insufficient  fat  digestion,  then  the  sus- 


SYMPTOMS  315 

picion  of  disease  of  the  pancreas  is  certainly  justified.  Some  forms  of 
altered  fat  digestion,  true  steatorrhea,  in  which  larger,  even  macroscopi- 
cally  recognizable,  amounts  of  fat  are  passed  with  or  without  the  stool, 
which  show  diminished  fat-splitting  with  a  certain  increased  amount  of 
fat  in  the  stools,  and  low  quantities  of  soaps  in  proportion  to  the  fatty 
acids  and  neutral  fats,  are  factors  which  point  with  great  likelihood  to 
disease  of  the  pancreas.  It  can  only  be  positively  proven,  however,  when 
other  symptoms  due  to  absence  of  function,  such  as  diabetes  or  insufficient 
nitrogen  absorption,  or  certain  clinical  symptoms,  such  as  tumor,  bronzing 
of  the  skin  or  pancreatic  colic,  are  present. 

Equally  important  is  the  absence  or  disturbance  of  albumin  digestion, 
which  is  observed  experimentally  and  clinically  in  diseases  of  the  pancreas. 
Abelmann  found  that  when  the  pancreatic  juice  is  absent,  only  a  portion 
of  the  proteids  is  absorbed;  this  averages  44  per  cent,  in  animals  in 
whom  the  pancreas  was  removed,  and  54  per  cent,  in  the  cases  of  partial 
extirpation  of  the  pancreas.  If,  on  meat  diet,  pig's  pancreas  was  simul- 
taneously given,  the  absorption  of  nitrogen  was  decidedly  increased,  and 
74  to  78  per  cent,  was  absorbed.  After  a  meat  diet  the  presence  of  numer- 
ous macroscopically  recognizable  undigested  muscle  fibers  was  conspicuous. 
Similar  results  were  obtained  by  de  Renzi,  Cavazzani,  Sandmeyer,  and 
Harley.  In  an  instance  of  total  extirpation  of  the  pancreas  performed 
by  Katz  and  myself,  and  which  was  followed  by  diabetes,  after  meat  was 
taken  for  the  first  time,  large  portions  of  undigested  meat  were  macro- 
scopically found  in  the  feces.  Under  microscopic  investigation  numerous 
muscle  fibers  with  distinct  transverse  striae  were  detected. 

Rosenberg's  investigations  were  most  thorough;  after  tying  the  excre- 
tory ducts,  injecting  into  them  an  acid  solution,  and  subsequently  tying 
again,  as  is  done  for  the  gradual  destruction  of  the  glandular  parenchyma, 
he  found  at  once  that  the  absorption  of  nitrogen  was  but  slightly  altered, 
even  before  he  could  determine  any  disturbance  in  the  absorption  of  fat 
and  carbohydrates.  Later,  after  the  removal  of  the  degenerated  glands, 
nitrogen  metabolism  fell  to  33  and  35  per  cent.,  while  41  per  cent,  of  fat 
and  50  per  cent,  of  carbohydrates  were  still  being  absorbed. 

Quite  as  positive  is  the  clinical  proof  based  upon  numerous  observations 
that  in  man  disease  of  the  pancreas  causes  disturbances  of  albumin  diges- 
tion. Deficient  meat  digestion  is  most  conspicuous.  In  the  feces  there 
are  numerous  imdigested  muscular  fibers,  as  may  sometimes  be  recognized 
with  the  naked  eye,  but  microscopic  examination  shows  them  very  dis- 
tinctly. In  the  case  of  a  diabetic,  reported  by  Fles,  the  dejecta  contained 
uncommonly  numerous,  undigested,  quite  distinct,  transverse  muscular 
fibers.  If  the  patient  took  calf's  pancreas  with  his  other  food,  the  meat 
was  again  perfectly  digested,  and  the  muscle  fibers  again  appeared  in  the 
stool  when  no  pancreas  was  added  to  the  food.  Harley  recognized  a  similar 
condition  in   a  case  of  pancreatic   abscess,     v.   Ackeren  noted   impaired 


316  DISEASES   OF  THE   PANCREAS 

dif'estion  of  meat  in  carcinoma,  Kiister  in  a  case  of  cyst,  and  Lichtheim 
in*a  case  of  calculus  formation  in  the  pancreas.  In  a  case  of  carcinoma 
of  the  pancreas  that  came  under  my  observation,  I  noted  numerous  remains 
of  transverse,  striped,  muscular  fibers  with  distinct  muscular  structure. 
Zoja  recently  reported  a  case  of  carcinoma  of  the  head  of  the  pancreas 
with  occlusion  of  Wirsung's  duct  and  of  the  common  gall-duct,  in  which 
numerous  fibers  of  meat  were  found  in  the  feces  with  distinctly  devel- 
oped transverse  striation.  A  similar  condition  was  observed  by  Auerbach 
in  a  case  of  carcinoma  of  the  pancreas,  and  by  Cipriani  and  Giudiceandrea 
in  pancreatic  calculi. 

The  insufficient  nitrogen  absorption  in  pancreatic  disease  has  also 
been  proven  by  exact  researches  in  metabolism.  Hirschfeld  conducted  a 
series  of  thorough  analyses  in  diabetes.  He  found  that  32  per  cent,  of 
the  nitrogen  substance  ingested  could  be  found  in  the  feces,  while  5  to  6 
per  cent,  corresponds  to  the  norm.  It  is  true  this  was  not  proven  by 
autopsy  findings.  But  this  proof  was  present  in  a  case  of  Weintraud's; 
45.2  per  cent,  of  the  albumin  of  the  food,  and  22.2  per  cent,  of  the  fat, 
were  lost.  At  the  autopsy  a  markedly  contracted,  indurated  pancreas  with 
decided  increase  of  the  connective  tissue  was  found,  and  in  this  only  iso- 
lated glandular  globules  could  be  seen.  Weintraud,  in  agreement  with  the 
results  of  Rosenberg's  animal  experiments,  lays  the  principal  stress  upon 
the  fact  that  in  diseases  of  the  pancreas  proteid  absorption  is  more  de- 
cidedly, or  at  least  as  greatly,  disturbed  as  fat  absorption;  while  in 
intestinal  diseases,  in  which  the  intestinal  apparatus  for  the  absorption  of 
fat  functionates  insufficiently,  as  in  amyloid  disease  of  the  intestine,  etc., 
the  absorption  of  fat  is  comparatively  as  much  affected  as  that  of  the 
albumin.  The  conditions  were  similar  in  a  previously  mentioned  case 
reported  by  Zoja,  of  carcinoma  of  the  pancreas  with  occlusion  of  Wirsung's 
duet.  More  than  70  per  cent,  of  the  nitrogen  of  the  food  was  excreted,  and 
liardiy  30  per  cent,  absorbed.  Unfortunately,  but  few  reports  of  experi- 
ments are  at  hand;  but  even  with  the  data  we  have,  there  can  be  no  doubt 
that  this  is  a  positive  method  for  the  recognition  of  diseases  of  the 
pancreas. 

Recently  Sahli  has  proposed  another  method  for  testing  the  digestive 
function  of  the  pancreas  for  proteids.  He  determined  by  exact  experiments 
that  gelatin  capsules  hardened  with  formaldehyd — he  calls  them  glutoid 
capsules — after  reaching  a  definite  degree  of  hardness,  are  soluble  neither 
by  water  nor  by  hydrochloric  acid  pepsin  digestion,  but  only  so  by  pancre- 
atic juice  (by  trypsin).  If  these  capsules  are  filled  with  a  substance  which 
can  be  recognized  in  the  saliva  or  in  the  urine — best  with  iodoform — in 
eases  of  arrested  pancreatic  digestion  a  reaction  for  iodin  does  not  occur 
at  all,  or  only  very  late.  With  normal  motility  of  the  stomach  and  suffi- 
ciently good  pancreatic  function  the  iodin  reaction  in  the  saliva  shows 
itself  in  from  4  to  8  hours.    According  to  Sahli,  from  the  absence  or  from 


SYMPTOMS  317 

the  delayed  appearance  of  the  iodin  reaction  we  may  determine  a  disturb- 
ance of  the  pancreatic  function,  provided  the  motility  of  the  stomach  is 
not  reduced.  These  reports  of  Sahli  are  very  interesting,  and  if,  in  a  large 
number  of  tests,  the  absence  or  the  late  appearance  of  the  "  glutoid  reac- 
tion "  coincides  with  anatomical  proof  of  a  pancreatic  disease  and  arrested 
secretion,  we  have  a  positive  and  infallible  sign  of  disease  of  the  pancreas. 

There  can  be  no  doubt  that  the  digestion  of  carbohydrates  suffers  when 
the  pancreatic  function  is  absent  or  disturbed.  Kosenberg  has  considered 
this  in  his  animal  experiments.  So  long  as  the  pathologic  process  in  the 
pancreas  is  not  too  far  advanced,  normal  or  almost  normal  absorption 
was  (found;  when  the  process  had  made  further  progress,  the  figures  de- 
creased decidedly,  so  that,  in  this  ease,  digestion  was  already  seriously 
damaged.  In  an  experiment  at  the  conclusion  of  which  the  degenerate 
glandular  remains  were  removed,  carbohydrate  absorption  as  well  as  fat- 
splitting  sank  rapidly  and  decidedly,  with  a  loss  in  the  absorption  of 
nitrogen  and  fat ;  on  pancreas  feeding,  in  all  the  experiments  a  conspicuous 
improvement  was  noted.  Clinical  reports  in  regard  to  this  factor  are  very 
few.  In  recent  isolated  cases,  as,  for  example,  by  Auerbach  and  Edoardo 
Italia,  it  is  expressly  stated  that  considerable  starch  was  found  in  the 
stools. 

When  the  pancreatic  function  is  either  absent  or  disturbed,  impaired 
digestion  occasionally  produces  conspicuous  symptoms  that  are  often  noted 
by  the  patient  himself.  The  stools  have  a  massive  appearance  which  is  out 
of  proportion  to  the  amount  of  food  ingested.  I  have  seen  a  number  of 
cases  in  which  this  symptom  led  me  to  suspect  a  disease  of  the  pancreas, 
and  the  further  course  of  the  affection  justified  this  assumption.  Much 
of  the  food  passes  through  the  digestive  tract  without  being  utilized.  In 
spite  of  plentiful  food,  there  is  constant  loss  of  weight,  and  conspicuously 
massive,  thick,  pappy  or  compact  dejecta,  whose  amount  appears  to  he 
decidedly  greater  than  the  ingested  food,  and  this  is  an  important  symp- 
tom which  calls  for  the  closest  attention  of  the  physician.  Exact  micro- 
scopic and  chemical  analysis  explains  this  massiveness ;  muscle  fiber  as  well 
as  fat  and  carbohydrates  are  excreted  without  being  assimilated. 

The  s}Tnptoms  due  to  absence  of  function  unquestionably  furnish  the 
most  important  aid  in  the  recognition  of  an  affection  of  the  pancreas,  and 
must  therefore  be  first  described.  There  are,  however,  a  few  symptoms 
which  cannot  be  regarded  as  denoting  absence  of  function,  which,  never- 
theless, enable  us  to  recognize  that  the  pancreas  is  diseased.  Among  these 
we  must  consider  the  following:  Bronzing  of  the  sTcin,  peculiar  colic  and 
pains  of  a  definite  character  in  the  epigastrium ;  tumor  or  resistance  in 
.  this  region,  and  certain  forms  of  jaundice.  These  signs,  with  the  excep- 
tion of  tumor  formation,  only  become  important  when  they  are  combined 
with  permanent  or  transitory  symptoms  of  absence  of  function  of  the 
gland. 


318  DISEASES  OF  THE  PANCREAS 

French  authors  were  the  first  to  direct  attention  to  a  peculiar  form 
nf  diabetes  with  deposition  of  pigment  in  the  skin — diabete  bronze.  This 
pio-ment  formation  is  the  expression  of  hemochromatosis,  which  develops 
in  the  skin  as  well  as  in  the  different  organs.  The  color  of  the  skin  is 
brownish,  brownish-black,  or  somewhat  grayish,  the  discoloration  is  diffused 
over  the  entire  body,  and  nowhere  are  pigmented  areas  observed,  not  even 
upon  the  mucous  membrane,  and  this  differentiates  the  condition  from 
Addison's  disease. 

The  cases  reported  up  to  the  present  time  are  few  in  number.  In  the 
book  I  published  in  1898  I  mentioned  23,  Anschiitz,  in  1899,  24  cases. 
In  most  instances  changes  were  foimd  in  the  pancreas.  It  was  sclerotic, 
rusty-brown,  the  excretory  ducts  were  patulous.  Jeanselme  had  already 
declared  diabetes  to  be  due  to  sclerosis  of  the  pancreas  which  develops 
as  a  result  of  deposition  of  pigment.  Anschiitz  recently  studied  an 
undonl)tod  case.  During  life,  besides  the  symptoms  of  diabetes,  there  were 
also  signs  of  disturbed  secretory  function:  distinct  fat-splitting  and  fatty 
stools.  For  this  reason  a  diagnosis  of  disease  of  the  pancreas  was  made. 
At  the  autopsy,  a  chronic,  indurated  pancreatitis  with  general  hemochroma- 
tosis was  found.  The  deposition  of  pigment  caused  chronic  inflammation 
of  the  pancreas,  and  this  in  turn  the  diabetes.  A  similar  report  and 
explanation  were  furnished  by  Opie. 

Bronzing  of  the  skin  diffusely  distributed,  from  which  hemochromatosis 
may  be  concluded,  absence  of  pigment  areas  in  the  skin  and  in  the  mucous 
membranes,  and  simultaneously  diabetes,  warrant  the  assumption  of  dis- 
ease of  the  pancreas,  particularly  if,  at  the  same  time,  secretory  disturb- 
ances, fatty  stools,  deficient  digestion  of  fat  and  albumin  can  be  deter- 
mined. 

Yyowx  the  pain  alone — no  matter  what  form  it  may  assume — disease  of 
the  pancreas  can  never  be  diagnosticated.  In  pancreatic  affections  pain 
may  be  of  many  varieties  and  degrees,  it  may  be  persistent  or  paroxysmal. 
The  former,  sometimes  remittent  or  paroxysmal,  or  gradually  becoming 
more  severe,  is  found  in  abscess,  in  hemorrhage,  in  acute  and  chronic 
pancreatitis,  and  in  tumor.  In  carcinoma  the  pain  may,  under  some  cir- 
cumstances, be  of  extraordinary  intensity,  so  that  the  patient  anxiously 
avoids  any  movement,  shrinks  at  a  loud  word,  and  rejects  food.  In 
combination  with  a  feeling  of  extreme  weakness  and  marked  prostration, 
this  pain  shows  certain  peculiarities  such  as  are  very  rare  in  other  tumors 
of  the  abdomen.  Whether  pressure  upon  the  celiac  ganglion  or  torsion  of 
the  same  causes  this  peculiar  pain  has  not  been  proven,  but  it  is  unques- 
tionably a  characteristic  feature,  and  we  are  justified  in  entertaining  the 
sus])ieion  that  the  seat  of  the  affection  is  the  pancreas. 

The  paroxysmal  pains  may  resemble  sharp  colic  limited  chiefly  to  the 
epigastrium,  and,  under  certain  circumstances,  may  also  point  to  disease 
of  the  ])ancreas.     By  some  authors  special  stress  is  laid  upon  this  pain. 


SYMPTOMS  319 

Epigastric  colic,  as  such,  naturally  proves  nothing,  not  even  that,  for  ex- 
ample, as  in  the  case  described  by  Miinnich  and  Holzmann,  its  main 
point  of  concentration  is  under  the  left  arch  of  the  ribs.  We  know  that 
renal  colic  or  gall-stone  colic,  colic  of  the  appendix,  and  a  beginning 
pericolitis  may  cause  similar  pains  in  the  region  of  the  splenic  flexure. 
We  are,  then,  only  justified  in  diagnosticating  a  disease  of  the  pancreas 
if  pancreatic  concrements  are  found  in  the  feces,  or  if,  after  prolongation 
of  the  disease,  s3Tnptoms  due  to  absence  of  function  appear,  such  as  dia- 
betes, or  insufficient  digestion  of  proteid  or  fat.  We  may  conclude  from 
this  that  the  same  process  that  gives  rise  to  prolonged  colic  also  brings 
about  changes  in  the  parenchyma  of  the  pancreas,  and  gradually  disturbs 
or  arrests  the  function  of  the  organ.  In  calculi  formation  there  are 
chronic  inflammatory  changes  with  connective  tissue  proliferation,  and 
these  gradually  displace  and  replace  the  gland  substance. 

Not  only  in  stone  formation  does  colic  occur,  but  also  in  all  cases  of 
occlusion  of  the  excretory  ducts  and  of  the  secretory  passages  in  the  in- 
terior of  the  gland,  as  from  cicatrices,  neoplasms,  indurated  inflammations 
or  hemorrhages.  In  cysts  of  the  pancreas  these  colics  play  a  particularly 
important  role.  In  104  cases  operated  upon  Takayasu  found  colic  a  symp- 
tom in  64  cases.  As  this  form  of  pain  is  evidently  very  much  more  rare 
in  other  cysts  of  the  abdomen,  its  presence,  as  Leube  emphasized,  is  an 
important  sign  of  pancreatic  cysts.  It  may  be  asserted  that  these  colics 
are  much  more  frequent  than  is  to-day  assumed.  How  many  so-called 
nervous  gastralgias  may  depend  upon  pancreatic  colic !  Minute  inves- 
tigations in  metabolism  and  absorption  may,  perhaps,  show  transitory 
or  permanent  anomalies  which  occur  in  the  course  of  a  pancreatic 
affection. 

A  feeling  of  resistance  or  a  tumor  in  the  region  of  the  pancreas  forms 
a  significant  symptom.  Naturally  we  must  be  certain  that  this  resist- 
ance, or  the  tumor,  actually  springs  from  the  pancreas.  This  proof,  on 
account  of  the  concealed  position  of  the  organ,  is  difficult  to  establish. 
Primarily  we  must  consider  carcinoma,  cysts,  and  indurative  inflamma- 
tion, as  the  acute  processes,  acute  hemorrhagic  pancreatitis,  abscess,  hemor- 
rhage and  necrosis  are  evidently  much  rarer  occurrences. 

In  a  small  number  of  cases  of  carcinoma^  in  about  -J^  to  ^,  a  tumor 
can  be  felt,  but  even  then  the  differentiation  from  carcinoma  of  the  duo- 
denum, from  carcinoma  of  the  choledochus  and  of  the  porta  hepatis,  from 
lymph-gland  tumor,  from  aneurysms  of  the  hepatic  artery,  from  products 
of  inflammation  of  a  tuberculous  nature,  even  from  carcinoma  of  the  colon 
or  pylorus,  is  very  difficult,  occasionally  impossible.  The  differentiation 
from  tumors  of  the  colon  or  pylorus  is  most  readily  made  since  pancreatic 
carcinomata  are,  as  a  rule,  fixed,  while  carcinomata  of  the  colon  and 
pylorus  are  frequently  movable.  By  artificial  inflation  of  the  stomach  and 
colon,  by  the  demonstration  of  symptoms  of  stenosis  in  the  stomach  or 
22 


320  DISEASES   OF  THE   PANCRE.\S 

intestine,  by  the  chemical  and  microscopic  investigation  of  the  gastric  and 
intestinal  contents,  as  well  as  by  other  clinical  signs  referable  to  disease 
of  the  stomach,  the  intestine,  or  of  the  pancreas,  the  diagnosis  may  occa- 
sionally be  made  with  certainty.  Much  more  difficult,  almost  impossible, 
is  the  differentiation  of  tumors  of  the  duodenum  or  the  biliary  passages. 
Here  the  appearance  of  symptoms  which  indicate  absence  of  function  of 
the  pancreas  may  clear  the  situation. 

The  appearance  of  a  cystic  tumor  in  the  region  of  the  pancreas  does 
not  at  all  prove  that  we  are  dealing  with  a  pancreatic  cyst. 

Echinococcus  of  the  liver,  of  the  spleen,  of  the  mesentery  and  of  the 
])(Titoncum,  hydronephrosis,  dropsy  of  the  gall-bladder,  cysts  of  the  omen- 
tum or  the  mesentery,  the  spleen,  the  kidney  or  the  adrenals,  soft  sar- 
comata of  the  liver,  accumulations  of  fluid  in  the  bursa  omentalis,  etc., 
mav  give  rise  to  confusion.  It  would  lead  us  too  far  afield  to  enter  upon 
the  details  of  the  diagnostic  factors;  frequently  the  diagnosis  can  only  be 
made  with  certainty  at  the  operation. 

The  inflammatory  tumor  is  rarely  recognized  during  life;  usually  it 
is  confounded  with  neoplasms.  Often,  however,  at  the  operation  it  is  not 
quite  clear  whether  an  indurative  inflammation  or  a  neoplasm  is  present, 
and  only  from  the  gradual  disappearance  of  the  tumor,  as,  for  instance, 
after  the  operative  removal  of  gall-stones,  do  we  recognize  that  a  chronic 
inflammation  of  the  pancreas  was  present,  and  this  appears  to  be  a  by  no 
means  rare  occurrence. 

One  of  the  most  frequent  symptoms  of  disease  of  the  pancreas  is 
ja  1(7} dice.  The  intimate  relations  existing  between  the  head  of  the  pan- 
creas and  the  common  gall-duct  sufficiently  explain  this.  Unfortunately 
there  is  no  characteristic  form  of  jaundice  which  indicates  disease  of  the 
])ancreas.  The  form  in  which  the  jaundice  slowly  but  steadily  increases 
and  finally  leads  to  complete  occlusion  by  compression  of  the  common 
gall-duct,  is  also  found  in  tumors  of  the  duodenum,  of  the  hilus  hepatis, 
and  in  lymph-gland  tumors,  all  of  these  causing  a  similar  development 
of  the  jaundice  as  well  as  the  Bard-Pic  syndrome:  Intense,  chronic,  grad- 
luilly  increasing  jaundice  with  enormous  dilatation  of  the  gall-bladder, 
rapid  onuiciation  and  cachexia  with  usually  subnormal  temperature,  and 
the  aljsence  of  decided  enlargement  of  the  liver  are  not  confirmatory,  even 
althnngh  it  cannot  be  denied  that  this  symptom-complex  occurs  more  fre- 
(luently  in  carcinoma  of  the  head  of  the  pancreas  than  in  tumor  of  the 
neighboring  organs,  or  in  stone  formation  in  the  biliary  passages.  The 
relatively  rare  appearance  of  the  cardinal  symptoms,  of  diabetes,  of  in- 
sutfieiont  fat  and  albumin  digestion,  may,  it  is  true,  here  also  indicate  the 
correct    diagnosis. 

Much  less  convincing  are  other  symptoms  which  are  observed  in  dis- 
ease of  the  pancreas:  Emaciation,  digestive  disturbances,  salivation,  vomit- 
incj,  constipation,  hemorrhagic  stools,  intestinal  occlusion,  fever.    It  is  true 


SYMPTOMS  321 

a  proof  of  a  sequestrating  pancreas,  or  of  pancreatic  concrements  in  the 
stools,  may  undoubtedly  lead  to  the  diagnosis  of  disease  of  the  organ. 

The  acute  inflammations,  hemorrhagic  pancreatitis,  pancreatic  apo- 
plexy and  necrosis  continually  appear  with  severe  symptoms :  Sudden, 
severe  and  paroxysmal  pain  in  the  gastric  and  umbilical  region,  nausea, 
vomiting,  immediate  and  severe  collapse,  great  anxiety,  enormous  increase 
in  the  pulse  rate,  and  not  infrequently  the  picture  of  acute  intestinal 
occlusion.  The  differential  diagnosis  between  internal  incarceration  and 
the  previously  mentioned  processes  is  exceedingly  difficult,  and  usually 
can  only  be  made  at  the  operation  or  at  the  autopsy. 

In  disease  of  the  pancreas  some  authors  lay  special  stress  upon  certain 
changes  in  the  urine  which  enable  us  to  make  a  diagnosis  of  involvement 
of  the  pancreas,  such  as  an  insufficient  excretion  of  indican  and  the  proof  of 
pentosuria  or  maltosuria;  unfortunately,  these  views  have  not  been  con- 
firmed. During  pancreatic  digestion,  as  is  well  known,  indol,  the  mother 
substance  of  indican,  develops.  For  this  reason  we  formerly,  with  a 
suspicion  of  disease  of  the  pancreas,  first  directed  particular  attention 
to  the  urine.  In  a  case  of  occlusion  of  the  small  intestine  Gerhardi  con- 
cluded from  the  fact  that  indican  was  not  increased  that  disease  of  the 
pancreas  was  the  cause  of  the  occlusion;  the  autopsy  confirmed  Gerhardi's 
view.  The  animal  experiments  of  Pisenti  appear  to  confirm  this  opinion. 
In  our  animal  experiments,  at  my  suggestion,  my  assistant,  Dr.  Katz, 
invariably  examined  the  urine  for  indican  and  always  found  this  sub- 
stance increased.  Reports  are  at  hand  showing  that,  in  the  course  of  dis- 
ease of  the  pancreas  in  man,  the  amount  of  indican  was  also  increased. 

Just  as  little  has  the  appearance  of  maltose  or  pentose  in  the  urine 
proven  itself  characteristic  of  pancreatic  disease. 

In  reviewing  the  important  sj^mptoms  which  have  been  mentioned  in 
this  article,  it  is  apparent  that  the  most  reliable  aids  in  the  diagnosis  are 
the  symptoms  due  to  absence  of  function  of  the  gland,  and  the  proof  of 
resistance  or  of  a  tumor  having  its  seat  in  the  pancreas.  In  a  detailed 
description  of  the  individual  forms  of  the  disease,  we  are  convinced  by 
the  careful  consideration  and  investigation  of  the  different  symptoms  in 
a  niimber  of  cases  that  the  diagnosis  may  be  made  with  certainty,  or  with 
more  or  less  likelihood.  In  many — probably  in  the  great  majority — of 
cases,  if  we  go  beyond  an  assumption  we  find  ourselves  upon  the  wrong 
track.  If  any  result  be  obtained  it  is  only  possible  by  persistent,  tireless 
investigation.  Such  a  result  is  not  only  of  theoretic,  but  also  of  great 
practical  value,  as  has  been  shown  by  the  efforts  of  surgeons,  who,  inter- 
fering at  the  right  time,  have  cured  many  affections  which  had  endangered 
life,  such  as  chronic  and  acute  inflammatory  processes,  and  neoplasms  of 
the  pancreas. 

We  are  now  at  the  dawn  of  rational  treatment  of  disease  of  the  pan- 
creas, and  undoubtedly  internal  therapy  will  also  produce  practical  results 


322  DISEASES  OF  THE  PANCREAS 

when  we  are  able  to  diagnosticate  the  by  no  means  rare  and  curable  affec- 
tions of  the  pancreas.  On  account  of  the  intimate  relation  between  the 
biliary  passages,  the  liver,  and  intestines  on  the  one  hand,  and  the  pan- 
creas on  the  other,  the  consecutive  changes  in  the  pancreas  will  un- 
(juestionably — I  might  say  will  unwittingly — be  cured  by  internal  treat- 
ment. When  we  gain  a  deeper  insight  into  the  pathology  of  the  pancreas, 
and  are  able  to  recognize  clearly  the  pathologic  changes  in  this  organ,  it 
will  perhaps  often  be  possible  not  only  to  prevent  the  implication  of  the 
pancreas,  but  to  restore  to  the  normal  the  already  diseased  organ  in  so 
far  as  this  is  at  all  possible. 


DISEASES  OF  THE   LIVER  AND    BILIARY 
PASSAGES 


JAUNDICE   AND    HEPATIC    INSUFFICIENCY 

By  O.  MINKOWSKI,  Cologne 

JAUNDICE 

GENERAL   CONSIDERATIONS 

When  a  patient  with  jaundice  presents  himself  to  our  notice,  certain 
peculiarities  are  conspicuous  at  the  first  glance.  In  a  yellow,  artificial 
light  the  yellow  discoloration  of  the  skin  may  easily  escape  observation, 
but  in  broad  daylight  this  is  strikingly  obvious,  and  we  then  perceive  the 
yellow  discoloration  of  the  conjunctival  sclerce;  the  transudation  of  the  tis- 
sues of  the  lips  and  the  mucous  membrane  of  the  mouth  with  the  same 
yellow  coloring  matter  also  becomes  visible  if  we  render  the  tissues  blood- 
less by  pressing  upon  the  mucous  membrane.  This  yellow  color  is  readily 
recognizable  upon  the  hard  palate  where  the  greater  tension  of  the  mucous 
membrane  makes  it  pallid. 

The  yellow  discoloration  is,  in  fact,  due  to  an  overflooding  of  the  organ- 
ism with  biliary  coloring  matter^  as  is  proven  by  the  composition  of  the 
urine  which,  with  its  brownish  tint  like  the  color  of  heer  and  the  yellowness 
of  its  foam,  shows  the  presence  of  bilirubin.  The  intense  staining  power 
of  this  coloring  matter  is  immediately  perceptible  on  dipping  a  piece  of 
filter  paper  into  the  urine,  and  is  also  manifested  by  the  yellow  stains 
which  may  appear  upon  the  linen  of  the  patient.  Certain  proof  of  the 
presence  of  biliary  coloring  is  obtained  by  the  positive  reaction  of  Gmelin's 
test,  which  is  as  follows: 

We  place  a  specimen  of  the  suspected  urine  in  a  test-tube,  and  with  a 
glass  pipette  introduce  beneath  it  a  layer  of  concentrated  nitric  acid  to 
which  nitrous  acid  has  been  added.  The  nitric  acid  should  have  only  a 
faint  yellow  color.  Chemically  pure  nitric  acid  is  Just  as  useful  as  the 
fuming  acid.  We  obtain  an  excellent  reagent  by  adding  to  a  larger  quan- 
tity of  pure  nitric  acid  a  few  drops  of  the  fuming  acid,  or  by  heating  the 
pure  acid  for  a  short  time  with  a  splinter  of  wood.  The  continuous  oxida- 
tion of  the  biliary  coloring  matter  will  then  produce  at  the  point  of  contact 
of  the  urine  and  acid  the  characteristic  green  zone  of  biliverdin  which, 
upon  allowing  the  test-tube  to  stand,  is  gradually  disseminated  upward  and 
is  subsequently  followed  by  a  ring  of  blue,  violet,  red  and  yellow,  which 
slowly  rises. 

325 


326  JAUNDICE  AND  HEPATIC   INSUFFICIENCY 

Even  with  a  great  dilution  of  the  urine,  these  bands  of  color  may  be 
distinctly  seen  if  the  test-tube  is  held  against  a  moist  piece  of  filter  paper 
or  a  plate  of  ground  glass  and  examined  in  a  clear  light. 

If  we  put  a  drop  of  nitric  acid  upon  the  filter  paper  through  which 
the  urine  has  been  filtered,  the  characteristic  colors  will  develop  in  con- 
centric rings.  By  adding  chloroform  to  some  of  the  urine  in  a  test-tube 
a  yellow  color  is  produced.  We  may  also  obtain  the  Gmelin  reaction 
with  chloroform  extract  by  adding  commercial  nitric  acid  or  bromin 
water. 

The  method  proposed  by  Marechal  and  Rosin,  of  covering  the  urine 
with  a  dilute  tincture  of  iodin,  will  also  produce  at  the  point  of  contact 
a  play  of  greenish  colors  which  denotes  the  presence  of  biliary  coloring 
matter. 

Besides  biliary  coloring  matter  other  constituents  of  the  bile  are  cer- 
tainly contained  in  the  urine,  chiefly  hile  acids.  Complicated  chemical 
methods  are  necessary  to  isolate  these  by  Pettenkofer's  test. 

The  urinary  sediment  obtained  by  centrifugation  shows  under  the  mi- 
croscope hyaline  casts  which,  in  the  case  to  be  described,  were  stained 
a  distinct  yellow.  The  presence  of  albumin  in  this  urine  could  not  be 
demonstrated  by  ordinary  reagents,  nor  was  sugar  present. 

The  overflooding  of  the  organism  with  biliary  coloring  matter  is  be- 
trayed also  by  the  intense  yellow  staining  of  the  blood  serum,  which  may 
be  recognized  in  a  thin  layer  of  the  blood  in  a  glass  capillary  pipette,  par- 
ticularly on  comparison  with  normal  blood  serum.  In  the  patient  under 
observation  the  blood  was  obtained  by  means  of  a  capillary  pipette  after 
pricking  the  lobe  of  the  ear,  and  a  Gruber-Widal  agglutination  test  was 
made  with  serum  which  was  negative  in  typhoid  cultures  as  well  as  in 
those  of  paratyphoid. 

The  serum  may  also  be  tested  by  Gmelin's  method.  With  nitric  acid, 
characteristic  colored  rings  will  be  observed  at  the  point  of  contact  with 
the  precipitated  albumin. 

In  tlie  case  under  consideration  this  accumulation  of  biliary  coloring 
matter  in  the  organism  was  coincident  with  the  absence  of  bile  from  the 
intestine.  The  peculiar,  whitish  gray  color  and  clayish  consistency  of  the 
feces  are  often  noticed  by  the  patient. 

Yet  such  appearance  in  normal  feces  is  not  proof  of  the  absence  of 
biliary  coloring  matter  or  its  reduction  products,  hydrobilirubin  and  uro- 
bilin. On  the  contrary,  it  is  demonstrable  that  the  grayish  white  color  is 
due  to  a  large  quantity  of  fats  and  soaps  in  the  dejecta.  Under  the 
microscope  we  may  discern  many  fat  globules  and  long  fatty  acid  crystals, 
also  a  large  number  of  fine  needles  of  sodium,  calcium  and  magnesium 
soaps.     These  soaps  give  to  the  feces  their  peculiar  glistening  appearance. 

If  the  feces  are  rendered  acid  by  an  addition  of  acetic  acid,  and  are 
then  shaken  up  with  alcohol  and  ether,  many  of  these  colorless  masses 


JAUNDICE  327 

may  be  dissolved,  after  which  the  residue  shows  a  dark  brown  discolora- 
tion due  to  the  undigested  remains  of  meat.  Neither  bilirubin  nor  uro- 
bilin can  be  demonstrated  in  the  pale  yellow  ethereal  extract,  and,  in 
fact,  an  occlusion  of  bile  from  the  intestine  may  be  assumed. 

The  abnormally  large  amount  of  fat  in  the  feces  is  unquestionably  the 
consequence  of  absence  of  bile  from  the  intestine,  although  it  is  possible 
that  an  obstruction  to  the  flow  of  the  pancreatic  juice  may  be  simultane- 
ously operative. 

The  constipation  and  flatulence  of  which  the  patients  complain  must 
be  referred  to  an  inhibition  to  the  flow  of  bile.  Primarily,  the  normal 
stimulation  of  intestinal  peristalsis  by  the  bile  is  lacking. 

Whether  the  absence  of  the  inhibitive  effect  of  bile  upon  decomposition 
may  be  regarded  as  the  cause  of  the  marked  production  of  gas  and  the 
somewhat  unusual  odor  of  the  feces  is  questionable.  Bidder  and  Schmidt 
have  assumed  that  the  bile  exerts  an  influence  upon  intestinal  decomposi- 
tion. Nevertheless  there  can  be  no  doubt  that  the  bile  itself  may  readily 
decompose,  and  it  certainly  exerts  no  powerful  antiseptic  effect.  Yet  we 
may  reasonably  suppose  that  the  absence  of  bile  from  the  intestine  favors 
the  development  of  certain  varieties  of  bacteria,  and  thus  diverts  the 
processes  of  decomposition  into  definite  tracts.  It  may  be  that  the  altera- 
tion in  the  composition  of  the  intestinal  contents  from  the  lack  of  bile, 
for  instance,  the  greater  proportion  of  fat,  is  the  sole  cause  of  the  abnormal 
processes  of  decomposition  in  the  intestine. 

The  probability  that  increased  decomposition  may  occasionally  result 
from  biliary  occlusion  is  favored  by  the  increased  excretion  of  ethyl  sul- 
phuric acid  in  the  urine  which  has  been  noted  by  various  authors  (Brieger, 
Biernacki,  Eiger,  Schmidt,  Bohm).  But  this  is  apparently  not  an  invari- 
able finding,  since  other  investigators,  such  as  Eohmann,  Pott,  and  v. 
Noorden,  found  no  marked  variation  from  the  normal  in  the  ethyl  sul- 
phuric acid  contents  of  the  urine  in  jaundice. 

The  symptom-complex  of  jaundice  is  met  with  in  very  unlike  but  more 
or  less  serious  affections:  In  occlusion  of  the  biliary  passages  from  gall- 
stones, in  neoplasms  of  the  biliary  channels  and  in  the  head  of  the  pan- 
creas, in  various  cases  of  diffused  and  circumscribed  disease  of  the  liver, 
especially  in  certain  forms  of  hepatic  cirrhosis.  Icteroid  discoloration  of 
the  skin  and  mucous  membranes  of  less  intensity  is  observed  in  other 
affections,  in  general  circulatory  disturbances,  in  those  produced  by  dis- 
ease of  the  heart,  in  some  cases  of  pneumonia,  in  general  sepsis,  and  in 
other  infectious  diseases.  In  all  of  these  cases  jaundice  appears  only  as 
an  accompanying  symptom  in  contradistinction  to  the  typical  symptoms 
of  the  disease  by  which  we  determine  the  character  of  the  affection  and  its 
probable  course. 

The  circumstances  are  different  in  the  case  under  consideration.  Here 
markedly  developed  icterus  dominates  the  entire  clinical  picture,  and  forms 


328  JAUNDICE  AND  HEPATIC   INSUFFICIENCY 

the  salient  feature  of  the  pathologic  condition.  Here  we  are  dealing  with 
simple  essential  jaundice,  with  icterus  simplex. 

This  diagnosis  corresponds  with  what  we  glean  from  the  history  of 
(lie  following  case:  The  patient,  a  strong  man,  26  years  of  age,  and  pre- 
viously healthy,  states  that  about  fourteen  days  ago  upon  the  occasion  of 
a  festivity  he  suffered  from  a  stomach  disturbance.  The  symptoms  which 
appeared  within  the  next  few  days  did  not,  as  on  similar  occasions,  soon 
pass  away,  but  continued;  a  sense  of  discomfort  in  the  gastric  region,  a 
disagreeable  taste,  loss  of  appetite,  a  tendency  to  nausea,  as  well  as  general 
nuilaise,  lassitude,  psychical  depression,  headache,  and  mild  vertigo  per- 
sisted. At  first  there  was  some  fever,  also  slight  diarrhea  followed  by 
constipation,  but  no  colicky  pain.  After  about  a  week  the  yellowness  of 
the  patient  became  noticeable  to  those  about  him.  Subsequently  he  re- 
iiH'inbcrod  that  his  urine,  even  for  a  few  days  before,  was  extremely  dark 
and  bad  stained  his  linen  yellow.  Until  the  present  time  the  patient  has 
been  able  to  follow  his  occupation,  but  has  felt  very  weak  and  has  emaci- 
ated decidedly.  Solid  food,  particularly  fatty  food,  has  been  repugnant 
to  him,  but  he  has  had  increased  thirst  and  a  special  desire  for  cool  and 
acid  drinks. 

l^'urther  examination  revealed  no  marked  change  except  the  jaundice; 
a  ft'w  scratches  upon  the  skin  showed  that  the  patient  was  annoyed  by 
itching.  There  was  no  elevation  of  the  temperature,  which  was,  on  the 
contrary,  somewhat  subnormal,  97°-98.1°  F. ;  the  pulse  was  slow,  64  to  68. 
'^^riiero  was  nothing  abnormal  in  the  thoracic  organs.  The  abdomen  was 
slightly  distended,  the  hepatic  region  somewhat  sensitive  to  pressure.  The 
liver  showed  some  enlargement  just  below  the  border  of  the  ribs,  but  was 
not  particularly  hard  to  the  touch.  The  gall-bladder  could  be  distinctly 
pal])ated  below  the  border  of  the  liver,  and  apparently  was  slightly  dis- 
tended. Splenic  dulness  seemed  somewhat  increased,  but  the  spleen  could 
not  be  palpated. 

We  therefore  recognized  the  clinical  condition  known  as  "  catarrhal " 
jaundice,  which  in  typical  cases,  as  a  rule,  runs  a  benign  course. 

^^'c  have  refrained  from  the  use  of  this  designation  because,  in  its 
conception,  a  definite  mode  of  development  of  the  jaundice  has  been 
assumed,  and  this  has  by  no  means  been  proven  in  all  cases.  The  term 
is  based  on  the  assumption  that  the  jaundice  is  caused  by  a  catarrhal  in- 
(1am  mat  ion  of  the  mucous  membrane  of  the  gall-ducts,  or  of  the  duodenum 
at  the  mouth  of  the  gall-ducts,  which  mechanically  inhibits  the  outflow 
of  bile.  The  finding  of  a  plug  of  colorless  mucus  at  the  mouth  of  the 
common  bile  duct  and  the  difficulty  of  forcing  the  contents  of  the  gall- 
hhiddcr  into  the  intestine  by  pressure  have,  since  the  time  of  Virchow, 
l)('cii   icgarded  as  the  anatomical  foundation  for  this  view. 

To-day  the  plug  of  mucus  is  no  longer  considered  to  be  the  actual  ob- 
struction to  the  flow  of  bile.     From  the  evident  lack  of  biliary  imbibition 


JAUNDICE  329 

which  the  mucus  reveals,  we  conclude  that,  at  most,  there  was  an  actual 
impediment  to  the  flow  of  bile  during  life.  The  mechanical  obstruction 
is  revealed  by  the  inspissation  of  the  bile  itself  as  well  as  by  the  catarrhal 
swelling  of  the  mucous  membrane  in  the  narrow  biliary  passages.  It  is 
true  that  little  of  this  swelling  is  to  be  seen  at  the  autopsy,  but  the  observa- 
tions of  those  who  have  inspected  the  mucous  membranes  during  life  have 
taught  us  that  swelling,  due  to  marked  hyperemia,  is  not  recognizable 
after  death. 

Nevertheless,  this  assumption  does  not  sufiBciently  explain  the  develop- 
ment of  jaundice  in  all  of  the  cases  which  are  included  under  the  term 
catarrhal  jaundice;  at  least,  it  does  not  coincide  with  our  ideas  of  catarrh 
of  the  biliary  passages,  of  cholangitis  catarrhalis.  The  symptoms  of  such 
a  cholangitis  are  often  found  in  cases  in  which  icterus  was  never  present, 
and  are  frequently  absent  when  the  clinical  picture  exactly  corresponds  to 
essential  jaundice. 

It  is  true  there  are  few  opportunities  for  the  anatomical  investigation 
of  typical  cases  of  this  affection,  since,  as  a  rule,  their  course  is  benign. 
But  their  purely  clinical  investigation,  the  nature  of  their  appearance, 
their  frequent  occurrence  under  certain  conditions,  their  relation  to  other 
forms  of  jaundice  and  to  diseases  of  the  liver  and  biliary  passages,  taken 
in  connection  with  the  results  of  experimental,  physiologic  and  pathologic 
investigation,  have  recently  led  to  other  hypotheses  which,  although  by 
no  means  clear,  are  in  many  respects  far  in  advance  of  earlier  conceptions. 

This  change  of  view  not  only  embraces  the  nosologic  position  of  this 
special  form  of  jaundice  but  also  explains  the  processes  brought  about  in 
these  cases  by  the  transference  of  biliary  constituents  into  the  blood  and 
the  fluids  of  the  tissues. 

ORIGIN 

Before  discussing  further  the  subject  of  jaundice,  we  must  express  our 
present  opinions  in  regard  to  the  development  of  jaundice  in  general. 

At  this  time  we  may  maintain  that  all  jaundice  is  of  hepatogenous 
origin,  i.  e.,  that  general  jaundice  cannot  occur  without  an  implication 
of  the  liver.  Every  case  of  jaundice,  therefore,  is  due  to  absorption  of 
hile  which  is  formed  in  the  liver. 

The  old  teaching  of  "  obstructive  jaundice/'  the  development  of  jaun- 
dice by  an  inhibited  excretion  of  coloring  matter  formed  outside  of  the 
liver  and  which  can  be  regarded  only  as  an  excretion  product,  has  been 
completely  disproven  by  the  investigations  of  Stern,  Naunyn  and  Min- 
kowski. But  the  opinion  also  that  the  icterus  in  "  hematogenous "  jaun- 
dice is  "  anhepatogenous  "  is  no  longer  tenable.  There  can  be  no  doubt 
that  hematoidin  (or  bilirubin)  may  be  formed  from  hemoglobin  outside 
the  liver,  for  example,  in  extravasations  of  blood.  It  is  also  certain  that 
processes  which  run  their  course  with  a  massive  dissolution  of  red  blood- 


330  JAUNDICE   AND  HEPATIC   INSUFFICIENCY 

corpuscles  and  an  increased  destruction  of  hemoglobin  may  lead  to  jaun- 
dice, but  in  such  cases,  as  in  hemoglobinemia  after  poisoning  with  arseni- 
iireted  hydrogen,  toluilendiamin  and  other  poisons,  the  transformation  of 
liemoo-lobin  into  biliary  coloring  matter  takes  place  in  the  liver  (Stadel- 
mann  Affanassiew),  and  its  presence  there  causes  the  outbreak  of  jaundice 
(N^aunyn  and  Minkowski).  The  latest  observations  of  loannovics  do  not 
alter  the  fact  that  by  hemolysis  the  spleen  plays  an  especial  role  in  the 
production  of  jaundice,  since  this  organ  is  actively  implicated  in  the  de- 
struction of  damaged  blood-corpuscles.  The  designation  of  such  forms  of 
jaundice  as  "  hematogenous  "  or  "  hematohepatogenous  "  is  even  less  justi- 
fiable, as  the  material  for  the  production  of  biliary  coloring  matter  is 
normally  furnished  by  the  hemoglobin.  If  we  desire  to  indicate  the  special 
mode  of  development  of  this  form  of  jaundice,  the  designations  "  cythemo- 
lytic"  and  "hemolytic"  are  certainly  preferable. 

The  most  likely  cause  for  the  absorption  of  bile  in  the  liver  is  a 
iiuH'hanical  impediment  to  the  flow  of  bile  in  the  biliary  passages.  There- 
fore, in  all  cases  of  jaundice  an  attempt  should  first  be  made  to  ascertain 
the  nature  of  this  mechanical  obstruction.  Naturally  it  is  easy  to  assume 
a  "  stasis  icterus "  when  either  the  lumen  of  one  of  the  large  biliary 
passages  is  occluded  or  there  is  external  compression  of  the  biliary  passages. 
When,  however,  the  impermeability  of  the  excretory  passages  cannot  be 
certainly  demonstrated,  more  or  less  hypothetical  explanations  of  the  ob- 
struction to  the  flow  of  bile  may  be  suggested.  The  fact  has  been  pointed 
out  that  the  secretory  pressure  of  the  bile  is  comparatively  low  (according 
to  Heidenhain  in  the  dog  about  200  mm.,  according  to  Biirker  in  the  rabbit 
75  to  80  mm.)  ;  therefore  even  a  slight  obstruction  to  the  flow  of  bile  is 
sufficient  to  cause  the  absorption  of  biliary  constituents  by  the  blood. 
Hence  it  was  believed,  as  has  been  stated,  that  the  development  of  simple 
jaundice  could  be  referred  to  catarrhal  swelling  of  the  mucous  membrane 
and  to  the  accumulation  of  mucus  at  the  mouth  of  the  common  bile  duct. 
Jaundice  in  infectious  diseases  was  attributed  to  complicating  intestinal 
catarrh  and  was  also  regarded  as  "  catarrhal."  When  jaundice  occurred 
in  pneumonia  it  was  assumed  that,  in  consequence  of  a  decrease  in  the 
respiratory  excursus  of  the  diaphragm,  an  important  adjunct  for  the  pro- 
pulsion of  bile  was  absent.  Jaundice  in  cardiac  disease  was  referred  to 
a  decrease  of  blood  pressure,  or  to  compression  of  the  finer  biliary  channels 
by  the  dilated  blood  capillaries.  In  the  case  of  icterus  neonatorum,  the 
condition  was  thought  to  be  due  to  the  altered  circulatory  relations  after 
birth,  to  a  patulous  ductus  arantii,  and  the  like.  Hepatic  cirrhosis  was 
at  one  time  attributed  to  a  compression  of  the  finest  interlobular  biliary 
channels  by  constricting  connective  tissue,  at  another  time  to  a  catarrhal 
affection  of  the  finest  biliary  passages  or  the  occlusion  of  their  lumen 
by  granular  pigmented  masses,  by  desquamated  and  swollen  epithelium 
and  the  like.     Some  authors  sought  for  the  explanation  of  the  obstruction 


JAUNDICE  331 

to  the  flow  of  bile  in  the  morphologic  changes,  the  swelling  and  displace- 
ment of  the  hepatic  cells,  and  the  "dislocation  of  the  hepatic  cell  tra- 
beculae/' 

"  Hemolytic "  jaundice  from  the  effect  of  blood  poisoning  was  first 
referred  by  Stadelmann  to  an  inspissation  of  the  bile  caused  by  the  in- 
creased destruction  of  blood-corpuscles  in  the  liver,  which  thus  formed 
coloring  matter.  Naunyn  and  Minkowski  therefore  employed  for  this  form 
of  jaundice  the  designation  "jaundice  from  polycholia"  and  Stadelmann 
proposed  as  a  more  concise  expression,  "  pleiochromia."  It  did  not  escape 
the  attention  of  these  authors  that  the  increased  formation  of  coloring 
matter  was  not  the  only  cause  of  the  obstruction  to  the  outflow  of  bile, 
but,  as  Stadelmann  emphasized,  besides  an  increased  secretion  of  mucus, 
the  occlusion  of  the  biliary  capillaries  with  decomposed  epithelia  and 
hepatic  cells  destroyed  by  the  poison  might  also  impede  the  outflow  of 
bile,  as  well  as,  perhaps,  the  compression  of  the  finer  biliary  passages  by 
swollen  glandular  cells  or  dilated  blood  capillaries  which  had  been  sub- 
jected to  toxic  influence. 

Although  a  conception  of  this  kind  relegated  "  polycholic  "  jaundice  to 
the  ranks  of  jaundice  due  to  mechanical  obstruction,  many  authors  have 
regarded  "polycholia"  as  a  welcome  adjunct  by  which  to  explain  the 
different  varieties  of  jaundice  whose  development  from  biliary  stasis  could 
otherwise  scarcely  be  proven.  Above  all,  icterus  neonatorum  was  ascribed 
to  a  suddenly  increased  formation  of  biliary  coloring  material  brought 
about  in  the  first  few  days  after  birth  (Hofmeier,  Silbermann,  Hayem) 
by  a  massive  destruction  of  the  red  blood-corpuscles.  The  development  of 
jaundice  from  polycholia  was  also  assumed  by  many  authors  (Rosenstein, 
Chauffard,  Girode,  Banti  and  others)  in  certain  forms  of  hepatic  cirrhosis 
as  well  as  in  the  different  varieties  of  "  infectious  "  jaundice.  This  was 
based  upon  the  observation  that  in  such  cases,  notwithstanding  the  jaundice, 
there  is  usually  an  intense  biliary  staining  of  the  feces,  Grawitz  found 
that  in  chronic  circulatory  disturbances  free  hemoglobin  was  demonstrable 
in  the  blood  serum;  he  therefore  believed  that  jaundice  in  cardiac  disease 
might  be  attributed  to  polycholia.  G.  Hoppe-Seyler  declared  icterus  in 
pneumonia  after  injections  of  tuberculin  and  in  Graves'  disease  to  be 
polycholic,  because  in  these  conditions  he  demonstrated  a  simultaneous 
increase  of  urobilin  in  the  urine  and  in  the  feces. 

In  those  forms  of  icterus  in  which  there  could  be  no  doubt  of  a  mechan- 
ical obstruction  to  the  flow  of  bile,  some  authors  went  so  far  as  to  ascribe 
the  jaundice  to  the  polycholia  which  caused  a  destruction  of  red  blood- 
corpuscles.  Browicz,  to  whom  we  are  indebted  for  very  valuable  investi- 
gations into  the  histology  of  the  liver,  attempted  to  prove  that  a  polycholia 
of  this  kind  was  the  foundation  of  all  forms  of  jaundice ;  even  in  occlusion 
of  the  common  bile  duct  he  believed  that  only  a  mediate  influence  upon  the 
development  of  jaundice  could  be  ascribed  to  the  mechanical  factor.    These 


332  JAUNDICE  AND  HEPATIC   INSUFFICIENCY 

theories,  however,  did  not  prove  satisfactory.  On  the  one  hand,  the  purely 
mechanical  explanations  were  incomplete.  In  some  cases  the  intensity  of 
the  jaundice  was  entirely  out  of  proportion  to  the  demonstrable  obstruc- 
tion ;  in  many  others,  no  obstruction  of  this  kind  could  be  determined,  and, 
finally,  in  the  liver  itself  signs  of  biliary  stasis  were  frequently  absent. 
Whon  these  siojns  were  present  there  was  undoubtedly  a  mechanical  ob- 
struction to  the  flow  of  bile:  Dilatation  and  flooding  of  the  biliary  passages, 
the  accumulation  of  bile  in  the  intralobular  bile  capillaries,  and  the  de- 
posit of  biliary  pigment  in  the  hepatic  cells.  On  the  other  hand,  the  mere 
assumption  of  polycholia  or  pleiochromia  did  not  sufficiently  explain  the 
entrance  of  bile  into  the  blood  and  into  the  fluids  of  the  tissues,  unless 
it  wore  assumed  that  occasionally  the  liver  ceased  to  excrete  bile  normally, 
wliile  at  the  same  time  bile  formation  was  increased. 

Thus  it  came  to  pass  in  the  last  few  years  that  a  new  view  received 
recognition  and  a  new  factor  entered  into  the  pathogenesis  of  icterus;  for 
an  attempt  was  made  to  attribute  the  appearance  of  biliary  constituents 
in  the  1)1  ood  to  special  functional  disturbances  of  the  hepatic  cells. 

1  was  probal)ly  the  first  definitely  to  express  this  thought,  for  in  a 
discussion  at  the  Congress  of  Internal  Medicine  in  1892  I  made  the  fol- 
lowing remarks:  "The  special  function  of  the  hepatic  cell,  which  enables 
it  to  introduce  certain  products  into  the  bile  channels,  others  into  the 
l)lo<)d-vesse]s  or  lymph  channels — ^therefore  biliary  coloring  matter  and  bile 
acids  into  the  biliary  passages,  and  sugar  and  urea  into  the  blood — is  appar- 
ently dependent  upon  the  normal  nutrition  and  normal  function  of  the 
cell  itself.  Disturbances  of  this  function  may  exist  without  mechanical 
hindrance  to  the  outflow  of  bile,  and  may  result  in  the  transmission  of 
biliary  constituents  to  the  blood."  I  compared  the  disturbance  in  func- 
tion of  the  hepatic  cells  here  described  with  the  disturbance  in.  function 
of  the  renal  cells  which  occurs  in  albuminuria,  and  pointed  to  the  analo- 
gous ap])earance  of  these  forms  of  disturbance  in  infectious  diseases,  in 
intoxications,  in  lesions  of  the  nervous  system,  in  circulatory  disturbances, 
and  in  parenchymatous  implication  of  the  organs. 

Liebermeister  followed  a  similar  train  of  thought  when,  a  year  later, 
lie  described  "  acathectic  "  jaundice,  which  was  said  to  be  due  either  to  a 
marked  change  in  the  liver  cells  or  because  in  the  process  of  destruction 
they  could  no  longer  retain  the  bile  or  hinder  its  diffusion  into  the  blood 
and  lymph.  Later  E.  Pick  voiced  the  same  opinion  when  he  declared 
most  varieties  of  jaundice  to  be  essentially  due  to  "  paracholia/'  a  disturb- 
ance of  the  flow  of  bile  in  a  much  more  general  form.  For  the  cases 
under  consideration  I  proposed  the  designation  " parapedesis  of  bile"  in 
(liirerentiating  the  close  analogy  with  hemorrhage  per  rhexin  and  per 
(liapedesin,  also  jaundice  "per  stasin  "  and  "per  parapedesin." 

Absolute  proof  of  this  origin  of  jaundice  is  extremely  difficult  to  ob- 
tain.    But  this  hypothesis  offered  not  only  a  plausible  interpretation  of 


JAUNDICE  333 

those  forms  of  jaundice  in  particular  for  which  former  explanations  were 
unsatisfactory,  but  it  coincided  with  many  other  common  pathologic  hy- 
potheses. It  was  unnecessary  to  combine  mysterious  "  vitalistic "  ideas 
with  the  theory  of  such  a  "  special  functional  disturbance  "  of  the  hepatic 
cells  as  might  lead  to  the  excretion  of  their  products  of  secretion  in  ab- 
normal directions.  We  know  that  nutritive  disturbances  and  pathologic 
changes  of  the  cells  not  only  modify  the  physical  and  chemical  processes 
which  occur  in  glandular  secretion,  but  the  function  of  the  cells  as  '*  semi- 
permeable membranes  "  may  be  so  altered  as  to  permit  the  passage  of  mole- 
cules which  cannot  pass  through  the  normal  cell.  And  particularly  in 
those  varieties  of  jaundice  in  which  this  explanation  seemed  necessary — 
jaundice  in  infectious  diseases  and  intoxications,  in  circulatory  conditions 
and  in  disturbances  of  innervation — such  a  damage  to  the  function  of  the 
cell  might,  doubtless,  readily  be  supposed.  Added  to  this,  the  histologic 
researches  of  Nauwerck  and  Fraser,  Browicz,  and  Szubinski  afforded  an 
anatomical  basis  for  the  assumption  of  an  irregular,  intracellular  exchange 
of  the  different  products  of  the  hepatic  function. 

Thus  the  teaching  of  parapedesis  of  bile  soon  found  general  accept- 
ance. Some  authors  went  so  far  as  to  emphasize  the  disturbed  function 
of  the  liver  in  all  forms  of  jaundice,  and  attached  little  importance  to  the 
mechanical  factor  in  biliary  stasis,  particularly  in  the  jaundice  occurring 
in  cholelithiasis  which  was  formerly  regarded  as  the  type  of  obstructive 
jaundice. 

Conflicting  opinions  were  not  lacking.  First,  D.  Gerhardt  opposed  the 
view  that  in  the  genesis  of  simple  stasis  icterus  the  main  point  was  the 
abnormal  direction  of  the  cell  secretion.  Subsequently  Hans  Eppinger 
attempted  to  overthrow  the  entire  principle  of  parapedesis  of  bile  because, 
by  painstaking  anatomical  investigations,  he  determined  the  factor  of 
biliary  stasis  to  be  of  much  greater  significance. 

Eppinger  devised  a  method  of  staining  by  means  of  which  all  the 
processes  of  the  interacinous  biliary  capillaries  were  made  distinctly  visible, 
and  he  employed  this  method  not  only  to  determine  the  normal  course 
of  these  biliary  capillaries  between  the  hepatic  cells  and  their  entrance  into 
the  liver  cells,  even  in  the  human  liver,  but  also  to  test  the  action  of  the 
biliary  capillaries  in  the  different  forms  of  jaundice.  He  observed  first 
that  in  pure  mechanical  stasis  icterus — after  tying  the  hepatic  duct — the 
accumulation  of  bile  in  the  biliary  passages  led  to  dilatation,  tortuosity, 
lengthening  and  varicose  distention  of  the  intracellular  biliary  passages 
until  they  finally  ruptured  and  their  contents  submerged  the  perivascular 
lymph  spaces.  Later  he  found  the  same  dilatation  and  rupture  of  the 
interacinous  biliary  capillaries  in  those  eases  in  which  jaundice  was  due 
to  hepatic  cirrhosis,  poisoning  from  phosphorus,  or  from  circulatory  dis- 
turbances. He  believed,  therefore,  that  these  cases  could  only  be  regarded 
as  special   forms  of  mechanical  stasis  icterus.     The  obstruction  to   the 


334  JAUNDICE  AND  HEPATIC   INSUFFICIENCY 

outflow  of  bile  was,  however,  not  in  the  large  bile  ducts  but  in  their  finest 
branches,  which,  as  in  the  case  of  hepatic  cirrhosis,  either  were  compressed 
by  ])rol  if  crating  connective  tissue  or,  as  in  the  case  of  toxic  and  cyanotic 
jaundice,  by  coagulated  masses  of  bile,  by  "  hilmry  thrombi." 

Investigations  similar  to  those  of  Eppinger  have  recently  been  made 
by  Abramow  and  Samoilowicz,  who,  in  the  main,  confirm '  the  former's 
results.  These  authors  also  assume,  as  an  absolute  prerequisite  for  the 
development  of  jaundice,  a  free  flow  of  bile  in  the  perivascular  lymph 
spaces. 

Elsewhere  I  recently  criticized  Eppinger's  views,  and  especially  empha- 
sized the  fact  that,  in  judging  such  conditions,  the  interchange  of  material 
occurring  in  the  organism  could  by  no  means  be  gauged  by  morphologic 
observations  alone.  The  appearance  of  the  previously  mentioned  biliary 
thrombi  proves  that  the  secretion  of  the  liver  is  no  longer  of  normal 
composition,  and  that  abnormal  processes  of  secretion  have  already  taken 
place  in  the  hepatic  cells.  We  know  that  in  certain  maladies,  especially 
in  infectious  diseases  of  the  liver,  the  bile  may  contain  albumin.  But  in 
these  cases  especially,  notwithstanding  an  existing  jaundice,  we  frequently 
fail  to  find  in  the  liver  any  signs  of  biliary  stasis,  even  upon  minute 
microscopic  examination.  Deposits  of  "  coagulated  bile,"  of  precipitates 
of  biliary  coloring  matter  in  the  intracellular  biliary  capillaries  and  within 
the  hej)atic  cells  themselves,  are  not  found  in  cases  of  recent  jaundice  but 
only  when  this  has  existed  for  considerable  time.  They  are  not  the  cause 
of  jaundice,  but  the  consequence  of  functional  disturbance  of  the  hepatic 
cells  leading  to  jaundice.  Biliary  thrombi  are,  at  most,  to  be  regarded 
as  predisposing  factors  for  the  transference  of  biliary  constituents  into  the 
blood  or  the  lymph,  just  as  the  occlusion  of  the  uriniferous  tubules  by 
urinary  casts  is  regarded  merely  as  a  predisposing  factor  for  a  functional 
disturbance  of  the  renal  capillaries  which  usually  causes  the  retention  of 
urinary  substances. 

For  the  present,  notwithstanding  these  objections,  I  believe  it  justifi- 
able to  maintain  the  importance  of  an  abnormal  direction  of  the  hepatic 
secretion  in  the  transference  of  biliary  constituents  into  the  blood,  and  I 
therefore  briefly  define  the  pathogenesis  of  jaundice  as  follows: 

General  jaundice  develops  only  from  the  absorption  of  bile  within 
the  liver. 

The  absorption  of  bile  may  be  due  to  the  following  causes: 

1.  An  obstruction  of  the  biliary  passages  which  inhibits  the  outflow  of 
hile  (stasis  icterus,  icterus  per  stasin). 

2.  A  disturbance  in  the  function  of  the  hepatic  cells  which  results  in 
the  excretion  of  biliary  constituents  in  an  abnormal  direction  (diffusion 
icterus,  icterus  per  parapedesin) . 

Xaturally  no  sharp  differentiation  of  these  forms  of  jaundice  according 
to  their  mode  of  development  can  be  made,  since  both  factors  may  be,  and 


JAUNDICE  •  335 

usually  are,  combined:  Mechanical  stasis  of  bile  leads  to  injury  of  the 
hepatic  cells  which  results  in  a  disturbance  of  their  secretory  function. 
And  any  damage  of  the  hepatic  cells  may  be  followed  by  a  mechanical 
obstruction  to  the  flow  of  bile,  either  because  the  lesion  may  at  the  same 
time  affect  the  mucous  membrane  of  the  intestine  or  of  the  biliary  passages, 
and  hence  obstruct  the  flow  of  bile,  or  because  from  the  pathologically 
altered  consistence  of  the  bile  its  outflow  becomes  difficult,  or  because  the 
finer  biliary  passages  are  occluded  by  a  swelling  of  the  hepatic  cells,  by 
dislocation  of  the  hepatic  cell  trabeculae,  by  connective  tissue  proliferation, 
or  by  biliary  thrombi. 

In  the  incipient  stages,  as  a  rule,  one  or  the  other  factor  preponder- 
ates, and  promotes  the  development  of  jaundice: 

Mechanical  obstruction  comes  into  question  in  the  following  conditions : 

(a)  In  occlusion  of  the  lumen  of  the  biliary  channels  by  gall-stones 
or  foreign  bodies  entering  from  the  intestine  (fruit  kernels,  thread  worms, 
distoma,  and  the  like),  by  neoplasms  and  cicatricial  strictures; 

(b)  In  external  compression  of  the  biliary  channels  by  tumors  which 
originate  in  the  stomach,  the  intestine,  the  head  of  the  pancreas,  the 
peritoneum,  the  portal  lymph-glands,  in  the  gall-bladder  or  the  liver  itself; 
by  perihepatic  bands,  by  floating  kidneys,  by  aneurysms  of  the  abdominal 
aorta,  of  the  celiac  axis,  the  hepatic  artery  or  the  superior  mesenteric 
artery,  in  rare  cases  even  by  tumors  of  the  uterus  and  ovaries,  or  by  the 
impaction  of  fecal  masses  in  the  right  flexure  of  the  colon. 

Functional  disturbances  of  the  hepatic  cells  promote  the  development 
of  jaundice: 

(a)  In  a  disturbance  of  the  circulation  of  the  blood  in  the  liver  due 
to  cardiac  disease,  thrombosis  of  the  portal  vein,  etc.; 

(b)  In  disturbances  of  innervation  of  the  liver,  as,  for  example,  in 
icterus  following  psychical  emotion,  icterus  ex  emotione; 

(c)  From  the  effect  of  poisons  (phosphorus,  arseniureted  hydrogen, 
and  others)  and  toxic  bacterial  products  introduced  with  tainted  food 
(ptomains)  or  those  formed  in  the  organism  in  infectious  diseases  (toxins), 
in  pneumonia,  septicemia,  relapsing  fever,  bilious  typhoid,  yellow  fever, 
syphilis,  and  the  like. 

SYMPTOMS 

We  have  seen  that  the  most  diverse  constitutional  diseases  and  the 
most  dissimilar  affections  of  the  liver  and  other  organs  may  lead,  in  one 
or  the  other  of  the  modes  here  described,  or  in  both  simultaneously,  to  the 
symptom-complex  of  jaundice.  The  importance  of  the  jaundice  in  the 
conception  of  the  pathologic  condition  of  the  individual  case  varies,  ac- 
cording to  whether  this  symptom-complex  is  distinctly  developed  or  less 
so,  and  whether  the  symptoms  that  accompany  it — which  at  one  time 
may  be  due  to  the  systemic  disease,  at  other  times  to  a  change  in  the  liver 
23 


336  JAUl^DICE   AND   HEPATIC   INSUFFICIENCY 

or  to  a  simultaneous  affection  of  other  organs — become  more  or  less  promi- 
nent in  the  entire  clinical  picture.  In  many  cases  we.  regard  jaundice 
only  as  a  symptom  or  a  complication  of  another  pathologic  condition. 
In  others,  however,  jaundice  assumes  the  importance  of  a  substantive 
affection. 

It  is  not  always  possible  to  draw  a  sharp  line  of  demarcation  between 
this  substantive  form  of  jaundice  and  the  jaundice  which  occurs  in  organic 
disease  of  the  liver  or  the  infectious  processes  or  intoxications  which  lead 
to  jaundice. 

The  conditions  are  nowise  different  from  those  of  other  pathologic 
changes  produced  by  the  effect  of  various  deleterious  agents  in  the  organ- 
ism. Whether,  for  example,  in  the  individual  case,  we  speak  of  septic 
nepliritis,  myocarditis,  and  the  like,  or  of  sepsis  with  albuminuria  and 
cardiac  insufficiency,  depends  only  upon  the  prominent  implication  of  indi- 
vidual parts  of  the  organism  in  comparison  with  the  general  symptoms. 

From  this  point  of  view  we  can  readily  understand  that  the  numerous 
cases  of  simple  jaundice,  no  matter  how  characteristic  the  mode  of  their 
appearance  and  their  development,  can  by  no  means  always  be  regarded 
as  of  the  same  nature.  And,  on  the  other  hand,  it  immediately  becomes 
obvious  that  in  simple  jaundice,  from  the  benign  to  the  most  severe  forms, 
those  with  decided  constitutional  affection  and  very  marked  changes  in 
the  liver,  icterus  gravis  and  icterus  infectiosus,  tliere  is  every  possible 
transitional  stage.  In  one  instance  various  factors  may  act  conjointly 
upon  the  liver  and  the  biliary  passages  so  that  the  symptoms  of  simple 
jaundice  are  produced.  In  another,  the  same  cause  may  generate  effects 
of  varying  intensity  so  that  at  one  time  serious,  at  other  times  mild, 
affections  result. 

The  milder  cases  of  simple  jaundice,  as  already  stated,  are  included 
under  the  conception  of  "  catarrhal "  jaundice.  In  fact,  catarrhal  cholan- 
gitis appears  to  be  the  primary  and  principal  anatomical  foundation  of  the 
pathologic  picture  which  has  been  described.  By  an  inflammation  of  the 
mucous  membrane  of  the  biliary  channels  and  an  increased  excretion  of 
mucus  this  cholangitis  may  obstruct  the  flow  of  bile,  and  thus  mechanically 
lead  to  stasis  icterus.^ 

Cholangitis,  like  all  inflammations  of  the  mucous  membrane,  may  be 
produced  by  toxic  or  infectious  processes  of  any  kind.  Deleterious  products 
may  enter  the  bile  from  the  hlood,  may  pass  through  the  liver  into  the 
biliary  passages,  or  enter  into  the  biliary  channels  from  the  intestine.  In 
the  case  first  mentioned,  secondary  infection  may  play  a  great  role  by  the 
entrance  of  bacteria  from  the  intestine. 

But,  as  has  been  stated,  the  theory  that  jaundice  originates  from  the 


'  In  a  case  of  catarrhal  jaundice,  Kiraura  estimated  the  viscosity  of  the  bile  at 
58.24  in  comparison  with  a  normal  viscosity  of  13.21. 


JAUNDICE  337 

mechanical  effects  of  a  catarrh  of  the  mucous  membrane  has  shown  itself 
to  be  unsatisfactory.  Here,  too,  we  must  allude  to  the  possibility  that 
cholangitis  may  be  the  cause  as  well  as  the  consequence  of  biliary 
stasis. 

It  is  true  we  know  that  bile  is  sometimes  neither  aseptic  nor  sterile, 
but,  under  normal  circumstances,  it  certainly  contains  but  few  bacteria 
and  these  are  non-pathogenic.  The  narrow  mouth  of  the  common  bile 
duct,  which  is  frequently  washed  by  the  flow  of  bile,  prevents  the  ingress 
and  development  of  microorganisms  from  the  intestine. 

As  soon  as  the  outflow  of  bile  is  impeded,  the  bile  duct  may  be  in- 
vaded from  the  intestine  by  the  most  varied  pathogenic  microbes :  The 
bacterium  coli,  the  different  varieties  of  proteus,  staphylococci,  streptococci, 
pneumococci,  typhoid  bacilli  and  others,  penetrate  into  the  bile  channels 
and  there  find  in  the  "  residual  bile  "  a  suitable  soil  for  their  development. 
Thus  any  check  to  the  outflow  of  hile  may  lead  to  infection  of  the  biliary 
passages  and  inflammatory  changes  in  its  mucous  membrane. 

Thus  all  mechanical  obstructions  of  the  biliary  passages,  whether  occlu- 
sion of  the  lumen  of  the  bile  ducts  or  their  compression  from  without, 
favor  the  production  of  cholangitis.  But  diseases  of  the  liver  which  lead 
to  a  disturbance  of  the  nutrition  and  function  of  the  hepatic  cells  may 
also  obstruct  the  flow  of  bile,  and  facilitate  the  development  of  cholangitis. 
As  a  matter  of  fact  we  frequently  find  cholangitis  to  be  a  complication  of 
the  most  varied  acute  and  chronic  forms  of  disease  of  the  liver  and  bile 
channels. 

This  complicating  cholangitis  increases  the  hindrance  to  the  propulsion 
of  bile  and  promotes  the  development  of  jaundice  in  the  diseases  we  have 
enumerated,  hence  Jaundice  in  gall-stones,  in  hepatic  cirrhosis,  and  the 
like,  has  usually  been  regarded  as  "  inflammatory,"  and  has  been  attributed 
to  a  complication  with  cholangitis. 

Of  late,  it  has  frequently  been  pointed  out  that  these  noxious  effects, 
toxic  and  infectious  influences,  which  we  consider  the  primal  cause  of 
cholangitis,  not  only  affect  the  mucous  membrane  of  the  intestine  and  the 
bile  channels  but  also  the  parenchyma  of  the  liver,  and,  therefore,  even 
in  simple  jaundice,  an  affection  of  the  hepatic  parenchyma  and  disturbance 
of  the  hepatic  cell  function  have  been  held  responsible  for  the  appearance 
of  the  clinical  symptoms. 

Some  authors,  among  them  Chauffard,  have  maintained  that  the  action 
of  poisons  which  are  introduced  with  the  food  or  which  develop  within 
the  digestive  tract  by  abnormal  fermentation  and  decomposition,  is  con- 
veyed to  the  liver  by  the  portal  vein.  Others,  such  as  Gilbert  and  Girode, 
Charrin  and  Roger,  attach  .the  greatest  significance  to  the  local  infection 
of  the  liver  by  the  ingress  of  bacteria  from  the  intestine.  Still  others, 
such  as  Botkin,  Kelsch,  and  Heitler,  in  these  cases  believe  only  in  a  general 
infection  which,  by  its  special  localization  in  the  liver  or  by  the  action 


338  JAUNDICE  AND  HEPATIC  INSUFFICIENCY 

of  the  toxins  which  the  organism  develops  in  the  liver,  brings  about  an 
obstruction  to  the  flow  of  bile. 

This  last  conception  found  a  firm  support  in  the  observation  of  cases 
of  jaundice,  which  are  on  the  increase,  in  which  the  action  of  the  infec- 
tious agent  betrayed  itself  simultaneously  in  the  clinical  course  of  the 
individual  case  and  in  the  epidemic  appearance  of  kindred  affections. 

Simple  jaundice,  as  we  may  perceive  from  the  history  previously  quoted, 
is  not  rarely  accompanied  by  more  or  less  well  developed  symptoms  of  a 
general  infection — fever,  enlargement  of  the  spleen,  albuminuria.  In  these 
cases  we  speak  of  "  infectious  jaundice."  In  the  mildest  cases  these  symp- 
toms of  general  infection  are  scarcely  perceptible  or  only  temporarily  so; 
often  they  appear  only  in  the  first  days  of  the  disease,  and  are  readily 
overlooked.  In  some  cases,  however,  they  become  much  more  noticeable 
as  the  disease  progresses,  and,  finally,  there  are  cases  which  run  their 
course  with  the  most  severe  symptoms  of  a  general  febrile  affection,  cases 
in  which  jaundice  is  merely  a  concomitant  phenomenon  of  the  entire 
pathologic  condition. 

Such  types,  the  severe  as  well  as  the  mild,  have  occasionally  appeared 
in  epidemics.  This  "  epidemic  jaundice  "  has  frequently  been  regarded  as 
a  special  specific  infectious  disease,  and  many  authors  have  attempted  to 
explain  isolated  cases  of  simple  jaundice  occurring  at  the  same  time  as 
"  sporadic  cases  "  of  this  infectious  disease. 

Numerous  observations  of  such  epidemics,  appearing  under  most  vary- 
ing circumstances,  have  been  reported.  These  observations,  however,  by 
no  means  confirm  the  view  that  the  disease  is  invariably  due  to  a  definite 
specific  pathogenic  agent.  It  is  true  that  for  the  development  of  the 
different  cases  occurring  in  a  single  epidemic  one  and  the  same  pathogenic 
agent  might  be  assumed  to  be  the  cause,  as,  for  instance,  in  those  epi- 
demics which  Liirmann  observed  in  Bremen  occurring  after  re-vaccination, 
or  those  which  Rizet  observed  in  soldiers  engaged  in  cleaning  the  moat 
of  a  fortress,  etc.  But  it  is  by  no  means  proven,  or  even  likely,  that  in 
these  epidemics  the  same  pathogenic  agent  was  always  operative.  Not 
only  have  the  bacteriologic  investigations  led  to  a  different  conclusion, 
but  all  which  has  been  learned  regarding  the  cause,  the  manner  of  dis- 
tribution, the  incubation  of  the  disease  in  the  various  epidemics,  is  opposed 
to  the  view  that  the  same  specific  pathogenic  agent  was  the  cause. 

Even  the  attempt  to  differentiate  from  the  numerous  cases  of  infec- 
tious jaundice  a  definite  group  characterized  by  a  peculiar  course  of  the 
disease  as  an  especial  infectious  disease,  the  so-called  "  Weil's  disease," 
lias  so  far  been  unsuccessful.^ 

In  the  year  1886  Weil  described  the  first  four  cases  of  a  peculiar  disease 
running  its  course  "  with  splenic  tumor,  jaundice  and  nephritis,"  which 

1  See  volume  "  Infectious  Diseases,"  page  808. 


JAUNDICE  339 

was  characterized  by  a  special  febrile  course  with  a  tendency  to  relapses; 
this  affection  was  subsequently  named  after  him.  Since  that  time  numer- 
ous publications  have  appeared  concerning  the  disease;  in  1901  Frankel 
collected  from  literature  no  less  than  150  cases.  Nevertheless,  even  to-day, 
the  views  regarding  the  nature  of  this  symptom-complex  are  wide  asunder. 
Some  authors,  such  as  Fiedler,  Neumann,  and  Miinzer,  share  Weil's  opinion 
that  it  is  a  special  infectious  disease  due  to  a  specific  pathogenic  agent. 
Many  others,  such  as  Brosch,  Cramer,  Stirl,  Pfuhl,  Frankel,  Nauwerck, 
Karlinsky,  and  Soupault,  assume  that  the  same  pathologic  picture  is  pro- 
duced by  various  causes,  and  that  the  cases  described  as  Weil's  disease 
have  masked  various  infectious  diseases  and  intoxications:  Enteric  fever 
and  relapsing  fever,  infectious  intestinal  catarrh,  tubercular  pericarditis, 
santonin  and  ptomain  poisoning  and  the  like,  and  many  others  which  have 
run  their  course  with  phenomena  resembling  Weil's  S3Tnptom-complex. 

During  an  epidemic  of  infectious  jaundice  in  the  year  1892  Jager 
isolated  a  special  microorganism,  the  pleomorphic  bacillus  proteus  fluores- 
cens,  which  he  regarded  as  the  pathogenic  agent.  The  specificity  of  this 
bacillus  was  doubted.  Yet  it  appears  to  be  a  fact  that  this  variety  of 
proteus  is  capable  of  producing  jaundice,  although  it  has  as  yet  by  no 
means  been  proven  that  a  definite  characteristic  course  of  the  disease  may 
be  attributed  to  the  action  of  this  special  bacillus. 

While  it  is  perhaps  true  that  many  isolated  cases  of  simple  jaundice 
may  be  referred  to  the  same  origin  as  cases  of  epidemic  jaundice — never- 
theless, the  former  need  not  be  regarded  as  sporadic  cases  of  a  well  marked 
infectious  disease,  but,  on  the  contrary,  even  in  these  a  very  different 
etiology  may  be  assigned  for  the  jaundice.^ 

Naturally  these  deleterious  agents  frequently  enter  the  stomach  and 
intestinal  canal  with  the  food,  and  develop  within  the  digestive  tract 
under  the  influence  of  abnormal  processes  of  decomposition  which  the 
ingesta  there  undergo.  This  enables  us  to  understand  why,  as  a  rule,  the 
symptoms  of  gastric  and  intestinal  catarrh  introduce  the  clinical  picture, 
and  why  the  development  of  jaundice  is  usually  referred  to  the  same  etio- 
logic  factors  which  we  are  accustomed  to  regard  as  the  causes  of  gastric 
and  intestinal  catarrhs:  The  immoderate  consumption  of  food,  the  inges- 
tion of  food  difficult  to  digest  or  that  is  tainted,  of  food  too  cold  or  too 
hot,  the  abuse  of  alcohol,  refrigeration,  infections  and  intoxications. 

1  From  this  point  of  view  the  recent  contradictory  reports  regarding  the  agglu- 
tinating properties  of  the  blood  serum  of  patients  with  jaundice  may  possibly  be 
understood.  Among  the  cases  of  jaundice  many  are  due  to  an  infection  with  typhoid 
bacilli  or  other  closely  related  varieties  of  bacteria. 


I 


340  JAUNDICE   AND  HEPATIC   INSUFFICIENCY 

HEPATIC    INSUFFICIENCY 

The  action  of  various  deleterious  agents  upon  the  liver  does  not  limit 
itself  to  a  mere  disturbance  of  the  excretion  of  bile.  Other  functions 
of  the  liver  also  may  be  impaired  to  greater  or  less  extent  by  the  same 
pathologic  causes,  and  hepatic  insufficiency  may  be  added  to  the  jaundice. 

The  disturbance  of  other  functions  of  the  liver  is  not  so  obvious  as 
the  obstruction  to  the  flow  of  bile  which  causes  jaundice.  Numerous  physi- 
ologic investigations  have  revealed  to  us  much  concerning  the  multiplicity 
of  the  functions  of  the  liver,  not  only  regarding  the  processes  by  which 
the  biliary  constituents  are  produced,  but  also  relative  to  the  part  which 
the  liver  plays  in  the  metabolism  of  the  most  important  foods  and  con- 
stituents of  the  body,  the  carbohydrates,  fats,  and  proteids.  Endeavors  to 
investigate  the  disturbance  of  these  functions  by  experimental  pathologic 
means  have  not  been  lacking.  But  in  diseases  of  the  liver  we  are  as  yet 
not  in  position  to  trace  these  disturbances  in  individual  organs. 

•  As  the  secretion  of  the  liver  is  insusceptible  to  direct  investigation 
except  in  certain  exceptional  instances,  such  as  biliary  fistula,  we  are 
unable  to  frame  a  positive  opinion  as  to  the  quantitative  and  qualitative 
changes  in  bile  production.  Studies  of  the  human  gall-bladder,  such  as 
were  recently  published  by  Tokuye  Kimura,  only  prove  primarily  that  in 
pathologic  lesions  there  are  marked  differences  in  the  condition  of  the 
bile.  No  definite  idea  can  be  obtained  from  these  investigations  in  regard 
to  the  secretion  of  bile,  for  here,  among  other  variations,  the  secretion  of 
the  mucous  membrane  of  the  gall-bladder  as  well  as  the  inspissation  and 
decomposition  of  the  bile  in  the  gall-bladder  must  be  considered. 

For  the  time  being  we  know  only  that  a  decrease  in  the  production 
of  bile,  a  hypocholia  or  oligocholia,  occurs  in  various  diseases  of  the 
liver  and,  as  a  rule,  also  in  consequence  of  prolonged  obstruction  to  the 
flow  of  bile,  and  that  an  increased  production  of  bile  or  biliary  coloring 
matter,  a.  polychoUa  or  pleiochromia,  may  appear  after  the  addition  of 
l)iliary  constituents  or  after  the  effect  of  poisons  which  produce  dissolu- 
tion of  blood-corpuscles* 

Whether  the  production  of  urobilin  instead  of  bilirubin  and  uroHU- 
nuria  may  be  regarded  as  the:  expression  of  a  disturbed  function  of  the 
liver  is  still  a  mooted  question;  In  most  cases  the  urobilin  excreted  in 
the  urine  is  of  enterogenous,  origin,  .and  develops  from  the  reduction  of 
liilirubin  in  intestinal  decomposition.  In  jaundice  an  increased  excretion 
of  urobilin  as  well  as  bilirubin  is  frequently  found  in  the  urine;  in  many 
eases,  or  in  certain  stages,  even  urobilin  exclusively  instead  of  bilirubin. 
However,  according  to  the  investigations  of  Fr.  Miiller,  even  in  these  cases 
urobilin  is  probably  formed  only  in  the  intestine.  According  to  Kimura 
even  the  urobilin,  that  is  urobilinogen  (Braunstein),  which  is  almost  in- 
variably found  in  the  bile,  appears  to  be  of  enterogenous  origin.     In  com- 


HEPATIC   INSUFFICIENCY  341 

plete  occlusion  of  the  bile  from  the  intestine  it  is  absent  both  from  the 
bile  and  from  the  urine. 

The  view  that  an  accumulation  of  urobilin  in  the  blood  may  produce 
an  especial  form  of  icterus,  the  "urobilin  icterus"  of  C.  Gerhardt  (Gub- 
ler's  "  ictere  hemapheique  "),  may  be  regarded  as  disproven.  It  has  been 
determined  by  numerous  researches  that  even  in  those  cases  in  which  the 
urine  contains  urobilin  alone  the  yellow  color  of  the  skin,  of  the  blood 
serum,  and  of  the  serous  effusions,  is  exclusively  due  to  bilirubin. 

As  additional  consequences  of  disturbed  hepatic  function  we  must 
consider  the  diminished  excretion  of  urea  with  an  increased  excretion  of 
ammonia,  so-called  alimentary  glycosuria,  as  well  as  an  increased  toxicity 
of  the  urine.  But  these  phenomena  cannot  as  yet  be  utilized  in  differen- 
tiating hepatic  insufficiency.  On  the  contrary,  the  disturbed  transformation 
of  other  carbohydrates  into  grape-sugar,  which  is  expressed  in  alimentary 
levulosuria,  has  a  certain  significance  as  a  sign  of  disturbed  function  of 
the  liver. 

In  the  clinical  picture  the  milder  grades  of  hepatic  insufficiency  mani- 
fest at  most  only  very  slight  and  varying  symptoms,  such  as  may  appear 
in  any  other  disease.  It  is  therefore,  at  present,  a  purely  arbitrary  assump- 
tion when  we  designate  certain  symptoms  of  dyspepsia  which  are  associated 
with  psychical  depression,  a  tendency  to  headache,  uncomfortable  sensa- 
tions in  the  abdomen,  and  more  or  less  distinctly  developed  jaundice,  as 
"  hepatic  dyspepsia,"  "  biliousness,-'  "  torpor  of  the  liver,"  and  the  like, 
as  is  commonly  done  both  in  England  and  America. 

But  there  can  be  no  doubt  that  certain  grave  symptoms  which  we  meet 
with  when  an  especially  severe  damage  to  the  liver  has  taken  place  are 
chiefly  to  be  attributed  to  an  absence  of  hepatic  function — to  acholia,  as 
the  condition  was  named  by  Frerichs,  with  particular  reference  to  the 
formation  of  bile,  or  to  hepatargy,  the  designation  proposed  by  Quincke. 

Usually  there  are  severe  disturbances  on  the  part  of  the  central  nervous 
system,  similar  to  those  observed  in  the  most  varied  autointoxications: 
Severe  headache,  nausea  and  vomiting,  implication  of  the  sensorium  even 
to  most  profound  coma,  a  state  of  men toZ  irritability  and  deliriurn,  even. 
maniacal  attacks,  muscular  twitchings,  and  general  convulsions.  T6  tlae^^ 
must  be' added-  the  development  of- th.e  hemorrhagic  didthesis,-a.  tendency 
to  hemorrhage  from  every  pos&ible- organ,  as  well- as  the  appearance -of 
circulatoty-disturbances,  and  finally  coZ?dpse  -which-  brings  ^iboiit  iha-faJxCl 
issue.  -■     ■■   '        ..  ^  .........  -     ,     . ,  .  , 

When  these  severe  symptoms  are  superadded  to  jaundice  we  have  the 
condition  known  as  icterus  gravis. 


342  JAUNDICE  AND  HEPATIC  INSUFFICIENCY 

ACUTE    YELLOW  ATROPHY 

The  clinical  picture  of  icterus  gravis  is,  as  a  rule,  associated  anatomi- 
cally with  an  acute  diffuse  degeneration  of  the  parenchyma  of  the  liver 
which  leads  to  the  destruction  of  the  hepatic  cells  and  a  rapid  decrease 
in  the  size  of  the  organ  which  usually  is  designated  as  "acute  yellow  atro- 
phy of  the  liver."  This  designation,  however,  applies  only  to  the  appear- 
ance of  the  liver  in  the  advanced  stage  of  anatomical  change  which  cases 
running  a  typical  clinical  course  usually  attain.  But  the  intensity  of  the 
clinical  symptoms  by  no  means  invariably  corresponds  with  the  intensity  of 
the  anatomical  changes.  Often  the  patient  perishes  before  the  anatomical 
lesion  of  this  characteristic  stage  is  reached,  therefore  the  term  "  icterus 
gravis "  does  not  aptly  describe  the  condition  known  as  "  acute  yellow 
atrophy  of  the  liver." 

In  these  cases  of  fatal  jaundice  it  is  difficult  to  differentiate  the  dis- 
turbances which  are  due  to  the  absence  of  hepatic  function  and  those  due 
to  the  consequent  alteration  in  the  composition  of  the  blood,  the  hepato- 
toxemia  or  hepatic  autointoxication  from  the  toxic  effects  of  biliary  con- 
stituents which  are  circulating  in  the  organism,  the  cholemia  from  tho2e 
symptoms  produced  by  the  primary  general  infection  or  general  intoxi- 
cation. 

Until  very  recently  attempts  have  been  constantly  made  to  prove  by 
experimental  investigation  that  these  severe  symptoms  depend  mainly  upon 
the  action  of  biliary  constituents  circulating  in  the  blood,  especially  of  the 
bile  acid  salts.  A  few  years  ago  Bickel  demonstrated  experimentally  that 
the  biliary  salts  when  brought  directly  into  contact  with  the  surfaces  of 
the  cerebral  hemispheres  prove  themselves  to  be  especially  potent  poisons 
to  the  nervous  system. 

Nevertheless  it  is  questionable  whether  the  biliary  salts  ever  attain  in 
the  organism  such  a  concentration  as  is  necessary  in  the  experiment  to 
produce  a  toxic  action. 

With  some  degree  of  probability,  we  may  refer  to  cholemia  in  a  re- 
stricted sense,  that  is,  to  the  over-flooding  of  the  organism  with  biliary 
constituents,  the  following: 

The  slowing  of  the  pulse  so  frequently  observed  in  jaundice,  which  is 
partially  due  to  the  direct  action  of  the  bile  acids  upon  the  heart  muscle, 
partially  to  central  stimulation  of  the  inhibitive  fibers  contained  in  the 
pneumogastric  nerve;  also  certain  milder  disturbances  in  the  nervous  and 
muscular  apparatus  which  are  expressed  by  itching  of  the  skin,  disturbance 
of  sight,  particularly  xanthopsia,  headache,  general  lassitude,  muscular 
w(>akness,  and  psychical  depression;  furthermore,  a  damage  to  the  kidneys 
wliifh  is  chiefly  revealed  anatomically  by  certain  alterations  in  the  epithelia 
aud  111  ihe  convoluted  uriniferous  tubules,  and  is  clinically  manifested  by 
the  appearance  of  albuminuria  and  the  excretion  of  easts  which,  as  ISToth- 


ACUTE  YELLOW  ATROPHY  343 

nagel  has  shown,  may  also  be  found  in  the  urine  of  jaundice  when  albumin 
cannot  be  demonstrated  by  the  ordinary  tests. 

Whether  the  property  of  the  bile  acids  to  dissolve  red  hlood-corpuscles 
is  also  called  into  action  in  jaundice  is  very  questionable  on  account  of 
the  slight  concentration  of  the  biliary  salts  in  the  organism.  Nor  is  it 
certain  that  we  can  refer  to  the  action  of  the  biliary  acids  the  changes  in 
the  walls  of  the  vessels  which  are  the  foundation  of  the  hemorrhagic 
diathesis,  and  which  occur  in  severe  cases  of  jaundice. 

On  the  contrary,  in  cases  of  icterus  gravis,  probably  all  of  the  other 
symptoms  of  severe  autointoxication  are  chiefly  due  to  a  damage  of  the 
hepatic  function  and  an  alteration  in  the  composition  of  the  fluids  produced 
by  hepatic  insufficiency.  For  these  phenomena  are  also  observed  after 
experimental  exclusion  of  the  hepatic  function  as  well  as  in  severe  hepatic 
diseases  in  which  there  is  no  marked  jaundice. 

The  special  cause  of  the  toxic  effect  here  produced  cannot  at  present 
be  decided  with  certainty.  Probably,  however,  the  substances  whose  accu- 
mulation in  the  organism  brings  about  this  autointoxication  are  to  be 
sought  for  in  certain  prior  nitrogenous  stages  of  urea  the  further  develop- 
ment of  which  occurs  in  the  liver;  or  in  the  toxic  products  of  intestinal 
decomposition  which,  under  normal  circumstances,  are  deprived  of  their 
deleterious  power  by  passing  through  the  liver;  or  in  the  products  of  de- 
composition of  the  hepatic  tissue  itself,  which  may  be  destroyed  by.  the 
action  of  the  same  deleterious  agent  which  generates  the  disease. 


SYMPTOMS 

If,  from  the  views  here  expressed,  we  consider  that  the  difference  be- 
tween benign  simple  jaimdice  and  that  running  a  fatal  course,  icterus 
gravis,  is  merely  a  difference  in  the  degree  of  intensity  of  the  action  of 
the  same  or  similar  factors  upon  the  same  tissue  elements,  it  is  imme- 
diately obvious  that  no  sharp  line  can  be  drawn  between  these  forms  of 
jaundice. 

As  a  rule,  these  forms  are  ushered  in  with  the  same  symptoms — those 
which  we  recognized  in  the  patient  whose  history  has  been  related.  Only 
the  subsequent  course  of  the  disease  varies.  ' 

In  ordinary  cases  of  simple  jaundice,  the  symptoms,  as  we  have  seen, 
last  for  a  short  time,  generally  from  two  to  three  weeks,  with  but  slight 
variation  in  their  intensity,  after  which  recovery  gradually  sets  in.  The 
appetite  returns,  the  patient  is  more  comfortable,  the  digestive  disturbances 
entirely  disappear.  The  feces  begin  to  show  biliary  staining,  the  return 
of  bile  to  the  intestine  often  being  indicated  previously  by  the  presence 
of  urobilin  in  the  alcoholic  ethereal  extract  of  feces  which  have  been  ren- 
dered acid.  The  biliary  coloring  matter  in  the  urine  gradually  decreases; 
often  a  more  decided  urobilinuria  may  transitorily  appear.     The  yellowish 


344  JAUNDICE  AND  HEPATIC   INSUFFICIENCY 

discoloration  of  the  skin  and  conjunctivaB  may  last  longer  than  the  other 
symptoms.  Finally,  this  also  completely  disappears,  and  in  three  or  four 
weeks  after  the  onset  of  the  disease  the  patient  entirely  recovers. 

But  there  may  be  deviations  from  this  course.  Not  rarely,  particularly 
in  epidemic  jaundice,  digestive  disturbances  and  constitutional  symptoms 
are  very  slight  from  the  onset,  or  may  be  absent  entirely.  Only  the  icteroid 
discoloration  of  the  skin  and  the  urine  and  the  clay-colored  stools  betray 
the  inhibition  to  the  flow  of  bile.  In  such  cases  the  duration  of  the  disease 
is  less,  being  only  from  ten  to  twelve  days. 

In  other  and  much  rarer  cases,  the  disease  is  very  protracted,  often 
lasting  three  or  four  months,  or  even  longer.  Occasionally,  in  spite  of  the 
prolonged  course,  the  reaction  upon  the  constitutional  condition  is  very 
slight.  As  a  rule,  however,  these  cases  gradually  increase  in  severity,  and 
produce  a  decided  loss  in  strength,  emaciation,  and  anemia.  Convalescence 
in  such  cases  may  be  correspondingly  protracted.  Finally,  however,  com- 
plete recovery  occurs.  Eosenstein  reports  a  case  in  which  catarrhal  jaun- 
dice lasted  more  than  a  year,  but  terminated  in  restoration  to  health.  In 
such  instances,  however,  the  diagnosis  must  be  consideried  very  ques- 
tionable. 

Occasionally  these  cases  become  more  grave.  More  or  less  suddenly, 
severe  symptoms  of  cholemic  intoxication  and  hepatic  insufhcieney  appear, 
combined  with  a  failure  in  renal  and  cardiac  activity,  or  the  patients 
perish  from  the  addition  of  the  hemorrhagic  diathesis.  These  cases,  there- 
fore, are  examples  of  a  transitional  change  into  the  critical  state  of 
icterus  gravis. 

Typical  cases  of  the  latter  form  usually  present  the  picture  of  benign 
jaundice  only  during  the  tirst  days.  From  the  onset  the  constitutional 
symptoms  are  somewhat  more  intense,  and  often  enlargement  and  marked 
sensitiveness  of  the  liver  upon  pressure  are  early  noticeable.  Splenic  tumor 
and  albuminuria  may  be  demonstrated  even  in  the  first  days  of  the  dis- 
ease. As  a  rule,  however,  these  cases  at  the  onset  do  not  differ  greatly 
from  those  previously  described.  .   . 

But  soon,  after  a  few  days,  toward  the  end  of  the  first  or  during  the 
second  week,  rarely  after  a  longer  course,  .a  change  ensues :  The  headache 
increases  and  sometimes  becomes .  ex:deedingly  severe,  the  patient  is  .restless, 
excited,  unable  to  slecp-.-and  hegins  to  be  delirious.  The  delirium  in- 
creases and  occasionally  assumes  a  furibund  character.  The  patient 
screams  and  tosses  about  and  can  hardly:  be  kept  in  bed.  In  other  cases 
tlie  delirium  may  be  of  a  more  quiet  nature,  or  from  the  onset  there  i> 
a  tendency  to  apathy  and  somnolence.  Finally  the  sensorium  is  more  and 
more  ])enumbed,  the  patient  becomes  soporous,  and  then  sinks  into  the 
deepest  coma.  During  this  time  there  are  convulsions  in  individual  muscle 
groups,  with  grinding  of  the  teeth,  attacks  of  trismus,  often  even  general 
convulsions.    Vomiting  repeatedly  occurs,  the  vomitus  sometimes  contain- 


ACUTE  YELLOW  ATROPHY  345 

ing  blood  in  greater  or  less  amounts.  Profuse  gastric  and  intestinal  hem- 
orrhages may  also  appear,  and  there  may  be  bleeding  from  other  parts 
of  the  body  in  addition:  Petechiae  and  ecchymoses  upon  the  skin  and 
mucous  membranes,  severe  epistaxis,  bleeding  from  the  gums,  hemorrhages 
from  the  urinary  passages,  and,  exceptionally,  also  pulmonary  hemorrhage. 

Meantime,  conspicuous  changes  take  place  in  the  liver.  The  organ 
which  was  at  first  enlarged  begins  to  decrease  in  size.  The  extent  of  this 
decrease  may  be  recognized  by  examinations  repeated  from  day  to  day. 
Finally,  the  organ  is  scarcely,  if  at  all,  recognizable  upon  percussion.  The 
spleen,  on  the  other  hand,  is  usually  enlarged. 

The  excretion  of  urine  is  diminished.  The  urine  shows  jaundice,  con- 
tains albumin  and  casts,  but  little  urea;  on  the  other  hand  leucin  and 
tyrosin  are  excreted  as  sediments,  or  in  testing  the  urine  are  readily 
demonstrated. 

During  this  time  the  temperature  is  frequently  subnormal;  sometimes, 
however,  it  may  be  normal  or  even  show  febrile  ranges.  The  pulse,  which 
after  the  appearance  of  jaundice  frequently  becomes  slow,  subsequently  is 
more  rapid,  smaller,  and  weaker.  Finally,  the  pulse  rate  shows  extraor- 
dinary rapidity  but  loss  in  strength,  and  it  rapidly  declines,  the  respiration 
becomes  irregular  and  interrupted,  pulmonary  edema  appears,  and  the 
patient  perishes  in  profound  coma. 

The  entire  course  may  be  so  extremely  fulminant  that  even  four  or 
five  days  after  the  appearance  of  jaundice,  and  one  to  three  days  after 
the  severe  cerebral  symptoms  have  become  prominent,  death  may  occur. 
In  a  few  rare  cases  a  course  even  more  rapid  has  been  observed.  A  some- 
what protracted  course  is  less  rare:  The  initial  stage  may  last  for  two  or 
three  weeks  or  even  longer,  and  after  the  appearance  of  the  severe  symp- 
toms the  duration  of  life  is  sometimes  from  twelve  to  fifteen  days. 

In  the  cases  with  characteristic  symptoms  which  have  just  been  de- 
scribed a  favorable  course  is  extremely  rare;  but  several  undoubted  in- 
stances of  this  kind  have  been  reported.  Kecovery  is  then  very  slow,  and 
convalescence  is  exceedingly  protracted.  Sometimes  recovery  sets  in  with 
the  sudden  appearance  of  profuse  diuresis  ("crise  urinaire  polyurique," 
Bouchard)  or  a  profuse  diarrhea.  Harmful  products  are  thus  apparently 
removed  from  the  body.  Gradually  the  hemorrhage  ceases,  the  mind 
clears,  the  general  condition  improves.  As  a  rule,  the  liver  regains  -its 
normal  size  very  slowly,  but  occasionally  this  may  be  with  extraordinary 
rapidity.  Many  months  may  pass  before  the  debilitated  and  extremely 
emaciated  patients  completely  recover  their  strength. 

Like  the  mildest  cases  of  jaundice,  the  symptom-complex  of  icterus 
gravis  may  occur  secondarily  in  the  course  of  various  chronic  diseases  of 
the  liver:  as,  for  instance,  in  the  different  forms  of  chronic  diffuse  hepa- 
titis, more  rarely  in  congestion  of  the  liver,  syphilis  of  the  liver,  hepatic 
carcinoma,  and  others.     In  such  cases  the  affection  often  shows  the  char- 


346  JAUNDICE  AND  HEPATIC   INSUFFICIENCY 

acteristics  of  a  terminal  complication.  The  disturbances  on  the  part  of 
the  nervous  system  rarely  appear  suddenly,  but,  as  a  rule,  insidiously  and 
gradually,  and  they  soon  increase  to  the  deepest  coma  or  to  delirium  and 
convulsions;  hemorrhages  are  added,  characteristic  changes  in  the  urine 
appear,  but  are  less  prominent  than  in  the  cases  of  primary  disease.  There 
may  be  no  decrease  in  the  size  of  the  liver;  the  fever  may  be  slight  or 
entirely  absent,  the  temperature  is  usually  subnormal;  death  results  in 
a  few  days. 

Icterus  gravis  sometimes  occurs  apparently  as  a  primary  disease,  with- 
out any  previous  symptoms  denoting  disease  of  the  liver,  and  runs  a 
characteristic  course;  only  the  autopsy  then  reveals  an  earlier  affection 
of  the  liver  the  course  of  which  has  been  entirely  latent. 


ETIOLOGY 

The  causes  of  the  disease  will  decide  the  character  of  the  pathologic 
picture,  especially  the  severity  of  the  clinical  symptoms  in  the  individual 
case  and,  above  all,  the  intensity  of  the  toxic  action  or  the  virulence  of  the 
pathogenic  agent.  Definite  noxious  agents  are  characterized  by  their  spe- 
cial effect  upon  the  liver.  Whether  they  lead  only  to  temporary  functional 
damage  of  the  liver,  or  to  acute,  rapidly  progressing,  destructive  processes, 
or  to  chronic  degeneration  and  inflammation,  depends  upon  their  mode  of 
introduction  into  the  organism,  and  upon  the  duration  and  intensity  of 
their  action. 

Thus,  for  example,  acute  phosphorus  poisoning  with  only  slight  toxic 
eifect  may  lead  to  mild  transitory  forms  of  jaundice.  Larger  quantities 
of  the  poison  will  produce  the  clinical  picture  of  icterus  gravis  and  develop 
the  characteristic  changes  of  acute  yellow  atrophy  of  the  liver,  unless  the 
other  effects  upon  the  organism  should  cause  death  before  the  changes  in 
the  liver  develop  to  such  an  extent.  Phosphorus  rarely  acts  so  powerfully 
in  man  as  to  cause  a  chronic  diffuse  hepatitis,  but  changes  which  corre- 
spond to  hepatic  cirrhosis  have  been  experimentally  produced  in  animals 
by  repeated  doses  of  small  amounts  of  phosphorus. 

On  the  other  hand,  we  know  that  alcohol,  which,  as  a  rule,  has  a  less 
intense  action  upon  the  liver  but  more  fr^equently  implicates  this  organ, 
produces  chronic  hepatitis.  A  fatal  icterus  gravis  or  acute  yellow  atrophy 
of  the  liver  has  been  only  exceptionally  observed  after  acute  intoxication 
with  alcohol.  After  acute  alcoholic  intoxication  followed  by  gastric  and 
intestinal  catarrh,  a  benign  icterus  has  been  seen  which  was  looked  upon 
as  "catarrhal,"  but  which,  perhaps,  was  also  dependent  upon  a  direct 
action  of  the  alcohol  upon  the  liver. 

Among  infectious  diseases  there  are  some  which  particularly  implicate 
the  liver  so  that  the  jaundice  or  acute  diffuse  hepatitis  actually  forms  a 
part  of  the  clinical  picture.     In  other  infections  it  appears  to  be  only  a 


ACUTE  YELLOW  ATROPHY  347 

temporary  complication.  In  the  first  group  yellow  fever,  above  all,  must 
be  included,  for  in  this  the  implication  of  the  liver  plays  such  a  role  that 
Liebermeister  remarked :  "  Yellow  fever  is  merely  an  acute  parenchyma- 
tous degeneration  of  the  liver  due  to  a  specific  infection,  and,  aside  from 
the  effect  of  the  toxins  of  the  disease  upon  the  liver,  there  is  no  reason 
to  assume  a  direct  action  of  the  same  in  other  organs."  Comparatively 
often  mild  and  even  severe  forms  of  jaundice  occur  in  relapsing  fever 
("bilious  typhoid"),  also  in  septic  and  pyemic  affections,  but  less  fre- 
quently in  enteric  fever,  cholera,  diphtheria,  malaria,  and  tuberculosis. 

The  occurrence  of  milder  forms  of  jaundice  as  well  as  highly  developed 
cases  of  acute  yellow  atrophy  in  syphilis  requires  especial  mention.  Where 
this  occurs  in  the  early  period  of  the  disease  during  the  time  of  the  erup- 
tion of  the  secondary  exanthems,  it  occasionally  appears  in  a  very  charac- 
teristic manner. 

Furthermore,  nearly  all  pathogenic  microorganisms  may  occasionally 
produce  an  outbreak  of  malignant  or  benign  jaundice,  so  that  we  have 
no  more  reason  to  regard  an  "  essential "  icterus  gravis  or  a  "  primary " 
acute  yellow  atrophy  of  the  liver  as  a  definite  specific  disease  than  in  the 
case  of  simple  jaundice. 

A  predisposition  to  the  severe  forms  of  the  disease  depends  upon  the 
non-resistance  of  the  organism  as  well  as  upon  the  intensity  of  the  effect 
of  the  poison.  This  resistance  of  the  organ  may  have  been  diminished 
by  a  previously  existing  pathologic  change.  We  observe,  therefore,  as 
stated,  that  the  mild  as  well  as  the  severe  forms  of  jaundice  frequently 
occur  as  complications  of  hepatic  cirrhosis,  congestion  of  the  liver,  hepatic 
syphilis,  etc.  Yet  any  impediment  to  the  flow  of  bile  may  damage  the 
'liver  and  diminish  its  power  of  resistance  to  poisons  and  toxins  of  any 
kind.  Therefore  every  jaundice,  no  matter  what  its  cause,  may  in  its 
further  course  lead  to  hepatic  insufficiency  and  terminate  in  icterus  gravis. 

As  another  factor  which  may  cause  a  special  predisposition  to  jaundice, 
and  particularly  to  the  severe  forms,  pregnancy  must  be  mentioned.  It  is 
remarkable  that  about  one-half  of  all  the  eases  described  in  literature 
of  "  primary  "  acute  yellow  atrophy  of  the  liver  occurring  in  women  have 
been  in  pregnant  women.  We  cannot  regard  these  cases  as  solely  due  to 
the  influence  of  puerperal  septicemia  since  only  a  few  occurred  in  the 
puerperium,  the  majority  having  been  observed  between  the  fourth  and 
seventh  months  of  pregnancy. 

The  special  predisposition  of  the  pregnant  woman  to  severe  attacks 
of  jaundice  is  revealed  by  the  fact  that,  in  different  epidemics  of  jaundice, 
even  in  those  which  were  largely  of  benign  character,  among  those  who 
perished  with  the  symptoms  of  icterus  gravis  the  number  of  pregnant 
women  was  conspicuously  large.  The  French  authors  ( Saint- Vel,  Carpen- 
tier),  in  particular,  have  described  such  epidemics. 

The  cause  of  this  extreme  susceptibility  of  the  pregnant  cannot  be 


348  JAUNDICE   AND   HEPATIC  INSUFFICIENCY 

found  in  the  mechanical  effect  of  the  gravid  uterus,  as  Klebs  has  sup- 
posed, since  the  disease  occurs  even  during  the  earliest  months  of  preg- 
nancy. It  is  probably  the  consequence  of  the  changes  which  the  hepatic 
cells  as  well  as  the  renal  epithelium  and  other  tissue  elements  undergo 
during  the  course  of  pregnancy. 

Brauer,  who  recently  reported  a  peculiar  case  in  which  jaundice  recurred 
during  four  successive  pregnancies,  refers  the  damage  of  the  liver  to  the 
preceding  action  of  placental  toxins  (Veit's  syncytiolysins),  connecting 
them  with  the  kidney  of  pregnancy,  with  eclampsia,  osteomalacia,  and  other 
expressions  of  gravid  toxicoses.  Brauer  attempts  to  explain  menstrual 
jaundice  also  in  a  similar  manner. 

That  a  congenital,  often  hereditary,  predisposition  may  bring  about  a 
lessened  resistance  of  the  liver  and  a  tendency  to  mild  or  severe  forms 
of  jaundice  is  extremely  likely.  Such  a  hereditary  predisposition  to  chronic 
icterus  occurring  in  families  is  shown  in  a  remarkable  manner  by  certain 
cases  to  which  I  shall  briefly  refer: 

Cases  of  chronic  jaundice  appearing  in  several  members  of  the  same 
family  have  been  described  by  earlier  authors  (Murchison).  Recent  pub- 
lications are  also  at  hand  (Minkowski,  Gilbert  et  Lerebouillet,  A.  Pick 
and  others).  Under  the  name  of  "hereditary  jaundice"  or  of  "cholemie 
faniiliale"  very  different  conditions  have  been  portrayed,  and  the  French 
authors  especially,  with  their  tendency  to  "  diatheses,"  have  attached  great 
significance  to  the  most  heterogenous  phenomena  as  expressing  hereditary 
predisposition  depending  upon  family  cholcmia.  In  some  cases  the  cause 
of  hereditary  jaundice  has  been  sought  in  a  congenital  and  hereditary 
constriction  of  the  biliary  passages.  Pick  assumes  for  his  cases  either  a 
congenital  communication  between  the  lymph  channels  and  biliary  passages 
or  a  congenital  insufficiency  of  the  hepatic  cells. 

To  me  it  appears  questionable  whether  in  all  cases  of  hereditary  jaun- 
dice a  primary  change  in  the  liver  or  in  the  biliary  passages  must  be 
assumed.  I  do  not  believe  this  to  have  occurred  in  the  cases  I  described 
as  a  "  peculiar  hereditary  affection  running  its  course  under  the  picture 
of  clironic  jaundice  with  urobilinuria,  splenomegalia  and  renal  siderosis" 
{VcrlKuullungen  des  XVIII.  Congresses  fiir  innere  Medicin,  1900). 

This  symptom-complex  occurred  in  at  least  eight  members  of  a  family 
in  three  generations  without  producing  any  serious  disturbance  of  the 
constitutional  condition.  In  one  case,  upon  which  an  autopsy  was  held, 
death  being  due  to  other  cause,  noteworthy  structural  changes  could  not 
be  dt't(irmined  either  in  the  liver  or  in  the  biliary  channels;  however,  in 
addition  to  the  marked  hyperplasia  of  the  spleen,  a  very  conspicuous 
deposit  of  iron  was  found  in  the  kidneys,  which,  so  far  as  I  am  aware, 
has  not  been  observed  in  any  other  condition.  At  that  time,  therefore, 
I  expressed  the  belief  that  this  was  due  to  an  especial,  transmissible,  hered- 
itary anomaly  in  the  metabolism  of  blood  pigment  which  only  seeonda- 


ACUTE   YELLOW  ATROPHY  349 

rily  led  to  disturbance  of  the  function  of  the  liver.  During  the  discussion. 
Senator  reported  similar  observations  and,  in  the  main,  agreed  with  me. 

In  their  clinical  course  the  cases  resembled  the  clinical  picture  de- 
scribed by  Hayem  and  Levy  as  "  ictere  chronique  infectieux  splenomega- 
lique,"  which  Gilbert  and  Lerebouillet  have  also  designated  as  "  cholemie 
familiale."  But  the  mere  fact  of  the  hereditary  appearance  in  successive 
generations  is  against  Hayem's  conception  of  jaundice  as  an  infectious 
disease,  a  conception  which  was  also  opposed  by  Bettmann  who  described 
a  similar  case. 

Bettmann  determined  periodically  in  his  case  a  hemoglobinemia  without 
hemoglobinuria,  and  therefore  considers  a  congenital  abnormality  of  the 
blood  to  be  the  basis  of  the  disease. 

Eeeently  I  met  another  family  which  shows  characteristically  the  affec- 
tion I  have  described.  One  member  of  this  family,  then  a  student  of 
medicine,  was  examined  by  me  twelve  years  ago.  On  account  of  jaundice, 
urobilinuria,  and  an  enormous  splenic  tumor,  I  diagnosticated  hepatic 
cirrhosis,  nothing  militating  against  such  diagnosis  except  the  absence  of 
an  etiologic  factor,  and,  since  that  time,  the  continuously  undisturbed 
general  condition.  After  the  appearance  of  my  publication  this  gentleman, 
who  has  since  become  a  physician,  brought  to  me  his  brother,  who  since 
childhood  has  also  shown  icteroid  discoloration  of  the  skin,  has  voided  a 
dark  urine  rich  in  urobilin,  and  has  also  had  a  large  splenic  tumor.  The 
father  of  the  patient  is  said  to  have  died  at  an  advanced  age  of  hepatic 
cirrhosis.  The  grandmother,  four  brothers  and  sisters,  and  two  children 
showed  the  same  anomalies  from  youth;  therefore  eight  persons  in  four 
generations.  The  cases  resemble  perfectly  the  first  ones  I  described.  They 
are  to  be  reported  more  in  detail  by  Dr.  Haal,  who  has  instituted  far- 
reaching  investigations  concerning  them.^ 

PATHOLOGY 

We  would  digress  too  far  were  we  to  discuss  more  in  detail  the  ques- 
tions which  arise  concerning  the  subject  under  discussion.  I  shall,  there- 
fore, not  enter  upon  the  pathologico-anatomical  findings  in  jaundice,  but 
will  only  remark  that  the  changes  which  develop  in  consequence  of  dis- 
turbances of  the  flow  of  bile  in  the  liver  are  only  in  part  to  be  referred 
*to  the  mechanical  and  chemical  ejfects  of  the  retained  bile.  To  a  great 
extent  they  depend  upon  secondary  infection  of  the  biliary  passages  and 
upon  the  decreased  power  of  resistance  of  the  organ  owing  to  the  stagnation 
of  bile,  as  opposed  to  the  various  deleterious  agents  capable  of  producing 

^  According  to  a  communication  of  Dr.  Haal,  the  number  of  erythrocytes  was 
decreased,  the  excretion  of  uric  acid  increased,  and  the  amount  of  iron  in  the  urine 
decidedly  increased. — Three  additional  cases  of  the  same  aiTection  have  just  been 
described  by  v.  Krannhals  in  the  Deutsches  Archiv  f.  klin.  Med.,  Bd.  81. 


360  JAUNDICE   AND  HEPATIC   INSUFFICIENCY 

inflammation.  To  the  most  common  signs  of  hepatic  jaundice,  as  demon- 
strated in  the  enlargement  of  the  liver  and  its  icteroid  discoloration,  the 
dilatation  of  the  biliary  passages  and  the  deposit  of  biliary  stained  masses 
in  the  hepatic  cells  and  bile  capillaries,  with  continued  obstruction  to  the 
flow  of  bile,  we  may  add  the  severe  changes  presented  by  the  picture  of 
diffuse  hepatitis  which,  in  its  mode  of  development,  presents  certain  pecu- 
liarities. These  peculiarities  are  noted  especially  in  the  appearance  of 
focal  necroses  in  the  parenchyma  of  the  liver  as  well  as  in  the  marked 
prominence  of  inflammation  and  processes  of  proliferation  starting  from 
the  interlohulary  biliary  channels. 

As  a  rule,  in  the  cases  which  perish  under  the  picture  of  acute  hepatic 
degeneration  very  conspicuous  and  peculiar  changes  of  the  organ  are  found. 
Upon  opening  the  abdominal  cavity  in  cases  of  well  developed  "  acute 
yellow  atrophy  of  the  liver,"  the  small  size  and  flaccidity  of  the  liver  are 
conspicuous,  and  the  organ,  covered  by  coils  of  intestine,  appears  to  have 
sunk  deep  down  alongside  the  vertebral  column.  The  weight  of  the  organ 
may  be  less  than  one-half  the  normal ;  in  consistence  it  is  flaccid,  withered, 
almost  fluctuating,  or  doughy  and  friable.  The  serous  covering  looks 
wrinkled.  The  color  of  the  liver  is  yellow,  often  uneven  upon  the  cut 
surfaces,  and  between  the  yellow  areas  large  or  small  red  foci  are  found. 
These  latter  show  a  more  advanced  stage  of  the  disease.  After  prolonged 
exposure  to  the  air  the  cut  surfaces  are  often  covered  with  a  wreath-like 
coating  of  tyrosin  crystals. 

Upon  microscopic  examination  of  such  a  liver  the  hepatic  cells  in  the 
yellow  areas  are  found  to  be  in  a  condition  of  more  or  less  advanced 
degenerative  destruction:  Cloudy,  swollen,  showing  fatty  degeneration,  de- 
formed, or  transformed  into  detritus.  In  the  red  areas  this  detritus  has 
been  absorbed,  and  we  note  between  the  capillaries  only  a  pale  homogeneous, 
or  striated,  open-meshed  connective  tissue,  in  which,  as  the  only  remains 
of  hepatic  cells,  isolated  fat  globules  and  granules  of  coloring  material 
are  found. 

In  the  cases  running  a  protracted  course,  in  addition  to  the  degenera- 
tion and  destruction  of  liver  cells,  proliferative  changes  take  place  in  the 
liver  by  which  the  destroyed  hepatic  tissue  is  replaced.  Besides  a  prolifera- 
tion of  hepatic  cells  by  indirect  division  of  the  nucleus,  new  formations 
appear,  starting  from  the  biliary  passages  and  consisting  of  epithelial 
tubules,  also  processes  of  proliferation  in  the  endothelia  of  the  blood- 
vessels, and  cell  accumulation  and  connective  tissue  proliferation  in  the 
interstitial  tissue.  Such  cases  form  transitional  stages  in  acute  and  sub- 
acute forms  of  hepatic  cirrhosis. 


ACUTE  YELLOW  ATROPHY  351 


DIAGNOSIS 


Before  entering  upon  minute  details  of  the  treatment,  we  must  con- 
sider the  diagnosis  and  prognosis  of  jaundice. 

The  diagnosis  of  simple  jaundice  is  readily  made  when  the  signs  of  the 
affection  become  marked.  Its  appearance  after  preceding  digestive  dis- 
turbances in  previously  healthy  persons  who,  as  a  rule,  present  but  slight 
constitutional  symptoms,  the  absence  of  pain  and  of  marked  changes  in 
the  liver,  above  all  its  benign  course,  do  not  leave  us  long  in  doubt  regard- 
ing the  nature  of  the  affection. 

In  my  opinion,  no  sharp  differentiation  is  possible  of  the  severe  forms 
of  icterus  gravis  which  run  their  course  with  acute  degeneration  of  the 
hepatic  parenchyma.  Such  differentiation  has  more  of  a  prognostic  than 
a  diagnostic  interest.  Clinically,  the  limits  must  be  drawn  where  the  dis- 
turbances of  hepatic  function  produce  the  symptoms  of  autointoxication. 
When  the  anatomical  changes  are  considered,  the  demonstrable  decrease  in 
the  size  of  the  organ  and  the  appearance  of  products  of  decomposition 
in  the  urine  appear  of  greater  significance. 

The  flooding  of  the  organism  with  the  products  of  decomposition  of 
the  liver,  above  all  the  appearance  of  amido-acids  in  the  urine  (and,  since 
the  discovery  of  Frerichs,  particularly  the  excretion  of  leucin  and  tyrosin) 
must  warrant  the  assumption  of  acute  yellow  atrophy  of  the  liver.  These 
substances  are  not  found  exclusively  or  even  invariably  in  the  above  men- 
tioned disease.  By  minute  methods  of  investigation  we  have  recently 
proven  that  the  presence  of  amido-acids  in  the  urine  is  not  rare ;  they  "have 
been  found  in  large  quantities  in  the  urine  in  gout,  in  pneumonia  and  in 
leukemia   ( Ignatowski ) . 

In  no  other  disease  are  such  large  quantities  of  amido-acids  found  as 
in  acute  degeneration  of  the  liver.  The  urine  here  needs  no  preparation 
with  sensitive  reagents  such  as  the  recently  employed  yQ-naphthalin  sulpho- 
chlorid.  On  the  contrary,  tyrosin  is  often  directly  deposited  in  the  urine 
as  a  crystalline  sediment  in  the  form  of  characteristic  bundles,  sheaves,  and 
strongly  refractive  needles.  The  more  readily  soluble  leucin  crystallizes 
in  the  urine  only  in  the  form  of  concentrically  layered  or  radially  striped 
globules. 

The  crystal  forms  may  readily  be  confounded  with  urate  salts.  It  is 
therefore  advisable  to  ascertain  the  presence  of  these  substances  either  by 
extracting  them  from  the  urine  which  has  been  boiled  with  alcohol,  or  by 
precipitating  them  with  lead  acetate  and  then  removing  the  surplus  quan- 
tity of  lead  with  hydrogen  sulphid,  by  which  means  we  obtain  a  solution 
free  from  urate  salts,  in  which  after  cooling  leucin  and  tyrosin  may  crys-' 
tallize. 

The  appearance  of  amido-acids,  which  have  been  recognized  as  the  prior 

stages  of  urea,  was  formerly  referred  to  a  cessation  of  the  formation  of 
24 


352  JAUNDICE   AND  HEPATIC   INSUFFICIENCY 

urea  in  consequence  of  a  deficiency  of  the  hepatic  function.  According 
to  my  investigations,  experimentally  excluding  the  liver,  as  well  as  accord- 
ing to  recent  researches  (Lang  and  others)  concerning  the  prevention  of 
amido-formation  in  the  animal  body,  it  appears  likely  that  the  splitting 
off  of  ammonia  from  the  amido-acids  may  take  place  outside  the  liver, 
and  only  the  synthetic  change  of  ammonia  into  urea  within  the  liver. 
As  a  consequence  of  disturbed  hepatic  function  we  may  therefore  assume 
at  most  an  increased  excretion  of  ammonia  with  a  simultaneous  decrease  in 
the  excretion  of  urea.  This  has  actually  been  determined  in  some,  but  by 
no  means  in  all,  cases  of  acute  yellow  atrophy  of  the  liver  (Minkowski, 
Miinzer,  Frankel,  Senator,  Soetbeer). 

Diagnostically,  however,  this  sign  cannot  be  utilized.  The  degree  of 
the  excretion  of  urea  and  the  total  nitrogen  excretion  cannot  readily  be 
determined  in  cases  of  extreme  insufficiency  of  the  liver,  because,  in  the 
first  place,  the  ingestion  of  food  as  well  as  t^e  digestion  and  absorption 
of  food  is  decidedly  limited;  secondly,  because  a  toxiferous  proteid  de- 
struction which  cannot  be  calculated  is  also  operative;  finally,  because 
the  excretion  of  nitrogen,  owing  to  the  severe  damage  to  the  kidney  which 
usually  occurs  simultaneously,  does  not  appear  to  be  uniform.  The  relative 
increase  of  the  excretion  of  ammonia  may,  however,  be  the  result  of  an 
excessive  production  of  acid  in  the  organism,  an  acidosis,  which  is  actually 
a  frequent  occurrence. 

The  abnormal  acids  which  in  such  cases  are  usually  found  in  the  urine 
probably  owe  their  origin  to  an  increased  destruction  of  tissue  elements. 
We  must  include  among  these  the  oxyacids  derived  from  the  amido-acids 
by  splitting  off  of  ammonia,  the  excretion  of  which  has  been  determined 
in  the  urine  in  acute  yellow  atrophy  of  the  liver,  also  hydro  par acumaric 
acid  derived  from  tyrosin  (the  homologous  oxymandelic  acid  found  by 
Schultze  and  Riess  in  the  urine  in  acute  yellow  atrophy).  Probably  many 
other  substances  belonging  to  this  category  are  also  found. 

Lactic  acid  (oxypropionic  acid),  which  has  been  detected  in  the  urine 
in  some  cases  of  severe  degeneration  of  the  liver,  is  probably  derived  from 
a  corresponding  amido-acid,  the  alanin  which  has  also  been  found  in  the 
urine  in  these  cases,  as  well  as  amidocaprionic  acid  and  leucin.  But  the 
excretion  of  this  (muscle)  lactic  acid  is,  perhaps,  connected  with  a  loss 
of  liver  function,  for  after  experimental  exclusion  of  the  liver  I  noted 
remarkably  large  quantities  of  lactic  acid  in  the  urine. 

Whether  the  albumoses  and  peptones  which  some  authors  have  found 
in  the  urine  in  acute  degeneration  of  the  liver  are  also  to  be  regarded  as 
the  results  of  the  abnormal  destruction  of  tissue  elements  is  at  least  ques- 
tionable. On  the  contrary,  the  increased  excretion  of  purin  substances 
(xanthin  bases  and  uric  acid)  may  undoubtedly  be  referred  to  an  increased 
destruction  of  cellular  nuclei.  No  special  diagnostic  significance  can  at 
present  be  attached  to  these  varied  occurrences. 


ACUTE  YELLOW  ATROPHY  363 

The  differentiation  of  simple  forms  of  jaundice  from  jaundice  due  to 
gall-stones  is  of  great  practical  importance.  We  cannot  here  enter  into  the 
details  of  the  diagnosis  of  cholelithiasis.  But  that  this  condition  is  a 
cause  of  jaundice  should  be  constantly  borne  in  mind  if  icterus  develops 
with  pain  or  if  colicky  attacks  of  pain  have  previously  been  localized  in 
the  region  of  the  gall-bladder,  if  the  jaundice  develops  very  suddenly  and 
soon  disappears^  and  if  repeated  attacks  of  icterus  occur  in  the  same  person. 

Above  all,  we  must  consider  the  possibility  of  incarceration  of  stone 
when  the  jaundice  lasts  for  an  extremely  long  time.  Although,  as  has  been 
stated,  there  are  exceptions  to  this  rule,  simple  jaundice  very  rarely  lasts 
longer  than  six  weeks.  When  the  course  is  more  protracted,  cholelithiasis, 
certain  forms  of  hepatic  cirrhosis,  and,  above  all,  neoplasms  of  the  biliary 
passages  come  into  question. 

Marked  enlargement  of  the  liver  and  spleen  generally  favors  diffuse 
hepatitis. 

The  diagnosis  of  simple  jaundice  in  an  elderly  person  always  demands 
the  careful  weighing  of  all  the  symptoms.  In  these  cases  neoplasms  of  the 
biliary  passages  and  the  head  of  the  pancreas  primarily  come  into  question. 

Close  investigation  of  the  various  pathological  conditions  and  their 
careful  consideration  will  usually  lead  us  to  a  correct  diagnosis.  But  the 
diagnostic  difficulties  may  sometimes  be  very  great.  Simple  jaundice 
rarely  fails  to  be  recognized;  much  more  frequently  this  is  diagnosticated 
when  instead  another  affection,  especially  cholelithiasis,  is  present. 


PROGNOSIS 

The  prognosis  in  jaundice  depends  mainly  upon  its  cause.  In  simple 
jaundice  it  is  usually  favorable;  but,  as  already  stated,  every  profound 
jaundice  brings  with  it  the  danger  of  a  more  or  less  sudden  hepatic  auto- 
intoxication. 

The  greater  the  development  of  the  typical  clinical  picture  of  acute 
yellow  atrophy  of  the  liver,  the  more  serious  the  prognosis.  The  fact  that 
this  affection  of  the  liver,  up  to  the  most  recent  times,  was  regarded  by 
many  authors  as  an  absolutely  fatal  disease,  and  a  termination  in  recovery 
as  a  signal  proof  of  diagnostic  error,  was  due  to  an  erroneous  idea  that 
the  process  was  of  peculiar  nature  and  produced  parenchymatous  degen- 
eration of  the  organ  which  led  to  atrophy,  and  the  connection  of  the 
disease  with  the  milder  forms  of  jaundice  and  of  acute  diffuse  hepatitis 
was  completely  overlooked.  If  we  consider  that  we  are  dealing  only  with 
different  degrees  in  the  intensity  of  the  disease,  it  will  not  surprise  us 
occasionally  to  find  a  case  running  a  severe  course  yet  terminating  in 
recovery. 

The  prognosis  in  the  individual  case  is  decided  mainly  by  the  severity 
of  the  general  symptoms  and  the  implication  of  the  central  nervous  system. 


354  JAUNDICE  AND  HEPATIC  INSUFFICIENCY 

Even  here  the  individuality  of  the  patient  must  be  taken  into  consideration, 
Leube  reports  a  case  in  which  the  appearance  of  delirium  and  convulsions 
indi(?ated  icterus  gravis;  but  the  further  course  proved  that  it  was  merely 
the  complication  of  simple  jaundice  with  severe  hysteria. 

When  a  rapid  decrease  in  the  size  of  the  liver  is  recognized  with  cer- 
tainty, or  when  leucin  and  tyrosin  appear  in  the  urine,  death  may  almost 
invariably  be  expected  in  a  short  time,  usually  in  two  or  three  days.  But 
exceptionally  a  favorable  outcome  has  been  observed,  even  in  these  cases. 

The  appearance  of  the  hemorrhagic  diathesis  is  a  most  unfavorable  sign. 
Occasionally  the  loss  of  blood  is  so  great,  particularly  in  hematemesis,  as 
speedily  to  cause  a  lethal  outcome. 

The  renal  function  is  to  be  regarded  as  an  important  factor  in  prog- 
nosis. Even  in  mild  cases,  the  intensity  of  the  clinical  symptoms  and, 
above  all,  of  the  subjective  symptoms  depends  chiefly  upon  the  secretion 
of  urine.  So  long  as  diuresis  continues  profuse,  there  is  no  immoderate 
accumulation  of  toxic  products  in  the  organism.  In  severe  cases,  the  renal 
function  decides  the  prognosis.  Therefore,  when  the  symptom  of  jaundice 
is  added  to  a  renal  affection,  it  must  be  regarded  as  a  very  serious  com- 
])lication;  the  state  of  the  kidneys  in  severe  cases  of  jaundice  is  even  more 
important,  for  the  affection  of  the  kidneys  is  here  the  consequence  of  a 
general  pathologic  condition,  and,  as  a  rule,  the  severity  of  the  renal 
disease  is  parallel  with  the  severity  of  the  hepatic  affection.  The  ominous 
symptoms  attributable  to  the  central  nervous  system  which  characterize 
the  picture  of  hepatic  autointoxication  are,  therefore,  usually  introduced 
by  an  excessive  decline  in  diuresis  and  an  extraordinary  decrease  in  the 
excretion  of  nitrogen,  and  these  may  be  regarded  as  an  expression  of 
the  increased  retention  of  toxic  substances  in  the  organism. 

Finally,  the  duration  of  the  jaundice  is  of  great  significance  in  the 
prognosis.  Isolated  cases  have  been  observed  in  which  jaundice  lasted  for 
several  months  and  even  for  a  year,  running  its  course  as  simple  benign 
icterus,  the  symptoms  at  last  completely  disappearing.  As  a  rule,  how- 
ever, a  prolonged  attack  of  jaundice  is  accompanied  by  special  dangers. 
We  frequently  attribute  the  jaundice  to  severe  organic  affections.  Jaun- 
dice in  itself  will,  in  the  course  of  time,  lead  to  nutritive  disturbances, 
emaciation  and  anemia,  which  may  remain  long  after  the  icterus  has  passed 
away.  If  the  flow  of  bile  is  not  brought  about  in  proper  time,  death 
usually  occurs  in  the  course  of  the  first  year,  most  often  between  the 
sixth  and  twelfth  months.  Cases  of  jaundice  lasting  several  years  are 
among  the  greatest  of  rarities. 

TREATMENT 

In  the  therapy  of  jaundice  we  must  first  take  into  consideration  the 
fact  tliat,  in  most  cases,  the  greatest  harm  is  wrought  in  the  digestive 
organs,  the  port  of  entrance  for  the  liver  and  biliary  channels.     When, 


ACUTE  YELLOW  ATROPHY  355 

therefore,  in  a  case  of  jaundice  special  circumstances  indicate  the  direction 
of  our  therapy,  it  must  be  our  first  endeavor  to  remove  any  deleterious 
agents  still  present  in  the  digestive  tract.  Various  intestinal  antiseptics 
that  are  recommended,  such  as  salol,  naphthol,  etc.,  are  in  these  cases 
much  less  effective  than  laxatives,  of  which  calomel,  rhubarb,  and  the 
saline  laxatives  are  preferable  for  this  purpose. 

Since  laxatives  also  stimulate  peristalsis  in  the  biliary  channels,  and 
thus  assist  in  the  evacuation  of  these  tracts,  they  may  also  relieve  the 
biliary  channels  of  deleterious  products  which  they  may  contain.  Whether 
the  biliary  passages  are  disinfected  by  the  introduction  of  substances 
which  pass  into  the  bile  and  there  exert  their  power  must  still  be  regarded 
as  doubtful.  The  salicylic  preparations  may  possibly  have  an  action  of 
this  kind.  Certainly  not  only  metals,  such  as  lead  and  mercury,  but  also 
other  substances  introduced  into  the  organism,  for  instance,  methylene- 
blue  and  alcohol  (Brauer),  are  excreted  with  the  bile. 

The  next  object  of  treatment  is  to  promote  the  flow  of  bile  into  the 
intestine. 

In  fulfilment  of  this  purpose,  we  attempt  the  following: 

1.  To  decrease  the  consistence  of  the  bile. 

2.  To  increase  the  motive  power  which  causes  the  propulsion  of  the 
bile. 

3.  To  reestablish  the  normal  hepatic  function. 

We  first  try  to  decrease  the  consistence  of  the  bile  by  a  profuse  intro- 
duction of  water.  It  is  quite  certain  that  the  intake  of  water  does  not  in 
the  slightest  degree  influence  the  quantity  of  the  hepatic  secretion,  as  it 
does,  for  instance,  the  quantity  of  the  renal  secretion;  water  is  by  no  means 
an  integral  constituent  of  the  excretion  of  the  liver,  as  it  is  of  the  kidneys. 
After  water  is  taken  into  the  stomach,  the  excretion  of  bile  is  increased, 
but  this  increase  in  the  amount  of  bile  does  not  exceed  the  increase  of  the 
biliary  secretion  which  occurs  after  the  ingestion  of  food.  If,  however, 
water  is  taken  upon  an  empty  stomach,  as,  for  example,  in  mineral  water 
treatment,  the  bile  to  a  certain  degree  is  diluted,  for  the  increase  of  the 
bile  is  out  of  proportion  with  the  simultaneous  increase  of  the  solid  biliary 
constituents.  There  have  been  no  accurate  investigations  of  the  effect  of 
the  introduction  of  water  upon  the  viscosity  of  the  bile.  Strauss  found  the 
molecular  concentration  of  bile,  measured  from  its  decrease  at  the  freezing 
point,  to  be  unchanged  after  the  introduction  of  water. 

It  has  been  believed  that  the  effect  of  water  upon  the  consistence  of 
the  bile  could  be  aided  by  the  simultaneous  administration  of  alkalies. 
But  from  the  results  of  experimental  researches  carried  out  by  Stadelmann 
and  his  pupils,  alkalies  do  not  appear  directly  to  influence  the  composition 
of  the  bile.  But  it  is  possible  that  they  may  have  a  certain  effect  upon 
the  mucin-like  substance  of  the  bile  upon  which  its  viscosity  is  chiefly 
dependent. 


356  JAUNDICE  AND  HEPATIC   INSUFFICIENCY 

The  effect  of  alkaline  waters,  such  as  those  of  Carlsbad,  Neuenahr, 
Vichy,  etc.,  has  at  present  only  an  empiric  foundation,  and  in  cholangitis 
as  well  as  in  other  affections  of  the  digestive  organs  it  is  attributed  to  the 
general  "  anticatarrhal "  action  of  these  waters.  But  the  influence  of 
mineral  water  treatment  upon  intestinal  peristalsis  as  well  as  upon  the 
circulation  of  the  blood  and  the  liver  is  possibly  even  more  important. 

The  propulsion  of  the  bile  may  be  promoted  by  any  remedies  which 
stimulate  intestinal  peristalsis.  This  probably  depends  upon  the  produc- 
tion of  contractions  in  the  musculature  of  the  biliary  passages,  and  espe- 
cially of  the  gall-bladder,  by  which  the  bile  previously  secreted  is  more 
rapidly  propelled  onward.  The  action  of  remedies  which  have  been  desig- 
nated as  "  cholagogues  "  is  probably  limited.  As  a  rule,  they  are  laxatives, 
such  as  calomel,  rhubarb,  aloes.  Jalap,  podophyllin,  evonynin  and  the  like. 
It  is  possible  that  the  action  of  olive  oil  and  the  oleate  salts,  of  which 
eunatrol  (sodium  oleate)  has  lately  been  praised,  is  founded  upon  this. 
But  it  is  difficult  to  understand  why  these  substances  in  particular  should 
be  administered  in  jaundice  when,  without  them,  there  is  already  a  de- 
ficient absorption  in  the  digestive  organs  of  fats,  fatty  acids,  and  soaps. 
The  apparent  effect  of  olive  oil  in  the  treatment  of  gall-stones  is  probably 
due  to  the  fact  that  the  calcium  and  magnesium  soaps  which  have  been 
reduced  to  soft  concrements  by  the  oil  have  been  mistaken  for  gall-stones. 

The  only  cholagogues  which  actually  increase  the  production  of  bile 
are  the  biliary  acid  salts.  It  is  obvious  that  their  administration  in 
jaundice  is  irrational. 

The  outflow  of  bile  from  the  liver  may  be  further  increased  by  remedies 
which  strengthen  the  abdominal  press,  and  thus  compress  the  liver  and  the 
biliary  passages.  The  action  of  the  emetics  formerly  employed,  such  as 
apomorphin  subcutaneously  injected,  probably  depends  upon  this  fact,  but 
in  general  they  are  not  advisable.  These  effects  in  a  milder  degree  may 
also  be  brought  about  by  physical  exercises  which  favorably  and  simul- 
taneously influence  the  portal  circulation  and  the  liver. 

Careful  massage  of  the  abdomen  may  be  very  beneficial.  Gentle  massage 
of  the  hepatic  region  with  the  flat  of  the  hand  or  by  stroking  in  small 
circles,  also  vibration  of  the  right  hypochondrium,  or  the  like,  is  generally 
preferable  to  that  brought  about  by  apparatus.  Kecently,  however,  the 
various  forms  of  instrumental  vibration  and  massage  have  been  said  to 
render  good  service.  One  author  particularly  advises  shock  of  the  entire 
body,  because  he  himself  was  cured  of  a  stubborn  jaundice  by  a  prolonged 
railroad  journey. 

The  method,  formerly  advised  by  C.  Gerhardt,  by  which  the  extended 
gall-bladder  was  encircled  with  the  fingers  and  expressed  has  quite  properly 
been  abandoned,  since  it  is  of  doubtful  utility  and  by  no  means  devoid 
of  danger. 

On  the  other  hand,  faradization  of  the  abdominal  wall,  which  occasion- 


ACUTE  YELLOW  ATROPHY  367 

ally  is  very  beneficial  in  the  treatment  of  jaundice,  is  still  less  harmless. 
It  appears  to  make  no  difference  whether,  as  Gerhardt  originally  advised, 
one  electrode  is  placed  in  the  region  of  the  gall-bladder  and  the  other  hori- 
zontally opposite  and  to  the  right  of  the  vertebral  column,  or  whether  the 
current  is  extended  to  other  areas  of  the  abdominal  wall. 

Active  gymnastic  exercises  are  said  to  promote  the  flow  of  bile,  par- 
ticularly deep  methodical  respiration  by  which  a  kind  of  auto-massage  of 
the  liver  is  attained. 

Injections  of  large  quantities  of  water  into  the  colon  are  very  valuable 
for  the  purpose  under  consideration,  since  they  produce  an  effect  by  stimu- 
lating peristalsis  as  well  as  by  direct  pressure  upon  the  liver  and  the  gall- 
bladder. According  to  Krull,  injections  of  cold  water  (12°  to  18°  R.) 
more  powerfully  stimulate  the  intestinal  mucous  membrane.  It  is,  how- 
ever, frequently  desirable  to  avoid  irritation  of  the  intestine;  in  such  cases 
water  of  the  same  temperature  as  the  body  is  slowly  injected  into  the 
bowel  with  the  least  possible  force.  By  this  means  the  intestine  is  thor- 
oughly cleansed  and  there  is  simultaneously  an  increased  absorption  of 
water  which,  for  various  reasons,  is  very  desirable  in  jaundice. 

In  order  to  restore  the  normal  hepatic  function,  the  best  method  is  to 
assist  the  curative  processes  in  the  diseased  organ  by  decreasing  the  labor 
thrown  upon  the  organ  as  well  as  by  facilitating  the  circulation  of  the 
blood  therein. 

The  labor  required  of  the  liver  depends  mainly  upon  the  quantity  and 
composition  of  the  food.  The  necessity  of  sparing  the  diseased  organ  there- 
fore primarily  necessitates  a  limitation  of  the  entire  food  mass.  The  ful- 
filment of  this  purpose,  particularly  at  the  beginning  of  the  disease,  is  in 
most  cases  greatly  facilitated  by  existing  anorexia  and  repugnance  to  food. 
Often  it  is  much  more  difficult  to  prevent  the  limitation  of  food  from 
exceeding  the  boundaries  necessary  to  maintain  the  body-weight  and  the 
activity  of  the  organism. 

As  to  the  composition  of  the  food,  it  must  be  remembered  that  the 
liver  is  implicated  in  the  digestion  of  all  organic  food  products,  carbo- 
hydrates and  fat  as  well  as  albuminates.  As  experience  teaches  us,  how- 
ever, the  absence  of  bile  in  the  intestine  results  chiefly  in  a  deficient  absorp- 
tion of  fats.  It  must  be  borne  in  mind  also  that  the  toxic  products  which 
cause  hepatic  autointoxication  most  likely  originate  in  changes  which  pro- 
teid  substances  undergo.  In  jaundice  there  is  almost  always  an  instinctive 
repugnance  to  fat  and  meat.  Therefore,  in  regulating  the  diet  in  jaundice, 
fats  must  be  limited  as  far  as  possible,  and  when  practicable  these  should 
be  given  only  in  a  well  emulsified  form,  as  in  milk ;  the  ingestion  of  albu- 
min should  be  kept  within  moderate  limits  and  not  exclusively  in  the 
form  of  meat;  and  the  total  amount  of  food,  principally  carbohydrates, 
should  be  given  in  an  easily  digestible  form. 

A  plentiful  supply  of  water  in  jaundice  is  desirable  for  more  than  one 


358  JAUNDICE   AND  HEPATIC   INSUFFICIENCY 

reason;  above  all  we  must  here  consider  that  the  acceleration  of  the  cir- 
culation of  the  blood  in  the  liver  and  the  absorption  of  water  are  simul- 
taneouslv  combined  with  the  dilution  of  all'  those  substances  which,  in  their 
passage  through  the  liver,  are  capable  of  damaging  the  cells  of  this  organ. 

Alcoholic  drinks  must  be  excluded,  as  there  can  be  no  doubt  of  the 
deleterious  effect  of  alcohol  upon  the  liver.  'Other  irritants  such  as  pun- 
gent spices  (pepper,  mustard,  red  pepper,  and  the  like)  must  also  be 
avoided,  since  experience  has  demonstrated  their  unfavorable  effect  upon 
the  liver,  and  also  because  the  relations  of  the  portal  vein  circulation  make 
it  appear  probable  that,  after  the  gastric  mucous  membrane,  the  hepatic 
cells  are  most  readily  damaged  by  the  action  of  these  substances. 

Moreover,  it  has  lately  been  shown  experimentally  by  Kobert  and  his 
pupils  (Carlau,  Jiirss)  that  substances  contained  in  mustard,  pepper,  nut- 
meg and  parsley  (oil  of  mustard,  piperin,  myristicin,  apiol)  exert  an  espe- 
cially toxic  effect  upon  the  liver  which  somewhat  resembles  the  effect  of 
phosphorus. 

In  the  nutrition  of  patients  with  jaundice  the  following  dietary  is  ad- 
visable: Milk,  milk  soups,  broths,  fruit  soups  and  flour  soups,  very  little 
meat  (150  to  200  grams),  without  fatty  sauce  and  with  but  little  spice; 
wheat  bread,  stewed  fruit,  and  light  starchy  food;  tender  vegetables  in 
inodorate  quantity  and  prepared  without  fat,  especially  as  puree;  weak  tea, 
abundance  of  ordinary  water,  or  alkaline  and  carbonated  mineral  waters, 
and,  if  desired,  fruit  syrups.  Naturally,  in  choosing  the  diet,  we  must, 
as  far  as  possible,  consider  the  individual  circumstances. 

The  rapidity  of  the  circulation  of  the  blood  through  the  liver  is  power- 
fully influenced  by  the  ingestion  of  food,  for  the  amount  of  -blood  which 
flows  through  the  liver  depends  chiefly  upon  the  quantity  of  blood  which 
passes  through  the  roots  of  the  portal  vein.  Reflex  hyperemia  of  the 
digestive  organs  following  the  administration  of  food  always  results  in 
an  increased  supply  of  blood  to  the  liver;  but  while  the  resorption  of 
digestive  products  caused  by  the  administration  of  solid  food  leads  to  an 
increased  exercise  of  the  functions  of  the  hepatic  cells,  water  causes  only 
an  advantageous  increase  in  the  rapidity  of  the  circulation  and  in  the 
nutrition  of  the  liver,  without  markedly  increasing  the  labor  of  the  organ. 
Herein  probably  lies  the  explanation  of  the  favorable  results  in  jaundice 
from  the  administration  of  water,  especially  of  the  mineral  water  cures, 
and  for  this  reason  it  appears  perfectly  reasonable  that  the  use  of  mineral 
water  should  be  restricted  to  the  early  morning  hours  when  the  stomach 
is  empty. 

It  is  obvious  that  the  various  physical  curative  methods  previously  de- 
scribed, as  well  as  the  stimulation  of  intestinal  peristalsis  by  laxatives, 
will  quicken  the  circulation  of  the  blood  in  the  liver.  And  here  the  chief 
cause  of  their  effect  in  jaundice  is  more  readily  recognizable  than  in  the 
mechanical  stimulation  to  the  flow  of  bile. 


ACUTE  YELLOW  ATROPHY  359 

Finally,  one  of  the  principal  aims  of  the  treatment  must  be  described, 
namely,  the  protection  of  the  organism  from  the  injurious  consequences 
of  the  impediment  to  the  flow  of  bile.  In  pursuance  of  this  aim,  the 
following  points  are,  above  all  others,  necessary: 

1.  To  increase  the  excretion  of  the  accumulated  biliary  constituents  by 
stimulating  the  vicarious  activity  of  other  glands. 

2.  To  combat  the  digestive  disturbances  due  to  the  absence  of  bile  from 
the  intestine. 

3.  To  treat  symptomatically  the  disturbances  arising  from  the  presence 
of  biliary  constituents  in  the  blood. 

To  promote  the  excretion  of  the  biliary  constituents  circulating  in  the 
organism,  the  activity  of  the  kidneys  comes  chiefly  into  consideration. 
Here  also  the  plentiful  intake  of  water  is  the  remedy  by  which  these 
harmful  substances  may  most  readily  be  washed  from  the  body.  The 
diuretic  action  of  the  salts  which  are  contained  in  mineral  waters  is  also 
beneficial  for  this  purpose.  In  special  cases,  particularly  with  threatening 
autointoxication,  more  active  diuretics,  such  as  caffein,  diuretin,  etc.,  are 
sometimes  of  use. 

In  most  severe  cases  of  cholemic  or  hepatic  autointoxication,  when  the 
condition  of  the  patient  will  not  permit  the  copious  introduction  of  water 
either  by  the  mouth  or  by  the  bowel,  we  must  attempt  by  subcutaneous 
or  intravenous  infusions  of  normal  salt  solution  to  restore  the  diuresis 
which  has  threatened  to  cease. 

The  excretion  of  biliary  constituents  by  other  secretions,  for  thera- 
peutic purposes,  scarcely  comes  into  question.  Biliary  constituents  are 
only  excreted  in  the  urine  and  in  the  sweat.  It  has  been  supposed  that 
the  yellow  discoloration  of  the  body  linen  frequently  observed  in  cases  of 
jaundice  was  due  merely  to  the  absorption  of  coloring  material  from  the 
desquamated  yellow-stained  epithelia  of  the  skin.  But  Fr.  Miiller  and 
Leube  have  obtained  the  undoubted  reaction  for  bile  in  sweat  produced 
by  injections  of  pilocarpin.  However,  the  amount  of  biliary  constituents 
excreted  in  this  manner  is  very  slight.  The  favorable  influence  of  warm 
baths  is  due  rather  to  their  effect  upon  the  circulation  of  the  blood  and  the 
entire  metabolism,  and  especially  upon  the  excretion  of  urine,  than  upon 
the  stimulation  of- excretion  by  the  skin. 

Biliary  constituents  pass  into  the  other  glandular  secretions  only  when 
there  are  pathological  changes  in  the  secretions  or  an  admixture  of  inflam- 
matory exudates  therein.  In  serous  effusions  there  may  be  a  very  decided 
admixture  of  biliary  constituents.  In  cases  of  jaundice  in  which  larger 
effusions  of  this  kind  are  present,  it  is  more  often  advantageous  to  relieve 
the  organism  of  biliary  constituents  by  aspiration  and  the  evacuation  of 
these  effusions  than  to  endeavor  to  bring  about  their  absorption  by  drugs. 

Digestive  disturbances  due  to  the  lack  of  bile  in  the  intestine  are  most 
actively  combated  by  such  regulation  of  the  diet  as  has  been  described. 


360  JAUNDICE  AND  HEPATIC   INSUFFICIENCY 

Good  service  may  also  be  rendered  by  laxatives,  by  mineral  water  treatment, 
bv  intestinal  irrigation,  and,  in  suitable  eases,  by  gastric  lavage.  For  the 
disagreeable  taste  complained  of  in  the  latter,  and  the  subjective  symptoms 
on  the  part  of  the  stomach,  hydrochloric  acid  or  carbolic  acid  may  be 
employed. 

In  regard  to  the  symptoms,  the  itching  of  the  skin  produced  by  the 
flooding  of  the  organism  with  biliary  constituents  is  one  which  requires 
special  treatment.  Among  remedies  which  have  proven  effective  and  which 
should  be  enumerated  here  are  the  following:  Cold  ablutions,  perhaps  with 
the  addition  of  vinegar,  citric  acid,  soda,  aluminum  acetate  or  a  one  per 
cent,  solution  of  carbolic  acid ;  inunctions  with  a  4  to  5  per  cent,  carbolic 
acid  salve,  10  to  20  per  cent,  bromocoll  salve,  or  with  a  2  to  3  per  cent. 
alcoholic  menthol  solution. 

In  stubborn  cases  the  internal  administration  of  potassium  bromid  (2 
grams  twice  daily)  and  injections  of  pilocarpin  (0.01-0.02)  or  of  atropin 
(0.0005-0.001)  are  recommended.  Often  we  require  narcotics  (morphin, 
chloral  hydrate,  and  the  like).  The  frequent  use  of  warm  baths  is  very 
beneficial. 

The  symptoms  of  severe  cholemic  intoxication  indicate  such  methods 
of  symptomatic  treatment  as  are  based  on  the  general  laws  of  the  treat- 
ment of  poisoning. 


CHRONIC    INFLAMMATION    OF   THE    LIVER 

Bv  E.  STADELMANN,  Berlin. 

Under  the  name  of  chronic  inflammation  of  the  liver  we  include  all 
those  inflammatory  processes  in  the  liver  which  are  distinct  from  acute 
inflammation,  hepatic  abscess.  Usually  the  term  "  chronic  interstitial 
hepatitis "  is  also  applied  to  them,  and  this  designation  simultaneously 
indicates  that  the  condition  consists  chiefly  in  an  inflammation  of  the 
connective  tissue.  Under  such  a  conception,  however,  difficulties  arise. 
Undoubtedly  there  is  an  increase  of  the  connective  tissue  in  every  chronic 
inflammation  of  the  liver,  but  this  is  by  no  means  to  be  regarded  as  the 
primary  element.  On  the  contrary,  eminent  authorities — I  shall  here  men- 
tion only  Weigert  and  Ackermann — have  affirmed  that  a  degeneration  of 
the  hepatic  cells  is  the  primary,  and  hypertrophy  of  the  connective  tissue 
only  the  secondary,  element.  Although  this  view  unquestionably  has  much 
in  its  favor,  and  receives  abundant  support  from  the  fact  that  a  number 
of  poisons  which  produce  chronic  inflammation  in  the  human  organism — 
I  shall  only  mention  alcohol,  phosphorus  and  arsenic — positively,  directly, 
and  primarily  attack  the  liver  cells,  producing  therein  contraction,  degen- 
eration, fatty  infiltration,  fatty  degeneration,  granular  cloudiness,  and  also 
cause  the  disappearance  of  nuclei  and  coagulation  necrosis,  etc.,  neverthe- 
less, in  my  opinion,  schematism  would  carry  us  too  far  if  we  were  to 
assume  that  all  increase  of  the  connective  tissue,  which  is  the  character- 
istic of  chronic  hepatic  inflammation,  is  only  secondary,  that  is  to  say, 
passive,  and  not  also  active.  I  do  not  believe  that  this  connective  tissue 
increase  is  produced  solely  by  the  primary  destruction  of  the  hepatic  cells 
in  such  a  way  that  by  distention,  distribution,  and  proliferation  it  fills 
the  spaces  present.  On  the  contrary,  I  think  we  must  take  the  standpoint 
that  many  of  the  etiological  factors  of  chronic  interstitial  hepatitis  act 
upon  the  hepatic  cells  as  well  as  upon  the  interstitial  connective  tissue, 
at  one  time  chiefly  upon  one,  at  another  time  chiefly  upon  the  other,  and, 
in  the  main,  with  such  effect  that  the  hepatic  cells  contract  under  this 
influence  and  perish,  while  the  connective  tissue,  on  the  contrary,  increases, 
that  is,  hypertrophies.  I  desire,  therefore,  to  express  my  conviction  that 
in  many  cases  of  chronic  interstitial  hepatitis  the  connective  tissue  hyper- 
trophy is  not  merely  a  passive  one,  but  is  also  active,  and  that  it  is  incor- 
rect to  exclude  by  the  name  "  chronic  interstitial  hepatitis  "  our  conception 

361 


362  CHRONIC   INFLAMMATION   OF  THE   LIVER 

of  primary  degenerative  parenchymatous  conditions.  Important  proofs  of 
the  correctness  of  this  view  are  at  hand.  Degeneration  of  the  hepatic 
cells,  as  well  as  connective  tissue  hypertrophy,  is  undoubtedly  present  in 
advanced  hepatic  cirrhosis — this  is  proven  by  the  investigations  of  Acker- 
mann  (1),  Hartung  (2),  and  others — but  in  itself  it  is  not  sufficient  proof; 
for  why  should  not  the  cell  degeneration  in  these  advanced  stages  of  disease 
be  a  secondary  effect  produced  by  the  pressure  of  the  hypertrophied  con- 
nective tissue?  The  reason  must  be  found  in  the  stage  of  onset  of  the 
process.  Is  the  affection  of  the  cells,  or  the  connective  tissue  proliferation, 
primary  ?  In  three  such  cases  which  he  investigated  Brieger  (3)  found  both 
conditions.  Orth  states  in  his  text-book  that  new  connective  tissue  forma- 
tion is  often  found  without  a  trace  of  cellular  change.  A  number  of  other 
authors  express  the  same  opinion.  Minute  microscopic  investigation  in 
chronic  interstitial  hepatitis  shows  that  connective  tissue  proliferation 
varies  in  different  cases.  While  in  one  instance  the  proliferation,  in 
the  main,  takes  place  in  the  interlobular  connective  tissue  encircling  one 
or  more  hepatic  lobules  (annular,  insular  form,  that  is,  monolobular  ancl 
multilobular  cirrhosis),  at  other  times  it  is  more  or  less  distributed  within 
the  individual  lobes  and  between  the  individual  hepatic  cells  (the  intra- 
lobular, that  is,  the  intracellular  form).  Connective  tissue  is  also  sometimes 
deficient  in  cells,  fibrous  (older  foci),  sometimes  rich  in  cells  (recent 
foci).  The  liver  cells  themselves  sometimes  show  decided  degenerative 
processes,  such  as  infiltration  with  fat  and  bile,  or  the  cells  are  small  and 
contracted ;  in  other  cases  they  are  nearly  normal,  or  even  enlarged.  In 
almost  all  processes  of  the  liver,  and  going  hand  in  hand  with  new  con- 
nective tissue  formation,  net-like  canals  are  found  with  lumen  which  are 
in  part  to  be  considered  the  remains  of  normal  biliary  passages,  partly 
as  newly  formed  bile  ducts,  or  their  development  may  be  attributed  to  a 
transformation  of  the  epithelia  of  the  true  hepatic  cell  trabeculae  which 
are  flattened,  so  that,  according  to  this  last  conception,  they  are  not 
related  to  the  actual  biliary  passages,  nor  do  they  possess  special  walls 
(Aufrecht).  It  is  only  certain  that  these  canals  have  a  lumen,  and  that 
they  may  be  injected  by  way  of  the  biliary  system  (Ackermann).  The 
macroscopical  appearance  of  the  liver  varies  in  different  cases;  sometimes 
the  organ  is  enlarged,  sometimes  decreased  in  size;  occasionally  smooth, 
at  other  times  nodular;  sometimes  it  is  of  normal  consistence  and  feels 
coarse  and  hard,  at  other  times  it  is  more  doughy  (fatty  degeneration) ; 
sometimes  the  liver  is  greatly  stained  by  bile,  at  other  times  not;  some- 
times the  organ  is  dark-brown  in  color  and  greatly  pigmented,  at  other 
times  whitish  and  massively  infiltrated  with  fat. 

We  shall  now  briefly  discuss  the  different  forms  of  hepatitis,  and  their 
mode  of  origin. 


CHRONIC  HEPATIC  INFLAMMATION  363 

A.  THE    VARIOUS   FORMS   OF    CHRONIC    HEPATIC 
INFLAMMATION 

The  various  findings  mentioned  above  have  led  to  the  differentiation 
of  many  individual  forms  of  hepatic  cirrhosis,  and  the  greatest  schematic 
development  has  been  attained  in  France  where  some  authors  have  elab- 
orated eight,  ten,  and  even  fifteen  different  forms  of  hepatic  cirrhosis. 
This  number  will  be  still  further  augmented  if  we  take  into  consideration 
the  etiology  of  new  connective  tissue  formation  and  the  clinical  course 
of  the  disease. 

Under  these  circumstances  we  may  maintain  comprehensively  that  new 
connective  tissue  develops  in  the  liver  from  the  following  causes: 

1.  Local,  chronic  foci  of  inflammation  develop  around  foreign  todies 
(particles  of  coal  dust)  which  have  entered  the  liver;  in  the  surroundings 
of  tumors;  around  parasites  (echinococcus) ;  from  implication  of  the  liver, 
from  chronic  inflammatory  processes  in  neighboring  organs  (stomach,  pan- 
creas) ;  from  trauma  which  produces  local  injury  to  the  liver,  and  when, 
in  consequence  of  a  primary  hepatitis,  a  secondary  connective  tissue  pro- 
liferation of  greater  or  less  extent  also  takes  place  in  the  hepatic  tissue. 
To  this  category  also  belong  the  small  interstitial  proliferations  caused 
by  foci  of  bacteria  from  various  infectious  diseases  (tuberculosis,  variola, 
scarlatina,  morbilli,  diphtheria,  etc.). 

2.  In  connection  with  the  abundant  and  regular  use  of  pungent  spices 
(particularly  curry)  and  the  abuse  of  drastics  (Cantani)  after  gout.  These 
modes  of  development  must  still  be  regarded  as  unproven.  The  same  is 
probably  true  of 

3.  The  appearance  of  cirrhosis  after  portal  vein  thrombosis,  to  which 
Botkin  and  Solowieff  (4)  have  called  attention.  Solowieff  has  endeavored 
to  prove  Botkin's  view  experimentally,  but  these  experiments  are  by  no 
means  conclusive.  Thrombosis  of  the  portal  vein  without  hepatic  cirrhosis 
is  unquestionably  observed  very  frequently  in  man,  and  where  these  occur 
simultaneously  the  assumption  is  obvious  that  cirrhosis  was  primary,  and 
thrombosis  of  the  portal  vein  secondary.  Simple  occlusion  of  the  portal 
vein  leads  to  atrophy  of  the  liver. 

4.  Cirrhosis  in  connection  with  arteriosclerosis  is  maintained  by  Du- 
plaix  (5)  who,  in  fact,  does  not  regard  hepatic  cirrhosis  as  an  independent 
local  disease,  but  as  an  affection  which  accompanies  systemic  disease. 
There  is  so  little  upon  which  to  base  this  view  that  discussion  hardly 
appears  necessary.  Arteriosclerotic  changes  may  occasionally  be  found  in 
the  hepatic  vessels,  and  may  lead  to  local  interstitial  proliferation,  but 
true  hepatic  cirrhosis  in  consequence  of  arteriosclerosis  may  be  regarded 
as  unproven. 

5.  In  chronic  states  of  stasis  hyperemia  of  the  liver  in  consequence  of 
continuous   pressure   from  the  dilated   blood-vessels,  an  atrophy  of  the 


364  CHRONIC  INFLAMMATION   OF  THE   LIVER 

hepatic  cells  and  hypertrophy  of  the  connective  tissue,  especially  about  the 
central  portions  of  the  lobules  (hepatic  vein),  which,  however,  may  also 
penetrate  into  the  atrophied  hepatic  cell  trabeculae  and  even  include  the 
interlobular  spaces  (nutmeg  liver),  so  that  at  last  the  picture  of  atrophic 
hepatic  cirrhosis  with  ascites,  etc.,  develops.  To  this  category  probably 
belong  the  chronic  perihepatitis  and  pericardial  pseudo-cirrhosis  lately 
described  by  several  authors  (H.  Eumpf  (6)  and  Fr.  Pick  (7)).  We  shall 
later  revert  to  these  forms  of  disease,  and  describe  them  somewhat  more 
in  detail. 

6.  The  quite  frequent  coincidence  of  hepatic  cirrhosis  and  tuberculosis 
is  remarkable,  particularly  tubercular  peritonitis.  Wagner  (8),  Moroux  (9) 
and  others  report  numerous  instances  of  such  simultaneous  occurrence. 
Wagner's  explanation  appears  to  me  to  be  correct,  namely,  that  cirrhosis 
is  the  primary  condition,  and  tuberculosis  the  secondary;  nevertheless, 
there  are  distinguished  authors  (Weigert)  who  hold  a  different  opinion, 
and  who  maintain  that  the  inverse  relation  of  these  diseases  to  one  another 
is  tlie  true  one.  According  to  these,  therefore,  tuberculosis  is  the  primary 
condition,  and  causes  the  cirrhosis. 

Tuberculosis  of  the  liver,  naturally,  is  frequently  observed  without  a 
simultaneous  cirrhosis.  The  tubercular  nodules  in  the  liver  frequently 
lead  to  no  inflammatory  proliferation  of  the  surrounding  tissue  worth 
mentioning.  In  other  cases,  however,  this  is  very  striking,  and  when  a 
great  number  of  tubercular  nodules,  which  naturally  must  have  existed 
for  a  long  time,  are  present,  the  picture  of  diffuse  interstitial  proliferation 
develops,  and  presents  some  similarity  to  that  of  hepatic  cirrhosis.  Con- 
traction of  the  organ  in  this  case  is  very  rare,  probably  because  the  under- 
lying condition  (tuberculosis)  early  causes  death,  for  tuberculosis  of  the 
liver  is  but  a  phase  of  general  tuberculosis.  We  do  not  deny  the  existence 
of  such  forms,  but  certainly  primary  cirrhosis  with  the  subsequent  develop- 
ment of  tubercles  is  more  frequent.  Occasionally  we  see  this  combined 
with  more  or  less  decided  fatty  infiltration  of  the  liver  cells.  That  tuber- 
culosis may  lead  to  fatty  liver  has  long  been  known,  and  cannot  be  regarded 
as  singular.  At  one  time  this,  at  another  time  that,  of  the  pathologic 
conditions  enumerated  preponderates,  and  thus  varying  pictures  are  pre- 
sented. We  are,  however,  scarcely  justified — and  this  is  evident  from  the 
al)ove  brief  discussion — as  the  French  maintain  (Hanot  and  Gilbert  (10) 
and  others),  in  differentiating  this  form  of  cirrhosis  as  a  special  one,  and 
then  proposing  numerous  subdivisions — not  less  than  six.  This  is  certainly 
carrying  schematism  too  far. 

7.  Here  we  must  mention  the  malarial  liver  which  in  Germany  is  quite 
rare.  We  therefore  quote  the  following  description  from  French  and  Ital- 
ian literature,  without  permitting  ourselves  the  right  of  criticism  as  to  the 
correctness  of  these  findings.  It  is  well  knowm  that  in  profound  malarial 
infection  a  large  amount  of  pigment  is  formed  from  the  destroyed  cor- 


CHRONIC   HEPATIC   INFLAMMATION  365 

puscles,  and  this  is  deposited  in  various  organs,  particularly  in  the  spleen 
and  liver.  The  pigment  enclosed  by  leukocytes  is  sometimes  found  in  the 
hepatic  capillaries,  producing  thrombosis  therein,  sometimes  within  the 
liver  cells,  and  to  some  extent  also  in  the  interstitial  tissue.  The  liver 
assumes  a  rusty  brown  or  dirty  grayish-brown  appearance.  The  pigment 
sometimes  gives  a  reaction  for  iron  (melanin),  sometimes  not.  The  liver 
is  rich  in  bile — as  in  mild  jaundice — enlarged,  hyperemic,  smooth,  and 
painful  upon  palpation. 

In  the  acute  cases  proliferation  of  the  interstitial  tissue  does  not  occur, 
as  is  the  case  in  chronic  malaria.  In  the  latter  disease  marked  enlarge- 
ment of  the  liver  is  found,  partly  in  consequence  of  hyperemia,  partly 
due  to  an  increase  of  the  parenchyma.  The  liver  cells  are  large,  swollen, 
opaque,  with  a  large  nucleus  frequently  beginning  to  segment.  If  the 
course  of  the  disease  is  prolonged,  from  this  stage  a  second  develops  in 
which  the  liver  becomes  atrophic.  The  liver  cells  degenerate,  the  con- 
nective tissue  is  but  little  increased,  the  organ  is  flaccid  and  smooth. 
Sometimes,  however,  a  different  condition  is  found  (Kelsch  (11)  and 
Kiener)  and  the  liver  is  more  voluminous,  is  soft,  irregular,  covered  with 
small  nodules,  which  are  whitish,  or  golden  yellow  to  greenish,  of  the 
size  of  a  pea,  projecting  from  the  reddish  parenchyma.  In  these  nodules 
the  cellular  trabeculae  are  greatly  thickened  (to  four  times  their  normal 
size).  The  individual  cells  are  very  large  and  opaque,  and  show  one  or 
more  large  nuclei.  The  normal  arrangement  of  the  hepatic  lobules  is 
broken  up,  the  peripheral  hepatic  trabeculae  being  centrally  flattened  by 
the  pressure  of  the  hypertrophied  tissue.  Sometimes  these  nodules  resemble 
adenomata.  In  about  one-third  of  the  cases  (probably  the  oldest  forms 
of  the  disease)  we  then  observe  more  prominent  interstitial  proliferations 
starting  from  the  interlobular  spaces,  and  resembling  the  process  in  ordi- 
nary hepatic  cirrhosis. 

These  forms  and  stages  of  hepatic  disease  may  be  combined  in  one  and 
the  same  case  to  a  varying  extent  and  thus  produce  very  different  pictures. 
According  to  Ughetti  (12)  the  malarial  liver  in  the  south  of  Italy  differs 
nowise  from  ordinary  hepatic  cirrhosis,  and  does  not  present  the  peculiar- 
ities described  by  Kelsch  and  Kiener. 

8.  Similarly  as  in  malaria,  hepatic  cirrhosis  also  occurs  in  diabetes 
meUitus.  Some  authors  have  included  both  forms — this  and  the  preceding 
— under  the  term  "  cirrhoses  pigmentaires."  Cirrhosis  in  diabetes — at  least 
in  Germany — is  a  rare  disease;  this  was  first  described  by  Hanot  and 
Chauffard  (13)  as  cirrhose  pigmentaire  hypertrophique.  The  patient  shows 
marked  cutaneous  pigmentation — similar  to  that  in  Addison's  disease — 
with  cachexia  and  moderate  diabetes.  The  liver  is  greatly  enlarged  and 
indurated,  and  shows  decided  pigmentation  as  well  as  profuse  cirrhotic 
connective  tissue  proliferation.  The  pigment  gives  a  reaction  for  iron, 
and  shows  itself  to  be  closely  related  to  hemoglobin.     Hence  we  may 


366  CHRONIC   INFLAMMATION   OF  THE   LIVER 

conclude  that  in  the  organism  of  the  patients  affected  great  and  long- 
continued  destruction  of  red  blood-corpuscles  plays  an  important  role. 
Quincke  (14)  called  attention  to  the  fact  that  in  diabetics  there  is  "  side- 
rosis,"  i.  e.,  a  deposit  of  iron-containing  pigment  in  the  different  organs. 
Occasionally  this  occurs  in  consequence  of  hepatic  cirrhosis.  Upon  the 
basis  of  Quincke's  investigations,  however,  the  view  so  widely  current  in 
French  literature,  that  siderosis  of  the  liver  is  the  cause  of  cirrhosis,  must 
be  rejected.  We  fail  to  see  why  a  diabetic  should  not  have  hepatic  cirrhosis, 
and,  on  the  other  hand,  why  a  patient  with  hepatic  cirrhosis  should  not 
contract  diabetes.  I  am  unwilling  to  acknowledge  any  causal  connection 
between  these  diseases.  In  fact,  patients  with  hepatic  cirrhosis  and  a 
simultaneous  diabetes  by  no  means  always  show  the  above  mentioned  pig- 
mentation. Why  diabetes  leads  to  hemosiderosis  is  not  quite  clear.  Perhaps 
acidosis,  the  production  of  oxybutyric  acid,  leads  to  the  destruction  of  the 
rod  blood-corpuscles  in  the  organism.  I  believe  this  a  subject  well  worthy 
of  discussion.  That  autointoxication  occurs  in  the  course  of  severe  dia- 
Ijetes,  in  consequence  of  acidosis,  that  is,  the  production  of  oxybutyric  acid 
(coma  diabeticum),  is,  in  my  opinion,  a  positive  fact.  That  the  circula- 
tion of  abnormal  products  of  metabolism  in  the  blood  must  exert  a  dele- 
terious influence  upon  the  red  blood-corpuscles  appears  to  me  to  be  quite 
obvious.  But  we  would  digress  too  far  to  follow  this  thought  at  the 
pi-esent  time.  I  desire  only  to  mention  that  in  two  patients  with  diabetes 
and  distinct  hepatic  cirrhosis,  whom  I  have  under  observation  at  the 
present  time,  the  one  without  acidosis  presents  no  sign  of  cutaneous  pig- 
mentation, while  the  second,  Avho  has  been  constantly  observed  for  about 
three  years,  and  who,  in  spite  of  a  very  strict  diet,  has  about  4  per  -cent, 
of  sugar  in  the  urine,  and  is  passing  three  liters  in  twenty- four  hours, 
has  severe  acidosis  and  presents  the  typical  picture  of  diabete  bronze.  The 
former  of  the  patients  just  mentioned  succumbed  after  a  continuous  ob- 
servation of  several  months,  and  in  him  ordinary  cirrhosis  hepatis  was 
found  without  any  peculiarities.  The  amount  of  sugar  in  the  urine,  which 
at  first  varied  between  7  and  8  per  cent,  (the  amount  of  urine  could  not 
be  definitely  determined,  as  the  patient  was  careless),  then  gradually  de- 
creased, notwithstanding  the  fact  that  no  dietetic  measures  could  be  car- 
ried out  with  the  patient,  and  during  the  last  two  or  three  months  of  his 
life  sugar  had  entirely  disappeared.  Besides  cirrhosis  and  diabetes  there 
was  also  decided  cystitis,  but  no  nephritis;  periodically  considerable  blood 
was  found  in  the  urine,  and  the  autopsy  proved  that  this  originated  in 
the  bladder.  The  urine  never  showed  the  iron  chlorid  reaction.  At  the 
autopsy  the  pancreas  was  found  to  be  perfectly  normal. 

The  second  patient  exhibited  marked  cutaneous  discoloration  (grayish- 
brown)  in  different  areas  (face,  hands,  testicles,  penis,  skin  of  the  abdo- 
men). The  pigmentation  has  increased  but  little  in  the  last  few  3'ears. 
Tlu'  liver  is  large,  reaching  to  the  umbilicus,  is  tough,  smooth,  and  reveals 


CHRONIC   HEPATIC   INFLAMMATION  367 

a  sharp  margin;  there  is  no  tendency  to  contraction.  The  spleen  is  not 
enlarged.  For  about  a  year  and  a  half  the  patient  has  employed  alkalies 
(sodium  citrate)  continuously,  maintains  his  weight  at  about  60  kilos, 
and  follows  his  occupation.  There  is  no  jaundice,  no  ascites,  no  edema. 
That  the  disease,  as  reported,  rapidly  leads  to  cachexia  and  causes  death 
from  ascites  and  edema,  therefore  does  not  appear  to  be  true  in  all  cases. 
Certainly  there  has  been  no  apparent  change  in  the  condition  of  my 
patient  for  about  three  years,  and  the  liver  invariably  shows  the  same 
abnormalities. 

In  diabetes  not  only  the  hypertrophic,  but  also  the  atrophic,  form 
(Hanot  (15)  and  Sehachmann)  is  occasionally  observed. 

That  there  is  an  undoubted  and  distinct  pigmentation  of  the  skin  in 
these  cases,  among  which  the  case  of  my  patient  above  mentioned  belongs, 
and  not,  as  Quincke  believes,  chiefly  a  cachexia,  I  positively  maintain 
from  my  own  experience. 

Siderosis  with  hepatic  cirrhosis  also  occurs  in  other  diseases  without 
diabetes;  for  instance,  in  pernicious  anemia  (Quincke)  and  phthisis  pul- 
monalis  (Marchand). 

9.  The  Italians,  for  instance  Galvagni  and  Ughetti  (16),  have  described 
a  form  of  hepatic  cirrhosis  as  "  hepatitis  interstitialis  flaccida."  But  our 
experience  regarding  these  observations  is  at  this  time  so  slight  that  we  can 
do  no  more  than  mention  the  name. 

10.  The  French  (Hutinel,  Sabourin  (17))  have  several  times  described 
a  type  of  hepatic  cirrhosis  as  "  cirrhose  graisseuse,"  and  have  differentiated 
it  as  a  distinct  form.  This  is  said  to  be  characterized  by  a  marked  fatty 
infiltration  of  the  hepatic  cells  as  well  as  the  distinct  proliferation  of  the 
interstitial  tissue.  The  liver  is  sometimes  increased  in  size,  at  other  times 
small;  this  form  is  found  in  alcoholics  as  well  as  in  the  tubercular.  I 
do  not  recognize  it  as  a  special  variety.  Any  one  who  frequently  examines 
cases  of  hepatic  cirrhosis  knows  that  the  amount  of  fat  in  the  cells  varies 
within  wide  limits,  and  occasionally  may  be  enormous.  Here  we  have 
probably  only  the  combination  of  cirrhosis  with  fatty  liver.  Which  affec- 
tion is  the  primary  one  is  of  less  importance;  that  alcoholism  produces 
fatty  degeneration  as  well  as  cirrhosis  has  long  been  known,  and  that  fatty 
liver  as  well  as  interstitial  proliferation  may  be  observed  in  tuberculosis 
has  just  been  stated  under  paragraph  6. 

11.  Chronic  inflammation  of  the  liver  in  consequence  of  the  chronic 
effect  of  poisons.  When  alcohol  is  habitually  taken  by  man  in  large  quan- 
tities, it  not  only  produces  fatty  infiltration  of  the  liver  but  also  hepatic 
cirrhosis.  This  statement  may  be  regarded  as  a  positive  fact.  The  only 
question  is  whether  chronic  alcoholism  produces  different  forms  of  inter- 
stitial hepatitis  or  only  that  form  which  we  designate  as  Laennec's  atrophic 
hepatic  cirrhosis,  or  also  granular  atrophy.  Later  we  shall  minutely  dis- 
cuss the  fact  that,  chiefly  for  clinical,  and  less  for  anatomical,  reasons, 

25 


368  CHRONIC   INFLAMMATION   OF  THE   LIVER 

we  differentiate  two  forms  of  hepatic  cirrhosis,  namely,  (a)  the  above  de- 
scribed atrophic  or  Laennec's  cirrhosis,  and  (b)  hypertrophic  hepatic  cir- 
rhosis. Some  authors,  particularly  Rosenstein  (18),  assume  that  the  latter 
are  not  attributable  to  the  abuse  of  alcohol,  while  most  authors  agree  in 
regarding  alcohol  as  the  causa  peccans.  The  question  is  so  important 
tliat  it  must  be  discussed  somewhat  more  in  detail. 

Hepatic  cirrhosis  is  most  often  caused  by  spirits,  and  it  is  especially 
noteworthy  that  the  quite  large  number  of  children  mentioned  in  literature 
as  addicted  to  alcohol,  and  who  are  found  with  hypertrophic  hepatic  cirrho- 
sis, are  made  drunkards  chiefly  by  the  deplorable  ignorance  of  their  parents 
and  relatives.  But  beer  and  wine  also  cause  hepatic  cirrhosis,  although 
much  more  rarely. 

In  France  the  immoderate  use  of  absinthe  is  often  alleged  to  be  the 
cause  of  hepatic  cirrhosis.  The  following  is  shown  by  statistics:  That  in 
about  one-third  of  all  cases,  according  to  Frerichs  (12  patients  in  36) 
as  well  as  Bamberger,  the  immoderate  use  of  alcohol  may  be  regarded  posi- 
tively as  the  cause.  Price  (19)  found  among  142  cases  of  hepatic  cirrhosis 
108  occurring  in  men  and  34  in  women  (i.e.,  about  3  to  1).  Abuse  of 
alcohol  was  positive  in  72  cases,  probable  in  8^or  9,  unmentioned  in  50, 
and  positively  denied  in  a  few.  But  in  these  statistical  compilations  the 
two  forms  of  the  disease  have  not  been  separated,  Mangelsdorf  (20)  found 
in  49  cases  of  hypertrophic  cirrhosis  that  19  might  be  etiologically  referred 
to  alcoholism,  in  5  alcohol  was  suspected,  and  in  17  it  could  not  be  ex- 
cluded. In  only  5  cases  was  there  no  history  of  alcohol  or  syphilis,  the 
latter  affection  being  the  positive  cause  in  3  cases,  and  likely  in  2.  With 
the  widely  prevalent  use  of  alcohol  by  all  classes  of  the  population,  it  is 
extremely  difficult  to  prove,  in  the  individual  case,  that  it  has  had  a 
deleterious  effect  and  has  caused  the  disease.  What  is  regarded  as  much 
by  one  person  another  considers  very  little.  One  person  who  takes  habit- 
ually a  certain  quantity  of  alcohol  regards  himself  as  strictly  temperate, 
another  who  drinks  the  same  quantity  suffers  from  pangs  of  conscience, 
and  regards  himself  as  an  alcoholic.  But  the  same  quantity  of  alcohol 
has  a  baneful  but  varying  effect  upon  different  persons.  Here  we  cannot 
reckon  toxicologically  by  the  kilo  of  weight.  One  person  on  a  moderate 
daily  amount  of  alcohol  is  attacked  by  hepatic  cirrhosis;  another  worships 
Gambrinus,  Bacchus,  and  the  god  of  alcoholic  spirits,  and  goes  unpunished 
all  his  days.  But  the  cases  which  Mangelsdorf  describes,  and  others  which 
I  have  found  in  literature,  are  so  positive  and  conclusive  that  there  can 
be  no  question  as  to  the  influence  of  alcohol  in  the  development  of  hyper- 
trophic hepatic  cirrhosis.  The  consumption  of  from  3  to  6  liters  of  wine 
daily  is,  nevertheless,  a  large  amount,  particularly  if  we  refer  to  its  use 
by  women.  These  reports  are  so  conclusive  that  we  can  hardly  reconcile 
with  them  the  view  of  Rosenstein  (20  a  and  65)  that,  in  his  cases,  alcohol 
as  an  etiologic  factor  could  be  excluded.    We  must  emphasize  that  Rosen- 


CHRONIC  HEPATIC  INFLAMMATION  369 

stein's  view  is  of  great  importance,  since  he  has  seen  a  large  number  of  cases 
of  hypertrophic  hepatic  cirrhosis,  and  it  cannot  be  denied  that  the  frequency 
of  the  occurrence  of  these  forms  varies  greatly  in  different  localities.  In 
spite  of  the  immoderate  use  of  spirits  and  the  great  prevalence  of  atrophic 
hepatic  cirrhosis  in  Berlin,  typical  forms  of  hypertrophic  hepatic  cirrhosis 
are  quite  rare.  Therefore,  we  conclude  that  some  unknown  factor  besides 
alcohol  must  be  operative  to  produce  hypertrophic  hepatic  cirrhosis. 

How  alcohol  causes  hepatic  cirrhosis  has  not  yet  been  made  clear.  It  is 
possible  that  it  first  produces  inflammation  in  the  vessels  while  it  is  passing 
in  a  concentrated  form  from  the  stomach  and  intestines  into  the  portal 
vein  vessels,  and  perhaps  it  has  also  a  directly  deleterious  influence  upon 
the  hepatic  cells.  We  cannot  say  more  than  "  perhaps."  None  of  the 
views  previously  expressed  are  positive,  and  each  requires  proof.*  It  is 
said  that  alcohol  is  not  excreted  by  the  hepatic  cells,  for,  according  to  the 
researches  of  Weintraud,  even  after  the  administration  of  large  quantities 
it  cannot  be  detected  in  the  bile. 

The  results  of  Weintraud's  investigations  are  diametrically  opposed  by 
the  recent  experimental  inquiries  of  Brauer  {Zeitschr.  f.  physiolog.  Chemie, 
XL,  H.  3  und  4).  This  author,  after  administering  large  doses  of  alcohol 
to  dogs,  readily  demonstrated  the  presence  of  alcohol  in  the  bile,  besides 
quite  decided  amounts  of  albumin.  These  findings  should  be  of  great 
significance  in  proving  the  correctness  of  the  view  above  expressed  that 
alcohol  enters  the  liver  unchanged,  passes  into  the  bile,  and  directly  irri- 
tates and  damages  the  hepatic  cells.  This  continuous  damage  would  finally 
lead  to  the  destrtiction  of  the  cells  and  to  the  development  of  hepatic 
cirrhosis.  Alcohol  is  also  found  in  the  urine,  but  less  abundantly  than  in 
the  liver.  Besides  being  affected  by  cirrhosis,  many  alcoholics  also  suffer 
from  nephritis,  and  these  affections  may  quite  properly  be  referred  to  the 
same  cause,  namely,  alcohol.  The  secretion  of  the  milk  glands,  however, 
does  not  contain  alcohol  (Klingemann),  consequently  nurslings,  at  least, 
are  protected  from  the  consequences  of  the  abuse  of  alcohol  on  the  part 
of  their  mothers  and  wet-nurses. 

Alison's  (21)  statistics  are  also  interesting;  he  found  in  the  country 
among  farm  hands  the  proportion  of  cirrhosis  to  alcoholism  as  1  to  85; 
in  the  city,  however,  with  a  sedentary  mode  of  life,  it  was  1  to  25,  and 
with  great  bodily  activity  the  number  of  city  cases  also  decreases  greatly, 
i.  e.,  to  about  1  to  42.  Therefore,  we  should  send  our  alcoholics  to  the 
country  and  assign  them  to  strenuous  corporeal  labor  if  we  desire  to  pro- 
tect them  from  hepatic  cirrhosis,  and  this  would  not  even  be  injurious; 
but  it  would  prove  as  difficult  to  enforce  this  prophylaxis  as  to  induce 
them  to  renounce  their  alcohol. 

In  comparison  with  alcohol  as  the  cause  of  hepatic  cirrhosis  other 
poisons  are  insignificant. 

In  man  phosphorus,  more  than  any  other,  destroys  the  hepatic  cells 


370  CHRONIC   INFLAMMATION  OF  THE   LIVER 

and  produces  marked  fatty  infiltration.  It  frequently  causes  the  anatomical 
picture  of  acute  yellow  atrophy,  but  rarely  true  hepatic  cirrhosis. 

Arsenic,  antimony  and  chloroform  are  also  said  to  produce  hepatic 
cirrhosis  in  man,  and,  according  to  Langowoi  (22),  this  is  also  true  of 
cantharides.  Here  it  seems  fitting  to  consider  somewhat  minutely  the 
experimental  investigations  which  have  been  made  in  the  hope  of  solving 
the  many  questions  under  discussion  which  have  just  been  enumerated. 
An  attempt  was  made  to  produce  hepatic  cirrhosis  in  animals,  and  for 
this  purpose  various  poisons,  especially  alcohol,  phosphorus  and  chloro- 
form, were  used.  Unfortunately,  as  we  must  admit  at  the  outset,  most 
of  these  endeavors  have  been  fruitless. 

It  has  been  impossible  to  produce  hepatic  cirrhosis  in  animals  by  ad- 
ministering alcohol.  This  is  shown  by  the  invariable  negative  trials  of 
Strassmann  (23),  Afanassiew  (24)  and  y.  Kahlden  (25).  Fatty  liver 
was  induced,  but  not  hepatic  cirrhosis.  In  my  opinion  these  results  con- 
tradict the  earlier  and  positive  reports  of  Dujardin-Beaumetz,  Pupier, 
Strauss  and  Blocq.  Afanassiew  claims  that  he  has  produced  degeneration 
of  the  hepatic  cells  by  prolonged  and  large  doses  of  alcohol,  especially  in 
rabbits,  while  v.  Kahlden  denies  such  a  pathologic  finding. 

Perhaps  the  toxic  effect  of  alcohol  with  large,  individual  doses  was  not 
long  enough  continued. 

H.  Mertens  maintains  that  he  has  lately  produced  typical  hepatic 
cirrhosis  in  rabbits  by  keeping  the  animals  continuously  in  an  atmosphere 
permeated  with  alcohol. 

According  to  Mertens  (26),  chloroform  in  subcutaneous  injections  has 
a  much  more  powerful  effect.  He  was  able  to  produce  typical  hepatic 
cirrhosis,  and  to  determine  that  the  liver  constantly  became  harder,  more 
granular,  and  more  contracted.  The  liver  cells  suffered  first;  they  became 
opaque,  atrophic,  and  showed  fatty  degeneration,  being  permeated  with 
vacuoles.  Later,  starting  from  the  portal  vessels,  connective  tissue  devel- 
oped which  became  diffused  through  the  hepatic  lobules  toward  the  center 
(the  hepatic  veins).  By  the  kindness  of  Professor  Heymanns  in  Ghent, 
where  Mertens  worked,  I  was  able  to  obtain  sections  of  such  livers  for 
examination.  These  livers  showed  typical  granular  atrophy  with  the  above 
described  microscopic  findings.  Nevertheless,  I  am  very  skeptical  in  regard 
to  experimental  investigations  in  rabbits  on  account  of  my  own  extensive 
experience.  These  animals  frequently  have  diseased  livers,  and  consequently 
we  are  easily  led  astray  in  regard  to,  at  least,  the  early  stages  of  cirrhosis. 

I  do  not  altogether  countenance  the  investigations  of  Boix  (27)  who, 
by  the  introduction  of  small  amounts  of  butyric  acid  (for  three  months), 
acetic  acid  (for  thirty-five  days),  and  also  of  lactic  acid  and  valerianic  acid, 
produced  typical  atrophic  hepatic  cirrhosis  in  rabbits. 

Recent  experiments  have  cast  a  doubt  upon  the  apparently  positive 
production  of  phosphoric  hepatitis  observed  by  Wegner.    Kronig  (28),  as 


GRANULAR  ATROPHY   OF  THE   LIVER  371 

well  as  Ziegler  and  Obolensky  (29),  found  almost  invariably  marked  epi- 
thelial degeneration,  but  the  inflammatory  phenomena  were  only  moderate, 
and,  according  to  my  investigations,  the  conditions  resembled  those  pro- 
duced by  toluylendiamin.  Ziegler  and  Obolensky  expressly  state  in  their 
report :  "  It  appears  impossible,  from  the  investigations  at  hand,  to  draw 
conclusions  from  poisoning  by  phosphorus  and  arsenic  as  to  the  genesis 
of  hepatic  cirrhosis  in  man.  At  present  the  latter  can  only  be  determined 
by  the  histologic  investigation  of  cirrhotic  livers." 

Aufrecht  (30),  it  is  true,  holds  a  diiferent  opinion.  He  maintains 
that  he  has  seen  connective  tissue  hypertrophy  follow  phosphorus  poison- 
ing without  any  epithelial  degeneration,  I  reiterate  the  fact  that  Aufrecht 
experimented  on  rabbits,  but,  as  mentioned  above,  in  these  animals  such 
experiments  are  not  conclusive. 

We  have  still  to  mention  four  other  forms  of  chronic  inflammation  of 
the  liver,  which  will  be  explicitly  described  later: 

12.  Cirrhosis  hepatis,  that  is,  Laennec's  cirrhosis,  which  has  several 
times  been  mentioned. 

13.  Hypertrophic  hepatic  cirrhosis, 

14.  Biliary  hepatic  cirrhosis. 

15.  Syphilitic  hepatic  cirrhosis. 

From  a  clinical  rather  than  from  a  pathologico-anatomical  standpoint 
it  appears  necessary  to  diiferentiate  the  two  fundamental  forms  of  hepatic 
cirrhosis,  (a)  the  atrophic  and  (b)  the  hypertrophic  hepatic  cirrhosis,  as 
two  contrasting  types,  between  which  are  numerous  transitional  forms; 
therefore  they  will  be  separately  considered. 

B.   CIRRHOSIS    HEPATIS— LAENNEC'S   CIRRHOSIS-GRANULAR 
ATROPHY    OF    THE    LIVER 

This  form  of  hepatic  cirrhosis  receives  its  name,  which  was  first  given, 
it  by  Laennec,  from  the  fact  that  in  advanced  stages  it  leads  to  contraction 
which  causes  the  anatomical  condition  to  resemble  the  granular  atrophy 
of  the  kidneys.  Etiologically  this  form,  as  described  above,  may  chiefly 
be  attributed  to  the  abuse  of  alcohol,  hence  the  affection  preponderates 
among  men.  Although  all  clinicians  are  unanimous  on  this  point,  it  must, 
nevertheless,  be  stated  that  there  are  cases  of  hepatic  cirrhosis  in  which 
the  abuse  of  alcohol  cannot  be  proven,  nor  can  any  of  the  causes  enumer- 
ated for  the  appearance  of  the  affection  be  found.  The  question,  there- 
fore, arises  whether  or  not,  as  with  alcohol,  other  toxic  products  in  large 
quantities  (products  of  metabolism)  may  not  occasionally  find  their  way 
from  the  intestine  into  the  portal  vein  system,  and  there  exert  a  deleterious 
influence  upon  the  liver  which  may  result  in  hepatic  cirrhosis.  We  all 
know  that  in  the  human  organism  an  antitoxic  function  is  quite  properly 
ascribed  to  the  liver,  and  the  inference  is  obvious  that  occasionally  under 


372  CHRONIC   INFLAMMATION   OF  THE   LIVER 

an  increased  virulence  of  the  toxins  which  are  normally  brought  to  the 
organ,  and  considering  the  amount  of  labor  to  be  performed,  this  anti- 
toxic power  may  not  be  exerted.  A  possible  support  for  this  view  may 
be  found  in  the  latest  investigations  of  Brauer  {Zeitschr.  f.  physiol.  Che- 
mie,  Bd.  40,  Heft  3  u.  4)  who,  after  administering  relatively  large  quan- 
tities of  methylene  blue  to  animals  by  the  mouth,  soon  after  found  it  in 
the  bile,  sometimes  even  in  larger  quantities  than  in  the  urine.  Methylene 
blue,  therefore,  in  concentrated  form,  passes  from  the  digestive  tract  into 
the  liver,  from  which  it  is  excreted  into  the  intestine  by  means  of  the 
bile;  therefore  it  passes  through  an  intermediary  circulation.  Similar 
processes  might  be  considered  in  the  case  of  toxins,  and  the  investigations 
of  Brauer  at  least  prove  that  this  is  not  impossible,  but  actually  occurs. 
Perhaps  the  unproven  reports  of  the  production  of  hepatic  cirrhosis  after 
the  use  of  pungent  spices  (particularly  curry),  after  the  frequent  admin- 
istration of  drastics  (Cantani),  after  taking  the  extract  of  male  fern 
(Grawitz),  after  gout,  etc.,  may  thus  be  satisfactorily  explained;  neverthe- 
less, we  are  forced  to  conclude  that  the  individual  predisposition  here  also 
plays  a  significant  role. 

PATHOLOGICAL  ANATOMY 

The  most  important  points  have  already  been  enumerated.  In  the  ad- 
vanced stage  the  organ  is  contracted,  small,  and  very  hard,  so  that  upon 
section  with  a  knife  a  grating  sound  is  produced.  It  is  misshapen,  the 
surface  is  irregular,  uneven,  and  covered  with  nodules  about  the  size  of 
a  pea.  The  serosa  is  frequently  thickened.  Microscopically  the  marked 
increase  of  connective  tissue  is  most  conspicuous,  and  this,  following  the 
interlobular  and  intralobular  vessels,  by  its  contraction  destroys  the  hepatic 
cells  as  well  as  the  blood-vessels  and  bile  capillaries.  Frequently  little 
remains  of  the  hepatic  parenchyma,  and  this  is  surrounded  by  wide  con- 
nective tissue  striae.  The  arrangement  of  the  hepatic  lobules  and  of  the 
hepatic  trabecule  is  everywhere  destroyed  by  the  connective  tissue  which 
permeates  it.  In  place  of  the  lost  liver  cells  we  see  occasionally  a  collection 
of  brown  pigment.  Regenerative  processes  may  also  be  observed  in  the 
shape  of  so-called  newly  formed  biliary  passages  and  blood-vessels  in  the 
newly  formed  connective  tissue.  The  latter  are  not  in  communication 
with  the  portal  vein,  but  with  the  hepatic  artery.  The  newly  formed  con- 
nective tissue  is  usually  fibrinous,  and  sometimes  rich  in  cells,  according  to 
tlie  age  of  the  new  formation.  Sometimes  the  liver  is  smooth,  in  spite 
of  considerable  connective  tissue  proliferation  in  the  organ,  but  only  when 
ilip  arrangement  of  this  tissue  is  somewhat  uniform.  The  cause  of  this 
difference  is  unknown. 

Of  those  advanced  forms  which  represent  the  terminal  stage  of  a  process 
existent  for  years,  the  earliest  stages  differ  very  materially.  The  organ  is 
then  uniformly  enlarged,  of  greater  consistence,  its  border  dull,  the  surface 


GRANULAR  ATROPHY   OF  THE   LIVER  373 

less  smooth.  Microscopically  the  previously  described  processes  are  present, 
but  only  to  a  slight  extent. 

By  the  pressure  of  connective  tissue,  many  of  the  portal  vein  branches 
are  destroyed;  the  consequence  of  this  is  stasis  in  the  larger  branches  of 
the  portal  vein.  The  formation  of  new  capillaries  of  the  hepatic  artery 
does  not  sufficiently  compensate  for  this.  Large  branches  of  the  portal 
vein  may  also  be  compressed  by  firm  connective  tissue  proliferation. 

The  beginning  of  the  process  can  scarcely  be  recognized  macroscopically, 
and  can  only  be  fully  determined  by  microscopic  examination  of  the  organ. 

Fatty  degeneration  of  the  liver  to  a  greater  or  less  extent,  associated 
with  the  extension  of  the  process  and  the  inconstancy  of  individual  phe- 
nomena, furnishes  very  varying  pictures,  and  presents  an  opportunity,  if 
Ave  have  a  tendency  to  schematism,  to  differentiate  many  dissimilar  forms, 
for  which,  however,  there  is  no  necessity. 

For  instance,  to  mention  but  a  few  of  these  individual  forms,  we  hear 
of  monolobular  and  multilobular  cirrhosis,  according  to  whether  few  or 
many  lobules  have  been  embraced  and  enclosed  by  individual  connective 
tissue  proliferation.  The  cirrhosis  is  called  bivenous  when  the  connective 
tissue  proliferation  starts  not  only  from  the  portal  vein  branches  but  also 
from  the  central  veins. 

Furthermore,  we  speak  of  a  "  cirrhose  hypertrophique  graisseuse,*'  of  a 
monocellular  or  intercellular  form,  of  a  "forme  mixte,"  etc.  Surre  (31) 
differentiates  eight  forms  of  hepatic  cirrhosis,  and  many  authors  consider 
this  as  by  no  means  exhaustive. 

The  question  has  been  mooted  whether  in  the  course  of  hepatic  cirrho- 
sis there  is  also  a  stage  of  hypertrophy  of  the  organ.  Great  importance 
has  been  attached  to  the  decision  of  this,  especially  in  the  discussion  re- 
garding the  justification  for  separating  hypertrophic  hepatic  cirrhosis  as 
a  special  pathologic  process.  In  this  disease,  which  will  be  described 
minutely  in  the  next  chapter,  a  permanent  and  quite  decided  enlargement 
of  the  organ  is  especially  characteristic. 

Xow  there  is  no  doubt  that  in  the  course  of  atrophic  hepatic  cirrhosis 
a  periodical  and  more  or  less  marked  enlargement  of  the  organ  takes  place. 
Any  one  who  has  seen  many  cases  of  hepatic  cirrhosis  will  confirm  this. 
This  hypertrophic  stage  of  the  organ,  besides  being  due  to  the  hyperemia, 
the  swelling  of  the  cells,  the  increased  and  not  yet  contracted  connective 
tissue,  is  also  attributable  to  a  more  or  less  decided  fatty  infiltration  of 
the  cells.  In  atrophic  hepatic  cirrhosis,  adenomatous  neoplasms  form  which, 
perhaps,  are  later  transformed  into  malignant  tumors  (carcinoma),  and 
which  naturally  increase  the  circumference  of  the  organ.  Therefore,  the 
causes  of  so-called  hypertrophy  of  the  liver  in  atrophic  hepatic  cirrhosis 
are  many,  and  this  alone,  even  when  it  persists  for  a  long  time,  does  not 
warrant  us  in  assuming  hypertrophic  hepatic  cirrhosis,  and  excluding 
Laennec's  atrophic  form. 


374  CHRONIC   INFLAMMATION   OF  THE   LIVER 

SYMPTOMATOLOGY  AND   COURSE    OF   THE   DISEASE 

The  disease  certainly  exists  for  a  long  time — occasionally  for  years — 
without  giving  rise  to  symptoms,  and  is  often  discovered  while  examining 
patients  who  come  to  us  in  consequence  of  some  other  affection.  In  keep- 
ing with  the  etiology,  symptoms  on  the  part  of  the  gastrointestinal  canal 
resembling  those  so  frequently  present  in  alcoholics  are  the  first  complaints 
of  the  patient.  These  consist  of  nausea,  anorexia,  eructations,  vomiting, 
constipation,  sometimes  even  diarrhea,  pressure  and  a  sensation  of  fulness 
in  the  epigastrium,  even  pains  in  this  region,  etc.  The  enlarged  liver 
causes  distress  by  pressure  upon  the  neighboring  organs.  The  patients  are 
debilitated,  the  general  condition  suffers.  Pain  is  rare  in  true  atrophic 
hepatic  cirrhosis.  It  occurs  only  when  the  inflammation  especially  attacks 
the  capsule  of  the  liver,  and  this  is  seldom.  In  the  course  of  the  disease 
irregular  rises  of  temperature  are  occasionally  noted,  which  come  and  go, 
and  for  which  no  cause  can  be  assigned.  Severe  symptoms  are  observed 
only  in  the  later  stages,  when  disturbances  appear  which  are  due  to  the 
portal  vein  circulation.  Mild  jaundice  may  be  present,  but  does  not  neces- 
sarily belong  to  the  picture  of  atrophic  hepatic  cirrhosis.  In  consequence 
of  the  destruction  of  so  many  small  portal  vein  vessels,  there  is  stasis  of 
the  blood  in  the  trunk  of  the  portal  vein  which  reacts  upon  the  stomach 
and  intestine.  The  consequence  is  an  increase  of  the  catarrhal  symptoms 
in  ])oth  organs  and  the  appearance  of  ascites,  which  then  becomes  promi- 
nent in  the  picture  of  hepatic  cirrhosis  and  continues  permanently.  Dis- 
tention of  the  abdomen,  and  an  increasing  sense  of  weight  and  fulness 
in  the  same,  are  frequently  the  first  symptoms  which  the  patient  observes. 
The  ascites  may  develop  to  an  extraordinary  extent,  and  by  forcing  up  the 
diaphragm  as  well  as  hindering  respiration  may  cause  the  patient  much 
distress.  Frequently  edema  of  the  lower  extremities  follows.  With  the 
constantly  increasing  symptoms  on  the  part  of  the  gastrointestinal  canal, 
the  nourishment  is  deficient  and  the  patients  rapidly  lose  weight.  The 
3normously  distended  abdomen  forms  a  striking  contrast  with  the  body 
emaciated  almost  to  a  skeleton.  Hemorrhages  occur  in  consequence  of 
decided  stasis  of  blood  in  the  esophagus,  stomach,  and  intestines.  These 
are  occasionally  only  of  the  capillary  form,  so  that  hemorrhagic  feces  and 
the  vomiting  of  black  mass6s  are  observed.  But  these  hemorrhages  may 
not  infrequently  be  also  very  copious,  and  threaten  life ;  then  large  amounts 
of  pure  blood  are  vomited,  and  the  dejecta  are  of  a  black,  tarry  color.  At 
the  autopsy  ruptured  varices  are  found  to  be  the  cause  of  this,  especially 
in  the  lowest  portions  of  the  esophagus;  but  pure  parenchymatous  hemor- 
rhages may  also  endanger  life  through  their  massiveness.  The  nutrition 
of  the  walls  of  the  vessels  also  suffers  and  leads  to  hemorrhages  in  various 
organs,  such  as  the  skin,  the  mucous  membrane,  the  retina,  etc. ;  fatal 
epistaxis    is    also    sometimes    observed.      The    slight    jaundice    is    partly 


GRANULAR  ATROPHY   OF  THE   LIVER  375 

due  to  compression  of  the  biliary  channels  in  the  liver  and  to  biliary 
stasis  due  to  the  resorption  of  bile,  in  part  it  may  be  referred  to  duodenal 
catarrh. 

The  examination  of  the  abdominal  organs  with  an  existing  ascites  is 
very  difficult,  and  often  is  only  possible  after  the  fluid  has  been  withdrawn. 
A  hard,  contracted,  nodular  liver  is  then  usually  felt;  sometimes  the  organ 
is  so  small  that  it  can  no  longer  be  palpated. 

The  condition  of  the  spleen  in  hepatic  cirrhosis  is  of  importance. 
Frequently  it  is  enlarged  to  two  or  three  times  its  normal  size;  and  this 
is  a  factor  of  great  significance  in  the  diagnosis  of  the  affection,  particu- 
larly in  its  last  stages  when  the  liver  can  no  longer  be  palpated.  Enlarge- 
ment of  the  spleen  is  not  only  due  to  stasis  of  the  blood  in  the  portal  vein, 
but  to  direct  hyperplasia  of  its  tissue,  with  an  increase  of  the  connective 
tissue.  We  must,  therefore,  assume  that  active  processes  are  going  on  in 
the  spleen,  similar  to  those  in  the  liver.  Sometimes,  however,  splenic  en- 
largement is  absent,  particularly  if  the  capsule  is  tough  and  thickened. 

Ascites. — Ascites  requires  a  somewhat  more  detailed  description.  The 
fluid  fluctuates  in  the  abdominal  cavity,  and  is  to  be  attributed  to  the 
passage  of  fluid  through  the  intestinal  serosa  into  the  peritoneal  cavity. 
According  to  Quincke  (32)  some  of  the  transudated  fluid  is  poured  out 
by  the  lymph-vessels  of  the  diaphragm  and  of  the  parietal  peritoneum,  and 
this  is  independent  of  the  portal  vein  circulation.  When  the  ascitic  fluid 
is  withdrawn  it  is  usually  clear,  amber-colored,  with  a  specific  gravity  of 
1.012  to  1.014,  and  contains  from  0.6  per  cent,  to  1.2  per  cent,  of  albumin. 
There  is  scarcely  a  trace  of  sugar  or  biliary  coloring  matter.  Turbidity 
to  any  extent  points  to  complicating  inflammation  of  the  peritoneum; 
blood  may  appear  in  small  or  in  large  quantities  in  consequence  of  stasis 
hyperemia  of  the  serosa. 

In  addition  to  the  previously  mentioned  stasis,  dilatation  of  large  venous 
areas  which  have  a  collateral  relation  to  the  portal  vein,  or  may  become 
thus  related,  plays  an  important  part  in  hepatic  cirrhosis.  Notwithstand- 
ing the  obstruction  to  the  circulation,  large  quantities  of  blood  from  the 
portal  vein  system  may  be  poured  into  the  veins  of  the  body  and  thus 
the  portal  system  is  greatly  relieved.  It  appears,  however,  that  the  com- 
pensatory importance  of  this  collateral  development  is  greatly  exaggerated; 
this  value,  at  least  clinically,  is  rarely  observed. 

Collateral  Circulation. — 1.  The  communication  of  the  mesenteric  veins 
with  the  veins  of  the  abdominal  walls.  2.  The  connection  of  the  gastric 
veins  with  the  inferior  esophageal  veins  and,  through  these,  with  the 
azygos  vein.  3.  The  conjunction  of  the  internal  hemorrhoidal  veins  and 
the  hypogastric  veins.  4.  The  communication  of  the  veins  of  Glisson's 
capsule  with  the  veins  of  the  diaphragm  through  perihepatitic  adhesions. 
5.  A  dilatation  of  the  incompletely  obliterated  umbilical  or  paraumbilical 
veins  which  run  along  the  ligamentum  teres,  from  which  point  blood  may 


376  CHRONIC   INFLAMMATION   OF  THE   LIVER 

then  be  carried  by  the  portal  vein  to  the  veins  of  the  abdominal  walls, 
particularly  to  the  epigastric  vein.  These  veins  of  the  abdominal  walls 
are  more  or  less  markedly  dilated,  and  form  a  figure  which  bears  a  re- 
mote resemblance  to  the  head  of  Medusa  {caput  Medusce),  and  accordingly 
has  received  this  name.  The  caput  Medusae,  at  least  in  its  well  developed 
form,  is  by  no  means  frequent;  we  must  not  mistake  for  it  simple  dilata- 
tion of  cutaneous  veins,  such  as  the  superior  and  inferior  epigastric  veins 
combined,  which  represent  nothing  more  than  collateral  tracts  of  the  com- 
pressed inferior  vena  cava;  these  may  be  found  in  any  form  of  abdominal 
dropsy,  and  not  only  when  they  are  the  consequence  of  an  implication  of 
the  portal  vein  circulation. 

Other  and  rarer  collateral  formations,  for  example,  communication  be- 
tween the  paraumbilical  and  the  right  iliac  vein  by  a  vein  of  the  abdominal 
wall   (Drummond),  require  no  further  mention. 

The  pulse  is  small  and  somewhat  accelerated,  but  it  is  regular  unless 
there  are  complications  on  the  part  of  the  heart. 

The  respiration  is  accelerated  when  ascites  is  present  because  the  dia- 
phragm is  forced  up,  and  its  action  is  limited. 

If  death  does  not  take  place  early  from  intercurrent  diseases  and  com- 
]ilications,  this  is  preceded  by  symptoms  of  increasing  weakness  and  ex- 
haustion. Not  rarely  the  patient  falls  into  a  comatose  condition  with 
delirium,  general  convulsions,  etc.,  and  from  this  he  never  awakens.  This 
gives  us  the  impression  that  we  are  dealing  with  a  condition  resembling 
cholemia,  such  as  is  observed  in  long-continued  stasis  jaundice,  or  in  acute 
yellow  atrophy  of  the  liver.  As  jaundice  is  absent  or  very  slight  in  the 
affection  in  question,  this  cannot  be  attributed  to  intoxication  with  con- 
stituents of  the  bile,  but  it  must  be  due  to  other  products  of  metabolism 
which  are  not  yet  sufficiently  known.  The  antitoxic  function  of  the  liver 
is  unquestionably  not  its  least  important  one — this  we  have  previously  re- 
ferred to.  But  in  this  respect,  as  well  as  in  many  others,  the  organ  cannot 
function  on  account  of  the  constant  and  increasingly  rapid  disappearance 
of  its  parenchymatous  cells.  The  toxins — probably  entering  from  the  in- 
testine— penetrate  the  protective  wall,  flood  the  organism,  and  produce  the 
condition  which  we  designate  as  autointoxication.  Perhaps  the  same  sub- 
stances, and  not  biliary  constituents,  cause  the  condition  known  as  ''  chole- 
mia "  or  "  acholia." 

Of  the  nature  of  these  toxins  we  have,  unfortunately,  as  yet  no  accu- 
rate knowledge,  and  in  my  opinion  here,  i.  e.,  in  the  study  of  this  toxin 
production,  scientific  investigators  should  lead  the  way.  Up  to  the  present 
time,  we  have  considered  only  ammonia,  the  aromatic  products  (phenol, 
skutol.  indol,  etc.),  the  alkaloidal  products  (putrescin,  cadaverin,  neuridin, 
etc.,  which  we  have  included  under  the  name  diamin,  and  a  knowledge  of 
wliich  we  mainly  owe  to  the  pioneer  investigations  of  Brieger),  and  the 
products  of  metabolism  of  the  bacteria  from  the  intestine  which  have  a 


GRANULAR  ATROPHY  OF  THE  LIVER  377 

toxin-like  effeci,  that  is,  in  other  words,  the  products  of  proteid  decom- 
position. 

In  regard  to  ammonia,  the  investigations  of  Nencki,  Pawlow,  Hahn  and 
others  in  dogs,  with  Eck's  fistula  (excluding  the  portal  vein  circulation) 
should  be  borne  in  mind.  In  their  experiments  upon  animals,  these  in- 
vestigators observed  symptoms  which  closely  resembled  those  of  cholemia, 
particularly  when  nitrogenous  food  was  administered. 

Many  authors  (Heger  (33),  Schiff  (34),  Lautenbach  (35)  and  others) 
found  that  the  liver  not  only  retains  certain  poisons  which  are  introduced 
with  the  blood  (nicotin,  strychnin,  hyoscyamin,  etc.)  but  also  destroys 
them  or  transforms  them  into  non-toxic  substances,  or,  at  least,  stores 
them  up. 

Special  credit  for  working  out  and  elucidating  this  question  is  due  to 
Bouchard  (36)  and  his  pupil  Roger  (37).  According  to  the  latter  the 
liver  acts  upon  poisons  in  three  ways:  1.  It  stores  them  (metallic  poisons 
such  as  copper,  iron,  arsenic,  etc.).  3.  It  excretes  them  with  the  bile  (a 
rarer  and  less  active  process).  3.  It  renders  the  poisons  more  or  less 
inert,  i.  e.,  destroys  them  or  changes  them  into  non-toxic  combinations 
(vegetable  alkaloids,  peptones,  toxic  products  of  intestinal  decomposition, 
ptomains). 

This  protective  action  of  the  liver,  according  to  Roger,  is  due  to  the 
glycogen  it  contains,  with  which  these  poisons  combine,  and  thus  become 
non-toxic.  It  must  be  confessed  that  these  teachings  have  not  been  gen- 
erally accepted,  and  that  they  cannot  as  yet  be  regarded  as  incontrovertible. 
We  shall  see  later,  when  discussing  the  treatment,  particularly  the  dietetics 
of  diseases  of  the  liver,  in  how  far  we  may  utilize  these  views.  Other 
experimental  investigations  to  determine  the  principle  on  which  is  based 
this  protective  action  of  the  liver  toward  poisons,  I  shall  not  discuss. 
They  have  given  us  no  additional  information. 

Bouchard  attempted  to  prove  this  important  property  of  the  liver  indi- 
rectly by  testing  the  toxicity  of  the  urine  in  various  diseases  of  the  liver, 
and  comparing  it  with  the  normal.  He  started  with  the  hypothesis  that 
the  soluble  poisons  circulating  in  the  body  were  excreted  in  the  urine. 
If  the  liver  had  an  antitoxic  action,  this  must  be*  limited  in  hepatic  dis- 
eases, and,  in  consequence,  the  urine  must  be  more  toxic  (the  "  urotoxic 
coefficient"  increases).  He  found  his  deductions  confirmed,  and  he  drew 
from  these  many  conclusions,  some  of  which,  however,  are  very  question- 
able. If  we  accept  all  that  has  been  stated,  notwithstanding  the  criticisms 
at  hand  as  to  the  results  of  experiments,  we  can  no  longer  doubt  the 
influence  of  the  liver  upon  numerous  poisons  (accordingly  upon  those  also 
which  reach  it  from  the  intestine). 

The  investigations  of  metabolism  in  hepatic  cirrhosis  have  not  been 
very  extensive,  biit,  nevertheless,  we  have  obtained  some  very  remarkable 
results.     In  regard  to  the  metabolism  of  nitrogen  in  hepatic  cirrhosis. 


378  CHRONIC   INFLAMMATION   OF  THE   LIVER 

Hallervorden  (38)  has  occasionally  found  very  large  quantities  of  am- 
monia in  the  urine  (up  to  2.5  in  the  daily  quantity).  I  also  (39),  and 
following  me  many  other  authors  (Fawitzky  (40),  Gumlich  (41),  v.  Noor- 
den  (42),  Miinzer  (43),  found  the  quantity  of  ammonia  increased  in 
comparison  with  the  total  amount  of  nitrogen  (10  to  18  per  cent,  instead 
of  the  normal  2  to  5  per  cent.),  but  the  absolute  figures  very  rarely 
reach  the  amount  determined  by  Hallervorden  (Momer  (44)  and  Sjoquist 
found  in  one  case  2.4  grams).  Yet  from  this  alone  we  cannot  determine 
a  diminution  of  the  urea-forming  function  of  the  liver,  which,  on  the 
contrary,  appears  to  be  extraordinarily  active,  usually  to  the  end.  For, 
besides  these  large  quantities  of  ammonia,  large  amounts  of  urea  also  are 
formed  (30  to  40  grams  in  twenty-four  hours).  With  the  decreased  ex- 
cretion of  urea  which  may  be  regarded  as  the  consequence  of  a  deficient 
ingestion  of  food,  of  inanition,  the  excretion  of  ammonia  is  also  lessened. 
The  relation  of  urea  to  the  total  amount  of  nitrogen  of  the  urine  is  also 
but  little  altered  (77  to  01  per  cent,  as  compared  with  the  normal  of  80 
to  90  per  cent.).  Some  time  ago  I  (45)  expressed  the  conviction  that 
other  factors,  and  particularly  an  increased  excretion  of  acid,  caused  an 
increased  excretion  of  ammonia.  In  the  urine  I,  as  well  as  v.  Noorden, 
occasionally  found  sarcolactic  acid,  as  has  lately  Calabrese  (46),  while 
V.  Jaksch  demonstrated  fatty  acids,  particularly  acetic  acid,  valerianic  acid, 
butyric  acid  and  propionic  acid.  Weintraud  (47)  administered  ammonia 
up  to  9  grams  in  hepatic  cirrhosis,  and  found  no  increased  excretion  of 
ammonia,  but  only  the  requisite  and  expected  increased  excretion  of 
urea.  Therefore,  if  urea  is  produced  in  the  liver  alone  and  not  in 
other  organs,  which,  however,  is  unlikely,  we  must  not  conclude  from 
these  findings  that  this  important  function  is  sufficiently  performed  by  the 
remaining  parts  of  the  hepatic  tissue,  and  that  life  ceases  before  the  disease 
leads  to  marked  and  distinctly  recognizable  anomalies  in  urea  formation. 
The  recent  conclusions  of  Schittenhelm  (Deutsches  Arch.  f.  Min.  Medicin, 
LXXA-'II,  H.  5  u.  6)  in  the  main  agree  with  my  views;  he  also  noted 
an  increase  of  the  excretion  of  ammonia  in  the  urine  in  destructive  hepatic 
atfections,  and  refers  this  to  the  acidity  of  the  organism.  Peptone  is 
positively  absent  from  the  urine  in  hepatic  cirrhosis;  albumoses  are  occa- 
sionally found,  but  they  are  rare  and  in  insignificant  amounts.  Uric  acid 
excretion' is  within  normal  limits,  as  well  as  the  alloxur  bodies  (prior  stages 
of  uric  acid)  which  have  lately  come  within  the  circle  of  scientific  inves- 
tigation. The  finding  of  leucin  and  tyrosin  is  more  than  questionable, 
von  Jaksch  (48),  who  has  made  very  extensive  investigations  in  regard 
to  the  nitrogen  excreted  in  the  urine  in  hepatic  diseases,  has  come  to  the 
couclusion  that,  in  the  main,  it  appears  as  urea,  and  that  other  nitrogenous 
products  are  not  found  in  increased  amount. 

The  lioat-generating  function  of  the  liver  must  naturally  suffer  as  soon 
as  the  activity  of  the  organ  is  decreased.    As,  however,  the  normal  function 


GRANULAR  ATROPHY   OF  THE   LIVER  379 

of  this  organ  in  proportion  to  the  heat-producing  power  of  the  entire 
organism  is  not  definitely  known,  in  pathologic  processes,  naturally,  little 
can  be  said  on  this  point.  I  believe  that  Ihis  function  of  the  most  important 
glandular  organ  of  the  body  is  not  insignificant.  However,  there  is  as  yet 
no  possibility  of  our  determining  the  effect  of  absence  of  its  function  in 
the  human  organism. 

Sugar  is  sometimes  found  in  the  urine  of  these  patients.  Yet,  on 
account  of  the  rarity  of  the  finding,  I  do  not  regard  it  as  in  organic  relation 
to  the  underlying  affection  (hepatic  cirrhosis),  but  merely  as  an  accidental 
complication. 

Steinhaus  (49)  found  in  the  majority  of  cases  of  hepatic  cirrhosis 
investigated  by  him  (in  11  out  of  12)  distinct  connective  tissue  prolifera- 
tion of  the  pancreas  resembling  that  of  the  liver,  and  he  believes  that 
occasional  diabetes  in  such  patients  may  be  attributed  to  this  condition. 
These  observations,  therefore,  coincide  with  the  opinion  expressed  above 
that  diabetes  is  here  not  directly  due  to  the  hepatic  disease. 

Alimentary  glycosuria  has  also  been  observed,  but  too  rarely  for  us  to 
deduce  diagnostic  conclusions  therefrom,  as  do  the  French  authors.  This 
is  true,  at  least,  regarding  grape-sugar  (intake  and  excretion).  With  the 
intake  of  levulose,  the  condition  is  different  (H.  Strauss  (50),  Lepine 
(51)),  for  it  has  been  observed  that  patients  with  disease  of  the  liver 
usually  develop  levulosuria  in  contrast  with  normal  persons.  In  26  of  39 
patients  examined  by  Strauss,  this  levulosuria  could  be  demonstrated. 

As,  however,  according  to  the  reports  of  Landsberger  {Deutsche  med. 
Wochenschr.,  1903,  Nr.  32),  similar  conditions  are  not  infrequent  in  healthy 
persons,  our  anticipation  of  having  found  an  important  aid  for  the  diag- 
nosis of  alimentary  levulosuria  has  met  with  disappointment. 


COMPLICATIONS 

Alcohol,  which  is  the  chief  cause  of  hepatic  cirrhosis,  also  damages  a 
number  of  other  organs,  such  as  the  heart,  kidneys,  vessels,  etc.  Combined 
with  hepatic  cirrhosis  we  also  frequently  find  myocarditis,  nephritis,  and 
arteriosclerosis,  but  rarely  pachymeningitis  or  chronic  meningitis.  The 
other  complications  of  hepatic  cirrhosis,  such  as  portal  vein  thrombosis  and 
fatty  liver,  have  already  been  mentioned.  Myocarditis  with  its  sequels, 
edema,  congestion  of  the  liver,  etc.,  as  well  as  nephritis,  is  often  the  cause 
of  the  fatal  termination  of  our  cases. 

The  not  infrequent  combination  of  hepatic  cirrhosis  and  primary  car- 
cinoma of  the  liver  is  remarkable,  as  is  the  connection  between  hepatic 
cirrhosis  and  peritoneal  tuberculosis  which  has  been  referred  to  previously. 


380  CHRONIC   INFLAMMATION  OP  THE  LIVER 


DIAGNOSIS  AND   PROGNOSIS 

Easy  as  the  diagnosis  of  hepatic  cirrhosis  may  be  in  many  cases,  in 
others  it  may  be  most  obscure.  In  alcoholics  with  enlarged  hard  liver, 
recognizable  enlargement  of  the  spleen,  and  moderate  ascites,  the  diagnosis 
presents  no  special  difficulty.  This  only  becomes  perplexing  when  we  are 
dealing  with  patients  in  whom  marked  ascites  makes  palpation  of  the 
abdominal  organs  impossible.  Then  we  must  first  determine  whether  a 
general  circulatory  disturbance  is  the  cause  of  the  ascites.  If  the  heart, 
lungs  and  kidneys  are  normal,  if  there  is  no  general  edema,  it  is  exceedingly 
likely  that  there  is  a  circulatory  disturbance  in  the  course  of  the  portal 
vein,  and,  when  combined  with  chronic  alcoholism,  hepatic  cirrhosis  may 
be  presumed  to  be  the  cause.  But  only  a  probable  diagnosis  can  be  made 
in  such  cases.  For  portal  vein  stasis  may  be  due  to  many  other  causes 
(compression  of  the  portal  vein  by  tumor,  thrombosis  of  the  portal  vein, 
carcinoma  of  the  peritoneum,  of  the  omentum,  etc.).  When  the  ascitic 
fluid  is  removed,  and  we  are  able  accurately  to  investigate  the  abdominal 
organs,  we  frequently  arrive  at  a  correct  diagnosis. 

The  differential  diagnosis  between  hepatic  cirrhosis  and  chronic,  as  well 
as  tuberculous,  peritonitis  is  especially  perplexing.  The  latter  affection 
combined  with  hepatic  cirrhosis  is  not  so  rare  as  was  formerly  supposed. 
The  proof  of  tuberculosis  in  other  organs,  the  character  of  the  ascites, 
which  in  peritonitis  is  frequently  hemorrhagic  and  also  shows  a  higher 
specific  gravity  with  a  greater  amount  of  albumin,  will  in  many  cases 
lead  to  a  correct  conclusion,  but  we  must  admit  that  errors  in  diagnosis 
cannot  always  be  avoided.  The  existence  of  a  chronic  perihepatitis,  peri- 
hepatitis chronica  hyperplastica,  must  also  be  considered  in  the  differential 
diagnosis.  The  great  thickening  of  the  capsule  leads  to  compression  of  the 
organ,  to  disturbance  of  the  portal  vein  circulation,  and  to  destruction  of 
the  hepatic  parenchyma.  The  organ,  in  consequence  of  the  marked  con- 
traction of  its  capsule,  becomes  small,  atrophic,  hard,  and  ascites  appears; 
in  brief,  a  picture  which  is  very  difficult  to  differentiate  from  atrophic 
hepatic  cirrhosis.  A  similar  affection  is  described  by  Pick  (Zeitschr.  f. 
klinisclie  Medicin,  Bd.  29,  Heft  5  u.  6),  pericardial  pseudo-hepatic  cirrho- 
sis, i.  e.,  perihepatitis  chronica  hyperplastica  combined  with  chronic  peri- 
carditis and  obliteration  of  the  pericardium. 

Duration. — The  duration  of  the  disease  cannot  be  determined  with  cer- 
tainty, since,  on  account  of  the  mild  symptoms,  the  time  of  onset  is  not 
known.  In  this  respect,  therefore,  individual  authors  express  very  varying 
opinions,  and  they  estimate  the  duration  of  life  at  between  one  and  ten 
years.  The  earliest  possible  recognition  of  the  disease,  the  whole  state 
of  the  patient,  his  circumstances,  the  avoidance  of  everything  injurious, 
and,  particularly,  abstention  from  alcohol,  etc. — all,  naturally,  have  an 
important  bearing  upon  the  course  of  the  disease. 


GRANULAR  ATROPHY  OF  THE  LIVER  381 

Prognosis. — As  to  the  prognosis  in  a  positive  ease  of  atrophic  hepatic 
cirrhosis,  all  authors  are  unanimous  in  declaring  the  disease  to  be  fatal. 
Yet  many  cases  of  recovery,  even  in  advanced  hepatic  cirrhosis  with  ascites, 
have  been  reported  (I  shall  only  mention  Liebermeister,  Rosenstein,  Sem- 
mola,  Leichtenstern).  Naunyn  especially  emphasizes  that,  in  his  experi- 
ence, the  cure  of  atrophic  hepatic  cirrhosis  is  sometimes  spontaneous. 
Ehret,  upon  the  basis  of  one  of  his  own  cases,  has  recently  expressed 
himself  on  this  point  most  explicitly,  and  entirely  agrees  with  Naunyn. 
I  have  never  seen  an  actual  cure  of  atrophic  hepatic  cirrhosis.  Where  this 
appeared  to  be  the  case,  there  was  some  doubt  as  to  the  diagnosis.  Syphi- 
litic hepatic  cirrhosis  will  be  described  separately. 


TREATMENT 

The  treatment  is,  in  the  main,  symptomatic.  The  removal  of  the  etio- 
logic  cause,  the  early  and  entire  withdrawal  of  alcohol,  and  the  forbidding 
of  pungent  spices  are  most  important;  in  malaria  we  employ  quinin,  in 
syphilis  potassium  iodid,  and  even  mercury  given  cautiously.  Where  syph- 
ilis cannot  positively  be  determined,  potassium  iodid  should  be  given  a 
trial.  The  patients  should  not  be  exposed  to  the  deleterious  action  of  lead, 
arsenic  or  phosphorus.  As  soon  as  the  pressure  of  ascites  causes  distress, 
paracentesis  abdominis  is  indicated;  early  puncture,  however,  is  not  ad- 
vised; the  value  of  this  is  very  problematical.  The  first  deposits  of  the 
newly  formed  ascitic  fluid  are  always  most  rapidly  excreted.  When  the 
pressure  of  fluid  in  the  abdomen  has  become  distinctly  positive,  accumu- 
lation takes  place  more  slowly.  By  early  and,  consequently,  frequent  punc- 
ture, a  large  quantity  of  albumin  is  withdrawn  from  the  body,  and  this 
hastens  the  destruction  of  the  patient.  In  contrast  with  this  is  the  value 
of  early  puncture  in  decreasing  venous  stasis  in  the  abdominal  organs ;  this 
is  supposed  to  hasten  the  establishment  of  the  collateral  circulation  between 
the  portal  vein  and  the  organs  of  the  body,  etc.,  which  is  so  desirable  to 
the  patient,  but  is  as  yet  by  no  means  proven.  In  regard  to  the  necessity 
of  tapping,  I  determine  this  from  the  symptoms  of  the  patient,  and,  since 
general  rules  cannot  be  given,  I  can  only  advise  it.  In  some  patients  we 
must  perform  this  little  operation  early  and  often;  in  others  enormous 
quantities  of  fluid  in  the  abdomen  occasion  no  special  symptoms. 

When  the  patients  complain  much  of  abdominal  pressure,  and  the  car- 
diac activity  and  respiration  are  implicated  by  the  displacement  of  the 
diaphragm,  aspiration  must  be  performed.  Not  only  these  difficulties,  but 
many  others,  then  seem  to  disappear  as  if  by  magic.  The  appetite  is 
stimulated,  a  sufficiency  of  food  is  ingested,  the  bowels  become  regular, 
and  diuresis  improves.  Aspiration  is  often  followed  by  an  amelioration 
of  the  entire  condition  which  lasts  for  some  time. 

In  atrophic  nutmeg  liver  due  to  diseases  of  the  heart,  lungs,  and  kidneys. 


382  CHRONIC   INFLAMMATION   OF  THE   LIVER 

the  treatment  of  the  underlying  affection,  particularly  of  the  heart,  must 
he  our  first  object.  Digitalis  is  then  the  most  valuable  remedy,  and  we 
must  attempt  by  diuretics  to  prevent  the  accumulation  of  fluid  or  to  remove 
tliat  which  has  been  formed.  Cream  of  tartar,  potassium  acetate  (always 
in  large  doses,  10,  15  to  20  grams  a  day),  juniper,  and  special  diuretics 
such  as  boneset  tea  (50  grams  macerated,  placed  in  a  liter  of  cold  water 
and  allowed  to  boil  for  three  or  four  hours,  then  poured  off  and  filtered; 
always  to  be  freshly  made,  and  the  entire  amount  taken  in  twenty-four 
hours).  Urea,  which  was  recently  strongly  advised  as  a  diuretic  by  Klem- 
perer  (10  to  20  grams  a  day),  I  have  not  found  specially  valuable.  In 
my  experience  it  acts  no  better  than  the  remedies  mentioned  above  when 
given  in  the  same  quantity,  and  these  may  be  prescribed  when  the  kidneys 
are  normal  without  damaging  these  organs  (in  the  diseased  kidney  urea 
is  even  witliout  effect  and,  possibly,  harmful).  In  England  balsam  and 
resin  of  copaiba  are  much  employed  (1  or  2  grams  daily  in  capsules). 
Potent  diuretics  which  enjoy  a  reputation  in  hepatic  cirrhosis  are  diuretin 
(4  to  G  grams  daily),  agurin  (1  gram  three  or  four  times  daily),  theophyl- 
lin  (0.3  to  0.3  gram  three  or  four  times  daily),  theocin,  the  double  salt 
of  caffein  (from  four  to  six  powders  daily,  each  0.2  gram),  and,  above 
all,  calomel.  This  last  remedy  calls  for  a  more  minute  description.  I 
advise  its  employment  only  when  the  kidneys  are  normal.  Then  0.2  of  a 
gram  of  calomel  are  given  three  times  daily  for  three  days,  followed  by 
a  pause  of  several  days.  The  oral  cavity  must  be  carefully  watched.  With 
marked  diarrhea,  opium  should  be  given  at  the  same  time.  I  am  afraid 
of  calomel,  which  occasionally  gives  such  excellent  results,  because  the 
stomatitis  which,  notwithstanding  the  greatest  care,  sometimes  follows,  may 
debilitate  the  patient  extremely.  Its  specific  action  upon  the  process  in 
the  liver,  which  is  presumed  by  some  authorities,  has  been  nowise  proven. 
Perhaps  smaller  doses  (0.02  to  0.06,  five  or  six  times  daily),  which  are 
specially  advised  by  Saccharjin  in  hypertrophic  hepatic  cirrhosis,  would  also 
be  of  value  here. 

Spa  treatment  of  the  affection  under  discussion  at  Carlsbad,  Marien- 
])ad  and  Kissingen,  etc.,  is  highly  recommended,  and  sometimes  also  the 
employment  of  artificial  Carlsbad  salt.  But  a  specially  beneficial  action 
\ipon  the  liver  and  the  processes  going  on  there  these  salts  cannot  have; 
oven  when  given  by  the  mouth  (54)  in  large  doses  they  do  not  enter  the 
bile.  Hence  the  value  of  alkalies  can  only  lie  in  their  favorable  effect  upon 
tlie  gastrointestinal  catarrh.  Symptoms  referable  to  the  gastrointestinal 
tract  are  often  very  prominent  in  these  patients,  and  primarily  demand 
treatment,  which,  unfortunately,  is  often  without  result.  Sometimes  these 
symptoms  point  unmistakably  to  gastric  catarrh  (pain  in  the  epigastrium, 
anorexia,  nausea,  vomiting),  at  other  times  to  involvement  of  the  intestine 
which  is  usually  manifested  by  uncontrollable  diarrhea,  more  rarely  by 
obstinate  constipation.     Disturbance  of  the  circulation  of  the  blood  in  the 


GRANULAR  ATROPHY  OF  THE  LIVER  ^ 

portal  vessels  is  certainly  the  cause  of  these  conditions.  In  this  case  the 
symptoms  of  gastrointestinal  catarrh,  which  are  prominent,  call  for  relief. 
Here  I  must  refer  to  the  special  treatment  of  these  affections,  and  shall 
only  mention  that  the  spa  treatment  is  very  beneficial  (besides  the  springs 
mentioned  above  also  the  waters  of  Vichy,  Neuenahr,  Ems,  Marienbad, 
Kissingen,  etc.,  as  well  as  the  salt  springs  of  Homburg,  Wiesbaden,  etc.), 
especially  when  constipation  and  meteorism  exist.  The  stagnant,  decom- 
posing masses  are  discharged,  and  absorption  of  the  freshly  digested  foods 
is  promoted,  hence  the  action  of  the  toxic,  deleterious  products  of  intestinal 
bacteria  (toxins,  ptomains)  is  limited.  In  regard  to  the  deficient  antitoxic 
function  of  the  liver,  the  French  (Bouchard,  Roger,  Dujardin-Beaumetz 
(55),  and  others)  assign  the  first  place  in  treatment  to  "intestinal  anti- 
sepsis." Charcoal,  bismuth  salicylate,  salol,  resorcin,  naphthalin,  sodium 
salicylate  or  sodium  benzoate,  etc.,  h3^drochloric  acid  (with  subacidity  of 
the  stomach),  have  all  been  warmly  advocated  by  them,  and  are  frequently 
employed  combined  with  a  diet  which  will  soon  be  described  in  detail.  So 
far  as  we  know,  antisepsis  is  carried  out  in  the  stomach  and  the  upper 
portions  of  the  intestine  by  hydrochloric  acid;  in  the  lower  portions 
of  the  small  intestine  possibly  (?)  by  the  bile  acids.  It  is  well  known 
that  in  advanced  hepatic  cirrhosis,  even  when  there  is  little  jaundice,  only 
small  quantities  of  bile  flow  into  the  intestine,  consequently  only  small 
amounts  of  biliary  acids  find  passage  there.  Connective  tissue  prolifera- 
tion in  the  liver  may  be  enormous,  and  the  greater  portion  of  the  hepatic 
cells  may  be  destroyed,  so  that  microscopically  but  scant  remains  of  these, 
which,  apparently,  are  in  great  part  atrophic,  are  to  be  found.  Deficiency 
in  bile  formation  and  the  resulting  incomplete  antisepsis  in  the  intestine 
become  more  pronounced,  and  the  antitoxic  property  of  the  liver,  on  ac- 
count of  the  few  undamaged  hepatic  cells  which  remain,  is  exerted  insuSi- 
ciently.  In  the  course  of  hepatic  cirrhosis  we  by  no  means  rarely  meet 
with  conditions  which  point  to  autointoxication  of  the  organism  with 
these  intestinal  toxins.  These  conditions  have  already  been  explicitly  de- 
scribed (56). 

In  Germany,  quite  correctly,  the  theory  of  "  intestinal  antisepsis  "  has 
met  with  little  acceptance.  The  extremely  artificial  superstructure  erected 
in  France  lacks  a  sufficiently  firm  foundation,  the  entrance  is  not  free 
from  danger,  and  it  may  very  readily  and  suddenly  collapse.  Preliminary 
studies  upon  which  to  found  this  treatment  must  be  characterized  as  en- 
tirely inadequate.  I  am  convinced  that,  in  the  disease  in  question,  as  little 
headway  has  been  made  with  intestinal  antisepsis  as,  for  example,  in  enteric 
fever,  which  in  France  is  treated  according  to  similar  principles.  The 
administration  of  small  doses  of  antiseptics  is  useless,  large  doses  are  de- 
cidedly dangerous.  A  combination  of  various  antiseptic  remedies  (of  each 
almost  its  toxic  dose)  has  given  no  better  results.  We  will  do  well  to  con- 
tinue to  be  skeptical  in  regard  to  this  therapy,  and  to  rely  upon  purgatives 
26 


384  CHRONIC  INFLAMMATION   OF  THE  LIVER 

such  as  aloes,  senna,  calomel,  rhubarb  (Helm's  pills  have  been  most  ex- 
tensively used  in  the  treatment  of  hepatic  cirrhosis),  and  the  laxative  bitter 
waters.  It  is  simply  impossible  to  disinfect  for  years  the  intestine  of  a 
human  being,  all  the  more  so  since  we  do  not  know  which  bacteria  should 
be  destroyed,  and  which  toxins  should  be  removed.  Continued  research  is 
here  necessary,  and  then  perhaps,  but  only  perhaps,  treatment  of  this  kind 
may  be  successful. 

A  chronic  disease,  the  course  of  which,  like  the  one  in  question,  is  so 
prolonged,  naturally  necessitates  care  in  the  diet,  and  here  the  patient's 
food  must  be  simple  and  non-irritating  with  a  sufficient  amount  of  calories. 
It  should  be  composed  of  milk,  carbohydrates  in  the  form  of  wheat  bread, 
crackers,  flour,  zwieback,  mashed  potatoes,  cocoa,  and  rice,  with  the  addi- 
tion of  butter  and  meat.  Only  the  more  easily  digested  and  nutritious 
vegetables,  such  as  green  peas,  turnips,  asparagus,  cauliflower,  and  spinach, 
are  to  be  allowed,  while,  on  the  other  hand,  those  which  cause  distention — 
such  as  all  kinds  of  cabbage — are  to  be  avoided. 

As  an  ideal  diet  in  hepatic  cirrhosis  the  French  have  praised  and  prac- 
tically employed  one  strictly  of  vegetables.  The  guiding  thought  is  this — 
that  in  its  employment  the  formation  of  toxins  (from  meat)  is  suppressed, 
and  intestinal  antisepsis  is  facilitated.  In  carrying  out  such  dietetic  rules, 
tlie  utmost  care  is  necessary.  Few  patients  with  hepatic  cirrhosis  can 
adhere  to  such  a  diet  on  account  of  their  especial  tendency  to  gastric  and 
intestinal  ailments.  For  individual  points  in  the  diet,  I  must  refer  to 
authoritative  text-books   (57). 

Surgical  Measures. — To  facilitate  the  establishment  of  the  above  men- 
tioned collateral  circulation  between  the  portal  vein  and  the  veins  of  the 
body,  that  is,  to  make  it  possible,  and  thus  relieve  the  dangerous  conse- 
quences of  congestion  in  the  portal  system,  efl'orts  have  been  made,  follow- 
ing Talma's  (57  a)  advice,  to  fasten  the  omentum,  and  also  the  spleen, 
to  the  abdominal  wall.  In  this  manner  adhesions  containing  new  vessels 
are  formed,  and  may  bring  about  the  desired  condition.  This  operation  is 
not  always  successful;  disappointment  and  even  serious  results  (gangrene 
of  the  omentum,  infections)  have  followed;  but,  on  the  other  hand,  some- 
times results  which  are  favorable.  In  some  cases,  after  the  operation,  the 
ascites  was  checked,  and  the  patients  left  the  hospital  in  the  best  condition 
and  able  to  carry  on  their  occupations  (Talma,  Drummond  and  Morison, 
Neumann  (57b)).  Such  favorable  results  as  these  from  Talma's  opera- 
tion justify  us,  in  suitable  cases,  in  resorting  to  it.  With  our  increasing 
experience  regarding  the  operation  itself,  and  in  the  choice  of  suitable 
cases,  we  can  hardly  doubt  that  in  the  future  these  results  will  be  even 
more  gratifying.  Experimental  investigations  (Tillmann  (57  c))  confirm 
the  practicability  and  the  benefits  of  Talma's  operation;  comprehensive 
reviews  by  Friedmann  (57  d)  and  Rohmer  (57  e)  give  critical  reports  of 
numerous  cases  operated  upon,   and  a  recent  publication  by  Lenzmann 


HYPERTROPHIC    HEPATIC  CIRRHOSIS  385 

may  be  referred  to  {Deutsche  med.  Wochensclir.,  1903,  Nr.  48,  p.  843)  in 
which  suggestions  have  been  given  regarding  the  choice  of  cases  to  be 
operated  upon. 


C.   HYPERTROPHIC    HEPATIC    CIRRHOSIS 

PATHOLOGICAL   ANATOMY 

In  important  points  this  affection  differs  pathologico-anatomically  as 
well  as  clinically  from  atrophic  hepatic  cirrhosis,  and  therefore,  as  is  now 
generally  admitted,  is  entitled  to  a  special  position. 

Up  to  the  time  of  death  the  liver  usually  remains  greatly  enlarged. 
The  surface  is  tumid,  it  is  of  firm,  elastic  consistence,  its  color  strongly 
icteroid,  yellow  to  green.  Upon  section  a  decided  increase  of  connective 
tissue  is  seen;  this  is  not  only  found  in  the  interlobular  spaces,  but  also 
in  the  hepatic  lobules  themselves.  In  spite  of  the  enormous  increase  of 
the  connective  tissue,  the  mass  of  the  hepatic  parenchyma  is  unaltered. 
The  connective  tissue  does  not  contract,  the  liver  cells  are  not  destroyed; 
on  the  contrary,  according  to  some  authors  (Ackermann  (58),  Aufrecht) 
they  are  enlarged,  hypertrophic,  and  mostly  polynuclear.  That  the  con- 
nective tissue  proliferation  in  hypertrophic  hepatic  cirrhosis  takes  place 
especially  around  the  biliary  passages  and,  according  to  the  view  of  the 
French,  chiefly  Charcot  and  his  pupils,  originates  from  these  and  not  from 
the  blood-vessels,  has  by  no  means  been  proven,  and  has  been  denied  by 
me  for  many  years  {Verhandlungen  des  Congresses  fiir  innere  Medicin, 
1892). 

Since  the  finer  biliary  passages  and  the  blood-vessels  coalesce  in  the 
same  interstitia,  it  is  hardly  possible  from  the  results  of  microscopic  in- 
vestigation to  maintain  with  any  degree  of  positiveness  that  the  one  system, 
and  not  the  other,  is  implicated  in  the  connective  tissue  increase.  This 
is  not  contradicted  by  the  fact  that,  in  many  areas,  connective  tissue 
proliferation  is  greatly  developed,  particularly  around  the  biliary  passages, 
that  their  walls  are  thickened  while  the  lumen  remains  open.  The  biliary 
channels,  on  account  of  their  structure,  form  a  prominent  part  of  the 
connective  tissue  masses.  The  incorrect  view  of  the  French  is,  as  was 
previously  remarked,  based  upon  the  fact  that  they  do  not  distinguish 
"  biliary  cirrhosis,"  which  we  shall  specially  describe  later,  from  hyper- 
trophic cirrhosis,  and  this  has  caused  much  confusion.  So-called,  newly 
formed  biliary  passages  are  more  numerous  than  in  the  atrophic  form. 
It  must  be  expressly  stated  that  the  differences  between  these  two  forms 
are  only  marked  when  we  compare  well-developed  classical  cases,  that  these, 
however,  are  by  no  means  always  typical,  and  that  these  forms  merge  into 
one  another.  Thus,  in  hypertrophic  hepatic  cirrhosis  there  is  sometimes 
contraction,  atrophy  of  the  cells,  etc.    The  French  have  easily  surmounted 


386  CHRONIC  INFLAMMATION  OP  THE  LIVER 

tliese  difficulties  by  creating  their  "  forme  mixte."  But  this,  at  the  same 
time,  indicates  that  special  differences  between  atrophic  and  hypertrophic 
hepatic  cirrhosis  do  not  exist.  The  pathologic  anatomy  of  the  disease, 
which  apparently  occurs  in  France  much  more  frequently  than  in  Germany, 
has  been  particularly  studied  by  the  French — I  mention  only  such  names 
as  Charcot  (59),  Ollivier  (60),  Hayem  (61),  Gombault  (62),  Hanot  (63), 
Schaehinann  (64)  and,  among  German  authors,  besides  Ackermann  (1.  c), 
Rosenstcin  (65)  and  Stadelmann  (66).  In  France  this  form  of  hepatic 
cirrhosis  is  named  after  the  most  eminent  authority  in  the  realm  of  this 
disease,  Hanot's  disease.  After  all  is  said,  we  must  frankly  admit  that 
the  true  cause  of  differences,  even  of  a  pathologico-anatomical  nature,  be- 
tween atrophic  and  hypertrophic  hepatic  cirrhosis  is  unknown.  It  is  worthy 
of  mention  that,  occasionally,  even  well-developed  cases  of  hypertrophic 
hepatic  cirrhosis  cannot  be  recognized  macroscopically,  but  are  only  de- 
termined by  microscopic  examination.  This  is  due  to  the  peculiar,  soft, 
but  only  slightly  prominent,  structure  of  the  richly  developed  connective 
tissue,  and  the  absence  of  contraction. 


SYMPTOMATOLOGY 

The  onset  of  the  disease,  like  atrophic  hepatic  cirrhosis,  is  accompanied 
by  indefinite  symptoms  on  the  part  of  the  gastrointestinal  tract.  The 
patient  complains  of  anorexia,  vomiting,  pressure  in  the  epigastrium,  con- 
stipation, and  diarrhea.  A  very  intense  jaundice  soon  appears,  so  that 
this  form  of  the  affection  has  been  designated  in  France  as  "  cirrhose  h)rper- 
trophique  avec  ictere."  The  liver  is  greatly  enlarged,  is  coarse  and  hard, 
with  a  rounded  margin,  and  remains  enlarged  to  the  end.  The  jaundice 
may  disappear  in  the  early  stages  of  the  disease  but  may  several  times 
recur  in  paroxysms  until  it  finally  becomes  permanent.  Besides  enlarge- 
ment of  the  liver,  we  usually  find  a  very  marked  enlargement  of  the  spleen. 
Ascites  is  almost  invariably  absent.  There  is  a  marked  tendency  to  hemor- 
rliage.  In  spite  of  the  jaundice,  the  feces  usually  show  bile.  Death  occurs 
from  exhaustion  after  a  prolonged  duration  of  the  disease,  which  runs  a 
longer  course  than  atrophic  hepatic  cirrhosis  (four,  five,  ten  to  twelve 
years),  and  is  frequently  preceded  by  the  symptoms  of  autointoxication 
and  by  cerebral  phenomena.  Irregular  rises  in  temperature  are  not  rare. 
The  cause  of  the  enlargement  of  the  spleen  is  doubtful;  it  cannot  be 
congestion,  as  in  atrophic  hepatic  cirrhosis,  for  this  is  entirely  absent  from 
llie  clinical  picture.  Nothing  remains  but  the  assumption  of  a  process 
in  the  spleen  resembling  that  taking  place  in  the  liver.  Rosenstein  has 
mentioned  a  decrease  of  the  red  blood-corpuscles. 

Disease  of  the  kidney  is  rarer  than  in  atrophic  cirrhosis. 

As  complications  there  are  to  be  mentioned  general  and  local  peri- 
tonitis (perihepatitis,  perisplenitis),  as  well  as  myocarditis. 


HYPERTROPHIC   HEPATIC  CIRRHOSIS  387 

ETIOLOGY 

Hypertrophic  hepatic  cirrhosis,  similar  to  the  atrophic  form,  occurs 
chiefly  in  men,  less  frequently  in  women.  It  is  quite  a  rare  disease,  and 
is  apparently  restricted  to  certain  localities.  Thus,  in  France  and  Holland 
(Eosenstein)  it  is  comparatively  frequent,  while  in  Germany,  at  least  in 
its  typical  forms,  it  is  very  rare.  Most  authors  attribute  the  affection  to 
alcohol,  others  contradict  this  (Eosenstein) ;  it  is  certainly  very  remarkable 
that,  notwithstanding  the  plentiful  ingestion  of  alcohol  in  Germany,  the 
affection  is  there  so  rare,  while,  in  other  regions,  in  spite  of  the  same 
conditions,  the  disease  is  often  noted.  This  forces  us  to  the  conclusion 
that  alcohol  cannot  be  the  only  cause,  but  that  an  unknown  factor  is  added. 
It  has  also  been  assumed  that  it  is  due  to  a  parasitic  disease  of  the  biliary 
channels  (bacteria,  protozoa).    Positive  proof  of  this  is  lacking. 

DIAGNOSIS   AND   PROGNOSIS 

In  the  stage  of  onset  the  affection  is  just  as  difficult  to  recognize  as 
atrophic  hepatic  cirrhosis.  The  gastrointestinal  symptoms  are  not  charac- 
teristic, the  jaundice  may  be  purely  catarrhal,  and  is  the  more  likely  to 
be  considered  such  because  this  symptom,  as  well  as  the  enlargement  of 
the  liver,  often  decreases.  Only  with  the  permanent  enlargement  of  the 
liver,  the  decided  splenic  tumor,  the  persistent  jaundice,  does  the  diagnosis, 
until  then  tentative,  become  positive. 

Prognosis. — The  prognosis  is  unfavorable.  Eecovery  from  the  well- 
developed  disease  is  unknown;  that  the  malady  may  be  arrested,  or  even 
cured,  in  the  stage  of  onset  by  suitable  treatment  is  possible,  but  not 
proven,  since,  in  this  stage,  the  diagnosis  is  still  uncertain.  It  is  at  least 
a  source  of  comfort  to  know  that  the  course  of  the  affection  may  be  very 
prolonged  without  decidedly  interfering  with  the  activity  of  the  patient. 

TREATMENT 

At  the  onset  of  the  malady  the  treatment  usually  employed  in  gastro- 
intestinal affections  is  to  be  instituted;  the  jaundice  present,  which  is 
generally  regarded  as  catarrhal  jaundice,  should  receive  appropriate — also 
dietetic — treatment.  The  effects  of  the  abuse  of  alcohol  must  be  combated, 
and  its  future  avoidance  always  be  insisted  upon  by  the  physician. 

In  the  case  of  hypertrophic  hepatic  cirrhosis  the  employment  of  calo- 
mel in  fractional  doses,  as  advised  by  Saccharjin  (0.02-0.05,  four  or  five 
times  daily),  is  particularly  valuable.  According  to  this  author,  the  drug 
has  a  specific  action  and  brings  about  a  cure.  But  that  a  specific  action 
upon  the  process  in  the  liver  is  not  produced  by  the  use  of  calomel,  and  that 
the  expected  result  frequently  does  not  follow,  must  be  especially  empha- 
sized.   Nevertheless,  with  all  necessary  precautions  (thorough  care  of  the 


388  CHRONIC   INFLAMMATION   OF  THE   LIVER 

mouth,  calomel  for  three  or  four  days,  then  a  pause  of  three  or  four  days, 
then  another  calomel  period,  etc.,  the  treatment  to  be  kept  up  for  about 
four  weeks),  the  calomel  treatment  is  advisable.  Potassium  iodid  should 
also  be  tried  in  hypertrophic  hepatic  cirrhosis,  although  I  have  seen  little 
success  from  its  employment,  nor  have  I  found  such  reported  in  literature. 
Ebstein  (6fi)  maintains  that  he  has  had  good  results  with  potassium  iodid. 
The  disturbances  of  metabolism  in  the  hypertrophic  form  do  not  differ 
from  those  in  the  atrophic.  Absorption  and  the  assimilation  of  food 
show  no  deviation  except  that,  perhaps,  on  account  of  the  deficiency  of 
bile  in  the  feces  and  the  jaundice  present,  the  absorption  and  assimilation 
of  fats  in  the  intestine  are  disturbed.  The  foundation  for  nutrition  is 
milk,  to  which  carbohydrates  and  proteids  should  be  added  as  required. 
Details  may  be  found  in  text-books  on  dietetics  (52). 

D.  BILIARY   HEPATIC    CIRRHOSIS 

In  France  the  disease  under  discussion  is  usually  grouped  with  hyper- 
trophic hepatic  cirrhosis,  as  has  already  been  mentioned,  and  this  has 
caused  great  confusion.  We  consider  it  advisable  sharply  to  differentiate 
the  two  conditions,  and  in  Germany,  so  far  as  I  can  see,  we  designate  by 
this  term  the  cirrhosis  which  arises  in  connection  with  mechanical  closure 
of  the  bile  channels,  especially  the  common  bile  duct,  either  by  stone,  by 
a  tumor,  by  adhesions,  by  cicatrices,  etc. 

ETIOLOGY   AND   PATHOLOGY 

After  prolonged  biliary  stasis  (Janowski)  necrotic  foci  due  to  destroyed 
hepatic  cells  are  found  in  the  liver.  These  are  absorbed,  small  cell  infil- 
tration appears  about  the  surrounding  tissue,  and,  later,  connective  tissue 
proliferation  develops.  The  bile  channels  are  also  thickened  by  infiltration 
and  connective  tissue  formation.  New  bile  channels  are  formed  in  the 
same  manner  as  in  ordinary  hepatic  cirrhosis.  The  connective  tissue  in- 
crease, as  well  as  the  atrophy  of  the  parenchymatous  cells,  may  finally 
attain  the  extreme  proportions  seen  in  atrophic  hepatic  cirrhosis.  Conse- 
quently, as  in  the  other  affection,  the  picture  of  portal  vein  stasis  appears, 
and  in  this  stage  biliary  cirrhosis  can  no  longer  be  differentiated  from 
cirrhosis  due  to  other  causes  (Litten  (67),  Mangelsdorf  (68)).  We  then 
find  fibrinous  connective  tissue  bands  which  constrict  and  permeate  the 
acini,  connective  tissue  proliferation  around  the  portal  vein  branches  which 
become  thickened  and  impermeable,  and  newly  formed  biliary  channels,  etc. 

Experimental  investigation,  in  the  main,  agrees  with  observations  in 
man,  but  the  consequences  of  experimental  biliary  stasis  are  much  less 
prominent  in  the  liver.  Infection  with  its  consequences  (purulent  inflam- 
mation, abscess)  may  complicate  the  situation  in  the  animal  experiment, 
and  it  is  not  always  absent  in  man. 


SYPHILIS   OF  THE   LIVER  389 

SYMPTOMS 

The  affection  runs  its  course  under  the  picture  of  severe  jaundice,  of 
cholemia,  that  is,  of  autointoxication,  and  usually  with  such  rapidity  that 
the  severe  hepatic  changes  above  described  do  not  have  time  to  develop 
completely.  The  disease  rarely  lasts  longer  than  two  years,  and,  by  its 
more  rapid  course,  as  well  as  by  the  absence  of  decided  enlargement  of  the 
spleen,  biliary  hepatic  cirrhosis  differs  from  hypertrophic  hepatic  cirrhosis 
to  which  it  otherwise  presents  great  similarity,  especially  if  the  liver  is 
greatly  enlarged,  which  is  often  the  case.  In  the  differential  diagnosis  the 
observation  of  the  feces  is  important.  In  hypertrophic  hepatic  cirrhosis 
they  are  more  or  less  bile  stained ;  but  in  biliary  cirrhosis  they  are  acholic, 
and  in  the  latter  affection  the  icterus  is  usually  more  intense.  Ascites, 
as  well  as  the  other  signs  of  portal  vein  stasis  (also  enlargement  of  the 
spleen),  may  develop  in  the  terminal  period  (Janowski  (69)). 

TREATMENT 

The  treatment  depends,  in  the  main,  upon  the  etiology.  As  the  affection 
always  depends  upon  mechanical  causes  which  cannot  be  removed  by  in- 
ternal treatment,  in  biliary  cirrhosis  we  are  therefore  compelled  to  resort 
to  surgical  measures.  Stones  must  be  removed  by  operation,  and,  in  the 
case  of  cicatricial  adhesions  and  tumors  which  cannot  be  removed,  chole- 
cystoenterostomy  is  to  be  performed,  that  is,  the  gall-bladder  is  to  be 
united  with  the  intestine.  This  operation  seems  to  be  too  rarely  performed, 
and  we  cannot  sufficiently  emphasize  that  it  is  calculated  to  save  the  life 
of  many  a  patient,  or,  at  least,  decidedly  to  prolong  it,  and  gives  us 
fresh  hope. 

The  greatest  attention  must  be  paid  to  the  nutrition,  and,  in  the  main, 
the  same  laws  are  operative  as  in  hypertrophic  hepatic  cirrhosis.  Carbo- 
hydrates and  proteids  are  preferable,  while  the  fats  should  be  as  far  as 
possible  excluded,  since,  in  acholia  of  the  intestine,  fats  are  insufficiently 
absorbed;  on  the  other  hand,  milk  should  be  employed  to  the  fullest 
extent. 

E.    SYPHILIS   OF   THE   LIVER 

That  syphilis  of  the  liver  produces  interstitial  hepatitis  may  be  regarded 
as  certain;  nevertheless,  one  and  the  same  poison,  as  must  be  admitted, 
may  produce  such  different  forms  of  disease  of  the  liver  that  we  cannot 
regard  it  as  strange  when  we  see  the  same  conditions  as  in  the  case  of 
alcohol. 

The  connection  between  syphilis  and  hepatic  cirrhosis  is  not  always 
easy  to  recognize,  and  often  can  only  be  determined  late,  provided  the 
history  of  our  patients  does  not  furnish  the  clue;  for,  clinically,  the  stage 
of  onset  of  syphilitic  hepatic  cirrhosis  very  rarely  differs  from  that  of  the 


390  CHRONIC   INFLAMMATION   OF  THE   LIVER 

alcoholic  form.  In  syphilitic  hepatic  cirrhosis  the  development  of  con- 
nective tissue  rich  in  cells  takes  place,  and  this  has  a  tendency  to  marked 
cicatricial  contraction,  so  that  the  tissue  later  becomes  tough  and  fibrous, 
and  the  cellular  elements  disappear.  The  parenchyma  of  the  liver  is  also 
destroyed,  and  fatty  degeneration  and  atrophy  occur  in  the  hepatic  cells. 
It  is  quite  necessary,  too,  to  differentiate  congenital  syphilitic  hepatic 
cirrhosis  from  acquired  hepatic  syphilis. 

The  first  is  found  in  children  with  congenital  syphilis,  and  here  the 
above  mentioned  characteristics  of  diffuse  hepatic  cirrhosis  are  most  evi- 
dent. The  liver  is  distinctly  enlarged,  tough,  brownish,  with  many  signs 
of  new  and  old  connective  tissue  in  the  interlobular  structure,  and  this 
may  also  permeate  the  lobules.  The  blood-vessels  are  greatly  thickened, 
their  walls  show  cellular  infiltration.  But,  besides  the  diffuse  connective 
tissue  increase  which  presents  the  greatest  similarity  to  that  of  ordinary 
hepatic  cirrhosis,  there  are  massive  connective  tissue  strands  in  individual 
areas  and  foci  with  an  accumulation  of  small  cells. 

In  such  children  the  liver  is  usually  hypertrophic,  probably  because 
these  children  early  succumb  to  the  underlying  affection  (syphilis  and  its 
consequences),  that  is,  before  the  atrophy  which  is  observed  in  some  cases 
that  live  longer  has  time  to  develop.  The  liver  is  sometimes  smooth, 
sometimes  flabby  and  notched,  sometimes  also  coarse  and  granular.  Be- 
sides the  diffuse  disease  of  the  organ,  we  find — however,  more  rarely — a 
formation  of  gummata  in  the  form  of  small  nodules  distributed  over  the 
entire  surface.  The  process  in  the  liver  strongly  resembles  syphilitic  dis- 
ease of  other  organs.  The  disease  without  doubt  begins  during  the  fetal 
period;  the  fetus  is  often  decomposed,  or  the  infants  die  a  few  weeks 
or  months  after  birth.  Syphilis  of  the  liver  is  the  most  frequent  phase 
of  hereditary  syphilis. 

Hepatic  syphilis  of  adults  is  a  late  phenomenon  of  acquired  syphilis 
appearing  in  the  tertiary  stage,  and  may  be  divided  into  two  different 
forms,  which,  however,  may  also  be  combined. 

1.  The  diffuse  form  corresponds  to  syphilitic  cirrhosis  of  children  and 
to  alcoholic  cirrhosis,  and  neither  pathologico-anatomically  nor  clinically 
can  it  be  positively  distinguished  from  the  latter.  Syphilis  and  alcohol 
aie  usually  combined  as  deleterious  factors  in  one  and  the  same  patient. 

2.  Sypliiloma  of  the  liver,  that  is,  gummatous  hepatitis.  Gummatous 
nodules  are  characteristic  of  this  form;  they  vary  in  size  from  that  of  a 
nut  to  that  of  an  apple,  are  mostly  found  upon  the  concave  surface  of  the 
liver  near  the  suspensory  ligament,  but  may  also  be  noted  at  the  porta 
hopatis  in  Glisson's  capsule.  These  nodules  show  a  tendency  to  caseation, 
to  decay,  and,  in  connection  with  this,  to  contraction.  Then  deep  furrows 
develop  and  cause  constriction  of  the  liver,  hence  the  organ  may  be  sepa- 
rated into  individual  lobes  ("lobulated  liver");  these  constrictions  con- 
sist of  hard,  tough  connective  tissue,  perhaps  also  of  remains  of  a  caseated 


SYPHILIS   OF  THE   LIVER  391 

gummatous  tissue,  and  sometimes  they  contain  unchanged  gummatous 
nodules.  Upon  the  smaller  and  larger  blood-vessels  (hepatic  arteries, 
portal  vein)  connective  tissue  proliferation  is  frequently  found  in  the 
form  of  syphilitic  endarteritis.  The  serosa  of  the  liver  is  usually  thick- 
ened in  consequence  of  inflammatory  processes  which  may  also  cause  ex- 
tensive adhesions  to  the  neighboring  organs. 

Finally,  in  hepatic  syphilis  of  adults,  as  in  that  of  children,  the 
syphilomata  may  be  of  such  a  miliary  form  that  a  certain  resemblance 
to  tubercle  is  noted.  In  adults  gumma  formation,  and  in  children  the 
diffuse  development  of  connective  tissue,  is  typical  of  syphilis  of  the  liver. 
But  in  adults  other  symptoms  of  tertiary  syphilis  are  usually  present 
(testicles,  meninges,  bones,  mucous  membranes,  etc.). 

SYMPTOMS   AND   CLINICAL   COURSE 

Syphilitic  hepatic  cirrhosis,  at  least  so  far  as  the  gummata  are  con- 
cerned, usually  runs  its  course  without  symptoms,  and  is  frequently  dis- 
covered only  at  autopsy.  In  inflammation  of  the  serosa,  if  adhesions  form, 
pain  in  the  hepatic  region  is  not  a  rare  complaint.  Frequently,  however, 
the  cicatricial  retractions,  the  lobulation  of  the  liver,  as  well  as  the  large 
gummata,  may  be  recognized  at  the  examination,  but  the  latter  by  their 
great  nodular  prominences  often  lead  to  errors  in  diagnosis  by  being  mis- 
taken for  malignant  tumors. 

If  the  gummata  and  the  cicatrization  are  situated  at  the  porta  hepatis, 
and  form  a  constriction  in  this  area,  the  well  known  symptoms  of  stasis, 
even  icterus  gravis,  may  arise  in  consequence  of  closure  of  the  common 
bile  duct. 

[Gummatous  hepatitis  frequently  produces  an  irregular  type  of  fever. 
This  is  sometimes  manifested  by  chills,  fever  and  sweats  occurring  at 
irregular  intervals  and  at  other  times  by  a  moderate  fever  of  intermittent 
or  remittent  type  without  chill.  Frequently  the  liver  is  palpable,  its  con- 
sistency increased,  and  it  is  tender  to  the  palpating  hand  during  the 
febrile  attacks.  Rest  without  medication  results  in  relief  in  some  in- 
stances. The  recognition  of  the  cause  with  appropriate  treatment  with 
mercury  and  iodids  is  followed  by  entire  relief. — Ed.] 

As  the  liver  is  otherwise  well  able  to  perform  its  functions,  and  diffuse 
processes  are  rare  in  the  adult,  as  has  been  mentioned,  the  constitutional 
condition  is  in  most  cases  not  affected,  nor  is  life  endangered,  by  the  dis- 
ease. Only  when  diffuse  syphilitic  hepatitis  develops  is  the  entire  clinical 
picture  of  atrophic  hepatic  cirrhosis  presented. 

Amelioration  and  arrest  of  the  affection,  particularly  under  proper 
treatment,  is  very  frequent. 

Amyloid  degeneration  of  the  liver,  spleen,  and  kidneys  may  follow,  as 
in  any  cachexia;  in  severe  syphilis  this  is  not  unusual,  and  it  may  then 
both  complicate  and  disguise  the  clinical  picture. 


392  CHRONIC   INFLAMMATION   OF  THE   LIVER 

In  children,  usiially  in  the  new-bom,  the  inverse  is  the  case.  The 
children  are  atrophic,  cachectic,  and  do  not  thrive;  ascites,  enlargement 
and  all  of  the  other  symptoms  of  diffuse  hepatitis  develop  rapidly,  and 
the  children,  as  a  rule,  soon  succumb  to  the  disease.  In  milder  cases, 
however,  the  affection  may  last  for  years.  Amyloid  degeneration  of  the 
liver  and  of  other  organs  is  then  a  frequent  complication.  The  children, 
even  the  mild  cases,  rarely  reach  puberty,  they  have  no  vigor,  they  develop 
slowlv,  and  remain  weak  and  thin — just  as  is  commonly  observed  in  syphilis 
hereditaria  tarda. 

DIAGNOSIS 

The  diagnosis  of  syphilitic  disease  of  the  liver  in  young  children  is 
usually  easy.  The  history  of  the  parents,  the  presence  of  other  symptoms 
of  hereditary  syphilis,  and  the  examination  of  the  children,  soon  make  the 
diagnosis  positive.  The  distended  abdomen,  the  enlarged,  hard  liver  which 
is  readily  palpable,  the  large  spleen,  the  symptoms  of  congestion,  ascites, 
etc.,  and  the  absence  of  other  etiology  pointing  to  hepatic  cirrhosis,  reveal 
the  true  nature  of  the  malady  even  when  the  parents  falsify  their  history 
during  tlie  examination,  and  conceal  their  own  syphilis. 

In  adults,  confusion  with  alcoholic  cirrhosis  on  the  one  hand,  and 
malignant  tumors  of  the  liver  on  the  other  hand,  is  easily  possible.  Even 
Avithout  a  history,  other  signs  of  tertiary  syphilis,  such  as  cutaneous  ulcera- 
tion, enlargement  of  the  bones,  and  ulceration  in  the  throat,  point  with 
certainty  to  the  correct  conclusion.  A  complicating  amyloid  degeneration 
should  he  remembered,  but  should  not  lead  us  astray.  If  there  is  no  other 
reason  for  its  existence,  in  doubtful  cases  it  favors  syphilis.  In  a  differ- 
entio-diagnostic  respect,  the  slight  cachexia  may  be  considered  as  against 
carcinoma. 

As  contra-indications  of  alcoholic  cirrhosis  there  are  varying  symptoms 
— longer-continued,  spontaneous  improvement,  the  enormous  spleen,  the 
size  of  the  nodules,  the  marked  globulation  of  the  liver,  and  the  possible 
absence  of  alcoholism,  etc. 

Confusion  with  simple  corset  lobe  liver  is  easily  possible.  But  this 
almost  always  occurs  in  women,  and  the  furrow  from  lacing  is  a  single 
one.  although  it  may  become  very  deep  and  almost  divide  the  liver  into 
two  ])arts.  while  in  syphilitic  hepatitis  there  are  several  cicatricial  bands, 
therefore  lobulation  occurs  in  several  areas  of  the  organ. 


TREATMERT 

With  early  and  proper  specific  treatment,  the  disease  may  be  arrested, 
the  process  retarded,  and  even  a  relative  cure  take  place.  The  etiology 
and  an  early  diagnosis  are,  therefore,  of  vital  importance  for  the  patient. 
Cicatricial  constriction  can  never  be  removed,  and,  according  to  our  present 


LITERATURE  393 

experience,  it  may  be  regarded  as  more  than  doubtful  that  a  well-developed 
diffuse  process  can  be  cured  or  even  arrested. 

Nevertheless,  when  syphilis  has  been  determined  and  disease  of  the 
liver  has  appeared,  a  careful  antisyphilitic  treatment  with  potassium  iodid 
and  mercury  is  not  only  invariably  advisable  but  directly  indicated,  and 
this  treatment  should  be  instituted  even  when  the  diagnosis  of  syphilitic 
liepatic  disease  is  doubtful.  Frequently,  as  is  not  unusual  in  syphilis,  the 
result  of  treatment  confirms  the  diagnosis.  Cautious  treatment  with  potas- 
sium iodid  and  mercury  is  not  injurious  if  the  patient's  kidneys  are  normal 
and  he  is  continuously  under  professional  observation.  The  physician 
should,  therefore,  first  try  potassium  iodid  or  sodium  iodid  in  increasing 
doses,  so  that  after  a  time  several  grams  of  the  iodin  salt  will  be  given 
daily,  and  in  combination  with  this,  as  soon  as  we  see  that  the  iodin  has 
had  its  effect  and  the  condition  of  the  patient  will  permit  it,  treatment 
with  mercury  should  be  begun  (preferably  a  thorough  inunction  cure). 
Decided  pain  in  the  hepatic  region  is  the  consequence  of  perihepatitis, 
and  may  justify  such  procedures. 

The  other  symptoms  of  hepatic  disease  are  to  be  treated  in  accordance 
with  the  method  established  for  the  treatment  of  atrophic  and  hypertrophic 
hepatic  cirrhosis. 

Literature 

(1)  Ackermann,  Virchow's  Archiv,  LXXX. 

(2)  Hartung,  "Ueber  das  histologische  Verhalten  der  Leberzellen  bei  der  Alko- 

holcirrhose."    Dissertation,  Halle,  1889. 

(3)  L.  Brieger,  Virchow's  Archiv,  LXXV. 

(4)  Virchow's  Archiv,  LXII. 

(5)  Arch.  gen.  de  Med.,  1885. 

(6)  Deutsches  Arch.  /.  klin.  Med.,  1895,  LV. 

(7)  Zeitschr.  f.  klin.  Med.,  1896,  XXIX. 

(8)  Deutsches  Arch.  f.  klin.  Med.,  XXXIV. 

(9)  These  de  Paris,  1888. 

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(11)  Archives  de  Physiologic,  1878;  "Maladies  des  pays  chauds,"  Paris,  1889. 

(12)  Quoted  from  Quincke,  "Die  Krankheiten  der  Leber,"  p.  420. 

(13)  Reime  de  Med.,  1882. 

(14)  Festschrift  fUr  Albrecht  v.  H alter,  1877. 

(15)  Arch,  de  physiol.  norm,  et  path.,  1886. 

(16)  Archivio  medico  italiano,  1882. 

(17)  Arch.  gen.  de  Med.,  1882. 

(18)  Berliner  klin.  Wochenschr.,  1890;  Verhandl.  d.  Congr.  j.  innere  Med.,  1892. 

(19)  Quoted  from  Ewald  in  Eulenburg's  Realencyclopddie,  XI. 

(20)  Deutsches  Arch.  }.  klin.  Med.,  XXXI. 
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(21)  Arch.  gen.  de  Med.,  1888. 

(22)  Fortschr.  d.  Med.,  1884. 


394  CHRONIC  INFLAMMATION   OF  THE   LIVER 

(23)  Vierteljahrschr.  /.  gerichtl.  Med.,  LXXXVIII. 

(24)  Ziegler  und  Nauwerk,  Beitrdge,  etc.,  IX,  Heft  2. 

(25)  Ziegler  und  Nauwerk,  Beitrdge,  etc.,  VIII. 

(26)  Arch,  de  Phannacodynamie,  1895,  II. 

(27)  These  de  Paris,  1894,  quoted  from  Quincke. 

(28)  Virchow's  Archiv,  CX. 

(29)  Ziegler's  Beitrdge,  II. 

(30)  Deutsches  Arch.  f.  klin.  Med.,  XXIII  und  LVIII. 

(31)  These,  Paris,  1879. 

(32)  Deutsches  Arch.  }.  klin.  Med.,  1882,  XXX. 

(33)  Journ.  de  Med.,  Bruxelles,  1877. 

(34)  Arch,  des  sciences  physiques  et  natureUes,  Geneve,  1877. 

(35)  Philadelphia  Med.  Times,  1877. 

(36)  "Lemons  sur  les  autointoxications,"  1887. 

(37)  "Action  du  foie  sur  les  poisons."     Thbse.  de  Paris,  1887. 

(38)  Arch.  /.  experim.  Path.  u.  Pharm.,  XII. 

(39)  Deutsches  Arch.  /.  klin.  Med.,  1883,  XXXIII. 

(40)  Deutsches  Arch.  f.  klin.  Med.,  1889,  XLV. 

(41)  Zeitschr.  f.  physiol.  Chemie,  XVII. 

(42)  "Lehrbuch  der  Pathologie  des  Stoflfwechsels,"  1893. 

(43)  Arch.  }.  experim.  Path.  u.  Pharm.,  XXXIII. 

(44)  Arch.  j.  Physiol.,  1891,  II. 

(45)  Verhandl.  d.  XI.  Congr.  /.  inncre  Med.,  1892. 

(46)  Morgagni,  1897. 

(47)  Arch.  f.  experim.  Path.  u.  Pharm.,  1892,  XXXII. 

(48)  Zeitschr.  /.  klin.  Med.,  XLVII. 

(49)  Deutsches  Arch.  f.  klin.  Med.,  LXXIV. 

(50)  Deutsche  med.  Wochenschr.,  1901. 

(51)  Sem.aine  med.,  1901 ;  Revue  de  med.,  XXI. 

(52)  Berliner  klin.  Wochenschr.,  1901,  Nr.  18. 

(53)  Milnchener  med.  Wochenschr.,  1903,  Nr.  8. 

(54)  "  Untersuchungen   von    Dr.    Glass   aus  raeinem    Laboratorium,"   Arch.    f. 

experim.  Path.  u.  Pharm.,  XLIII. 

(55)  "Traitement  des  maladies  du  foie,"  Paris,  1893. 

(56)  Compare    also    Staddmann,    "Ueber    chronische    Leberentziindung."     Ver- 

handl. d.  XI.   Congr.   j.   innere  Med.,  Leipzig,  1892,  and  Staddmann, 
"Der  Icterus  und  seine  verschiedenen  Formen,"  Stuttgart,  1891. 

(57)  Staddmann,  "Die  Ernahrungstherapie  bei  Leberkr^nkheiten "  in  v.  Leyden's 

"Handbuch  der  Ernahrungstherapie,"  II. 
(57a)  Berliner  klin.  Wochenschr.,  1898,  Nr.  38,  u.  1900,  Nr.  31. 
(57b)   Deutsche  med.  Wochenschr.,  1899,  Nr.  26. 
(57c)   Deutsche  med.  Wochenschr.,  1899,  Nr.  18. 
(57d)  Ce.ntralbl.  /.  d.  Grenzgehide  d.  Med.  u.  Chir.,  1900. 
(57e)  Deutsche  Aerzte-Zeitung,  1901,  Heft  14-15. 
(5S)    Virchoiv's  Archiv,  LXXX. 

(59)  "Maladies  du  foie,"  1877. 

(60)  UUnion  med.,  1871. 

(61)  Arch,  de  physiol.,  1874. 


LITERATURE  395 

• 

(62)  Arch,  de  phydol.,  1876. 

(63)  Thtse  de  Paris,  1876;  Arch.  gen.  de  med.,  1877-79. 

(64)  Arch,  de  physioL,  1887. 

(65)  Rosenstein,  Stadelmann,  Verhandl.  d.  XL  Congr.  /.  innere  Med.,  1892. 

(66)  Verhandl.  d.  XI.  Congr.  f.  innere  Med.,  1892,  p.  128. 

(67)  Charite-Annalen,  1880. 

(68)  Deutsches  Arch.  f.  klin.  Med.,  1882,  XXXI. 

(69)  Ziegler's  "Beitrage  zur  pathologischen  Anatomie,"  1892. 


NEOPLASMS   OF   THE    LIVER    AND    BILIARY 

PASSAGES 

By  FR.  KRAUS,  Graz 

The  development  of  the  surgery  of  the  liver  and  gall-bladder  in  the 
last  few  decades,  gradual  at  first  but  lately  proceeding  with  more  rapid 
strides,  has  steadily  intensified  the  practical  interest  of  the  profession  in 
neoplasms  of  the  liver.  There  are  surgeons  who  dream  of  the  complete 
eradication  and  actual  cure  of  these  diseases,  even  of  malignant  growths, 
by  the  aid  of  a  diagnostic  exploratory  incision.  Even  more  may,  perhaps, 
be  expected  on  account  of  the  positive  etiologic  relation  of  carefully  chosen 
cases  of  carcinoma  of  the  biliary  passages  (perhaps  also  of  the  liver)  to 
cholelithiasis  if  the  operative  treatment  of  gall-stone  disease  is  resorted  to 
early  enough.  If,  however,  the  knife  can  actually  aid  us,  and  to  avert  the 
dangers  in  general  of  cholelithiasis,  of  which  lithogenous  cancer  is  only 
one,  a  very  limited  but,  as  I  believe,  sufficient  experience  has  taught  us 
that  in  permanent  jaundice  which  is  the  result  of  an  already  present  car- 
cinoma of  the  common  bile  duct,  operative  interference  is  of  comparatively 
little  use,  and  even  exploratory  laparotomy,  in  individuals  whose  common 
bile  duct  is  occluded  by  a  malignant  tumor,  is  very  badly  borne.  The 
danger  involved,  therefore,  in  the  operation  for  gall-stones  is  one  of  the 
practical  reasons  why  so  much  depends  upon  a  knowledge  of  diagnosis; 
that  is,  an  exact  recognition  of  the  factors  which  bring  about  chronic 
obstruction  of  the  common  bile  duct  by  concrements  and  by  neoplasms  of 
the  biliary  passages  themselves,  of  the  duodenum,  or  of  the  head  of  the 
pancreas,  etc.,  enables  us  to  differentiate  them. 

The  very  complex  clinical  picture  occasionally  makes  the  decisive  differ- 
entiation of  malignant  neoplasms  of  the  liver  itself  from  those  of  the 
gall-bladder  and  of  the  biliary  passages  very  difficult,  as  primary  cancer 
of  the  gall-bladder  proliferating  into  the  liver  there  reaches  its  greatest 
development,  and  as  all  carcinomata  which  occlude  the  duodenal  end  of 
tbe  common  bile  duct,  no  matter  what  their  origin,  give  rise  to  metastases 
in  the  liver,  etc.  The  simultaneous  description  of  these  various  neoplasms, 
therefore,  appears  to  me  to  clear  the  situation  but  Ifttle,  and  after  full 
consideration  of  the  varying  practical  indications,  I  believe  a  separate  de- 
scription of  this  subject  to  be  necessary.  On  account  of  the  prevailing 
opinions  concerning  carcinoma  of  the  liver  as  a  primary  or  secondary 
396 


NEOPLASMS   OF  THE  GALL-BLADDER  397 

affection,  its  interesting  histogenetic  development,  its  manifold  varieties,, 
and  probably  also  because  of  considerations  to  which  the  system  of  tumors 
of  the  liver  gives  rise,  purely  clinical  interest  in  the  latter  is  far  less; 
hence  the  following  order  of  arrangement  will  be  different. 

As  indicated,  we  shall  discuss  manifold  clinical  pictures,  but  the  com- 
bination of  the  following  guiding  symptoms  will  always  be  observed: 
General  digestive  disturbances,  and,  in  connection  with  these,  rapid  and 
unarrested  progressive  cachexia,  the  appearance  or  the  absence  of  a  tumor, 
metastases  in  the  liver  itself  or  elsewhere,  cirrhosis  of  the  liver  (secondary), 
compression  of  the  biliary  passages,  particularly  that  form  accompanied  by 
permanent  jaundice,  portal  vein  stasis. 

1.   NEOPLASMS   OF   THE    GALL-BLADDER 

As  a  type  of  tumor  of  the  gall-bladder  carcinoma  may  be  considered, 
for  the  other  forms  of  tumor  mentioned  in  literature  are  either  so  rare  or 
of  such  subordinate  importance  as  to  be  of  only  slight  interest  to  the 
physician.    Sarcoma  has  the  same  significance  as  carcinoma. 

Among  the  granulation  tumors  of  the  gall-bladder,  tubercle  must  be 
mentioned  (Lanceraux,  Heddaeus,  Hermann) ;  of  benign  tumors  there  are 
to  be  considered  trite  cystic  tumors  (Wiedemann),  mucus  polypi,  submu- 
cous fibromata  (Albers),  papillomata  (Riedel,  Kiimmel),  lipomatous 
structures  (subperitoneal  upon  the  gall-bladder,  Cornil-Eanvier),  aneurysm 
of  the  cystic  artery  opening  into  the  gall-bladder  (Chiari),  echinococcus ; 
finally,  of  other  malignant  growths  we  must  enumerate  papillary  myxomata 
(Schiippel),  sarcomata  (Czerny,  Eiedel,  Destree,  etc.). 

Cancer  of  the  gall-bladder  is  a  pathologic  condition  which  has  only 
recently  been  accurately  studied.  Early  descriptions  were  given  by  Stoll, 
Hall,  Baillie,  Heyfelder  and  others  (1777-1839).  The  first  positive  cases 
were  probably  described  by  Durand-Fardel  (1837-1840).  Villard  (1871), 
in  his  "  Etude  sur  le  cancer  primitif  des  voies  biliaires,"  collected  24  cases 
of  primary  cancer  of  the  biliary  ducts,  of  which  21  were  carcinomatous 
degeneration  of  the  gall-bladder.  In  a  subsequent  series  of  reports,  the  most 
important  are  those  of  J.  Krauss  and  H.  Zenker,  the  latter  author  having 
most  thoroughly  and  convincingly  described  as  the  most  important  factor 
in  the  etiology  of  cancer  of  the  gall-bladder  the  presence  of  gall-stones. 
Noteworthy  anatomical  indications,  in  addition  to  those  already  mentioned, 
are  contained  in  a  publication  by  Ohloff.  The  most  comprehensive  statistics 
have  been  compiled  by  Courvoisier  and  Musser.  Among  recent  compre- 
hensive publications  from  a  surgical  standpoint,  that  of  A.  Heddaeus  must 
be  mentioned.  At  the  present  time,  the  pathologic  anatomy  and  the  sjrmp- 
tomatology  of  cancer  of  the  gall-bladder  are  well  understood,  and  only  a 
few  questions  touching  the  border-line  between  internal  medicine  and 
surgery  call  for  further  explanation. 


398  NEOPLASMS   OF  THE   LIVER   AND  BILIARY   PASSAGES 

•  Cancer  of  the  gall-bladder  is  only  very  rarely  secondary,  that  is,  pro- 
liferating into  the  gall-bladder  from  neighboring  organs  (the  pancreas, 
the  duodenum,  the  stomach,  etc.).  The  earlier  view  (Baillie),  according 
to  which  the  gall-bladder  was  said  to  be  most  rarely  attacked  by  cancer 
except  when  the  disease  had  previously  developed  in  the  liver,  has  been 
entirely  abandoned.  There  are  numerous  cases  on  record  in  which  the 
gall-bladder  was  the  only  organ  which  showed  malignant  involvement,  the 
liver  being  entirely  free.  And  this  is  favored  by  the  fact  that  cancer 
of  the  liver  which  occurs  simultaneously  has,  as  a  rule,  proliferated  by 
contiguity,  or  is  to  be  looked  upon  as  metastasis  of  the  gall-bladder.  In 
old  complicated  cases  with  disease  extending  to  all  the  organs  in  the  region 
of  the  liver,  at  the  present  time  the  gall-bladder  is  always  assumed  to  be 
the  primary  seat  if  it  show  but  a  moderately  severe  implication.  In  such 
cases  we  occasionally  find  in  the  liver  a  tumor  mass  with  indefinite,  limited 
borders,  embedded  in  cicatricial  adhesions,  in  the  center  of  which  upon 
incision  a  cavity  is  disclosed  with  irregular  borders  and  a  pappy  or  puru- 
lent mass  containing  concrements.  The  carcinoma  proliferating  from  the 
gall-bladder  to  the  adjacent  liver  naturally  gives  rise  to  a  tumor  which, 
at  first  sight,  may  resemble  a  primary  massive  cancer  of  the  liver.  Only 
in  one  case,  Tyson's,  was  the  carcinoma  of  the  gall-bladder  of  purely 
metastatic  origin,  and  this  growth  was  found  at  the  autopsy  in  a  case 
in  which  three  operations  for  cancer  of  the  lip  had  been  performed. 

As  a  rule,  cancer  of  the  gall-bladder  arises  primarily  either  from  the 
fundus  or  the  neck,  rarely  from  the  middle  portion,  or  the  wall  adjacent 
to  the  liver.  It  occurs  either  as  scirrhus  or  adenocarcinoma.  The  soft 
cancerous  alveoli  readily  break  down  and  form  a  malignant  ulcer.  Colloid 
cancer  (Villard,  Aezel,  Biach,  Eoberts,  Janeway,  Brodowski)  and  villous 
cancer  (Heschl,  Klob,  Moxon,  Voss,  Fifield)  occur.  Conspicuous,  yet 
particularly  mentioned  only  by  Mulat,  is  the  pavement  cell  epithelium  with 
the  well  known  onion-like  microscopic  configuration.  Either  the  cancer 
surrounds  the  gall-bladder,  and  only  implicates  a  small  portion  of  the  walls, 
or  the  entire  wall  is  uniformly  infiltrated.  Often  there  is  but  a  small 
tumor,  which  nevertheless  has  become  the  focus  for  a  large,  secondary 
cancer  of  the  liver,  or  has  produced  extensive  metastases.  The  entire 
malignant  gall-bladder  has  contracted  upon  one  or  a  few  gall-stones.  In 
other  cases  the  gall-bladder  appears  as  a  nodular  tumor  of  the  size  of  a 
fi.^t.  Occasionally  at  its  fundus  it  forms  a  diverticulum  which  is  separated 
from  the  rest  of  the  organ  by  a  thickened  ring  and  contains  gall-stones; 
this  ring  is  usually  the  seat  of  the  cancerous  development.  As  is  obvious 
fi-om  the  foregoing,  the  carcinoma  usually  proliferates  to  the  surrounding 
areas.  Widely  extended  dendritic  infiltration  of  Glisson's  capsule  is  not 
rare.  In  particular,  the  adjacent  liver,  the  parietal  peritoneum,  the  omen- 
tum and  the  intestine  (above  all,  the  colon)  are  primarily  implicated  by 
pericystitic  adhesions,  and  the  secondary  growth  penetrates  the  connective 


NEOPLASMS  OF  THE  GALL-BLADDER  399 

tissue  membranes.  Extending  by  way  of  the  hepato-duodenal  ligaments 
the  cancer  reaches  the  portal  lymph  nodes,  which  become  markedly  en- 
larged, and  by  pressure  upon  the  portal  vein  produce  ascites.  Thrombosis 
of  the  trunk  or  of  the  larger  branches  of  the  portal  vein  is  not  rare.  By 
continuity  through  the  cystic  duct  the  neoplasm  attacks  the  common  gall- 
duct  and  the  hepatic  duct,  and  by  stenosis  causes  obstruction  to  the  outflow 
of  bile,  dilatation  of  the  gall-bladder,  and  stasis  jaundice.  The  hepatic 
duct  and  common  gall-duct  may  also  be  implicated  externally  by  the  car- 
cinoma. In  some  cases  a  further  distribution  into  the  small  intra-hepatic 
gall-ducts  has  been  observed,  so  that  upon  transverse  section  they  appear 
as  cancerous  rings.  This  gives  rise  to  the  formation  of  new  bile  passages 
and  atrophy  in  the  trabeculae  of  the  cells  of  the  liver  acini,  causing  the 
retention  of  bile  in  the  liver  and  the  formation  of  small  cysts  which  are 
covered  with  the  epithelium  of  the  biliary  passages.  In  the  further  course 
of  the  affection,  inflammatory  products  collect.  ^  The  malignant  mass  breaks 
down  upon  the  inner  surface,  the  tissue  threads  reach  the  bile,  which  also 
decomposes,  and  is  changed  into  a  dirty,  grayish-brown  fluid  admixed  with 
blood  and  pus.  The  process  of  destruction  usually  extends  even  further, 
to  the  adjacent  tumor  masses  between  the  stomach,  the  large  intestine  and 
the  liver,  and  thus  an  ichorous  cavity  develops  which  is  filled  with  a  dirty, 
gray  mass,  permeated  with  cancerous  nodules.  Continued  stasis  of  bile 
and  consequent  infection  produce  a  distributed  cholangitis.  Not  rarely 
fistulas  form  which  perforate  into  the  liver,  into  the  gastrointestinal  canal, 
and  into  the  abdominal  wall  (navel). 

Although  cancer  of  the  gall-bladder  by  continuous  proliferation  is  prone 
to  attack  the  adjacent  liver  and  the  biliary  passages,  as  well  as  quite 
commonly  the  porta  hepatis,  it  may  also  give  rise  to  metastases,  as  I  must 
here  reiterate  in  opposition  to  the  opinion  which  has  been  generally  main- 
tained since  the  time  of  Courvoisier.  The  metastases  are  not  only  found 
in  the  liver,  but,  considering  the  brief  duration  of  the  disease,  often  in 
other  and  quite  distant  organs  (in  the  peritoneum,  the  omentum,  the  re- 
gions of  the  umbilicus  and  the  urinary  bladder,  the  recto-vesical  fold,  the 
kidney,  the  spleen,  the  intestine,  the  lung,  the  pleura,  the  ovaries,  the  portal, 
retroperitoneal,  mesenteric,  and  omental  lymph-glands).  I  know  of  a  case 
in  which  an  incorrect  diagnosis  was  made  because  the  first  and  chief  ob- 
jective symptom  consisted  of  tumors  which  were  found  in  the  pelvis. 


ETIOLOGY  AND   PATHOGENESIS 

The  etiology  and  pathogenesis  of  carcinoma  of  the  gall-bladder  there- 
fore necessitate  the  most  minute  investigation  on  the  part  of  the  practi- 
tioner, because  of  the  difficulties  which  up  to  the  present  time  have  suc- 
cessfully resisted  a  surgical  treatment  of  the  affection,  and  which  depend, 

in  no  small  degree,  upon  the  fact  that  the  chief  cause  of  cancer  of  the 
27 


400  NEOPLASMS   OF  THE   LIVER  AND  BILIARY  PASSAGES 

gall-bladder  is  not  sufficiently  considered,  and  operation  is  generally  de- 
ferred until  too  late.  Almost  all  investigators  have  been  struck  by  the 
extraordinary  frequency,  more  than  mere  coincidence,  with  which  stones 
(or  ulcers  and  cicatrices  due  to  stone)  as  well  as  cancer  are  found  in  the 
gall-bladder.  Naturally  the  question  arises.  What  causal  relation  exists 
between  the  presence  of  gall-stones  and  the  formation  of  cancer?  While 
some  authors  were  formerly  inclined  to  regard  the  development  of  cancer 
as  primary,  for  30  years  past  there  has  scarcely  been  a  pathologist  who 
doubted  that  cancer  is  due  to  the  irritation  of  stones  that  have  previously 
formed  (Klob,  Frerichs,  Klebs,  Willigk,  Schiippel,  Krauss,  Zenker,  Cour- 
voisier,  Naunyn,  and  others).  This  connection  is,  in  the  first  place,  borne 
out  by  statistics.  Courvoisier  found  gall-stones  simultaneously  with  cancer 
of  the  gall-bladder  in  about  90  per  cent,  of  all  cases,  Siegert  in.  almost 
all,  and  Lobker  in  all  cases.  According  to  Schroder,  14  per  cent,  of  all 
patients  with  gall-stones  are  attacked  with  carcinoma  of  the  gall-bladder; 
according  to  Naunyn  among  150  such  cases,  14  developed  cancer  of  the 
biliary  passages.  Of  172  patients  with  gall-stones  operated  upon  by  Lobker, 
17  suffered  from  carcinoma  of  the  gall-bladder,  and  Riedel  assumes  that 
about  10  per  cent,  of  all  patients  suffering  from  cholelithiasi's  subsequently 
acquire  carcinoma.  The  presence  of  stones  prior  to  the  development  of 
cancer  can  be  proven  clinically  as  well  as  pathologico-anatomically.  It  has 
long  been  known  that  carcinomata  are  prone  to  form  in  cicatrices,  particu- 
larly in  the  stomach,  as  has  recently  been  clearly  proven  by  G.  Hauser, 
and  H.  Zenker  conceived  the  idea  that  the  development  of  cancer  of  the 
gall-bladder  might  be  similarly  connected  with  preceding  ulcerative  proc- 
esses which  might  be  attributed  to  pressure  necrosis  due  to  stones.  Zenker 
demonstrated  clearly  that  the  successive  cicatrices  cause  an  atypical  glandu- 
lar proliferation  which  predisposes  to  carcinoma.  The  increased  growth 
of  the  remaining  glandular  portion,  the  shooting  forth  of  sprouts  and 
their  extension  in  various  directions,  the  more  marked  lobular  formation, 
are  primarily  but  the  expression  of  a  regenerative  endeavor  of  the  tissues; 
tlie  character  of  the  excessive  and  atypical  growths  gains  prominence  by  the 
clironic  irritation  of  the  stones.  Hauser  also  considers  the  absence  of 
physiologic  resistance,  and  Ribbert  the  constriction  of  portions  of  the  glands 
by  connective  tissue,  as  important.  Ohloff's  conception  is  somewhat  dif- 
ferent; he  believes  the  metaplasia  of  the  cylindrical  and  plate  epithelium 
as  the  result  of  stone  formation  is  causative.  The  composition  of  the  newly 
formed  plate  cells  becomes  horny,  concentric  layers  form,  and,  finally, 
nest  formation  takes  place.  This,  however,  is  probably  true  in  only  a  few 
of  the  cases. 

Cancer  of  the  gall-bladder  is  by  no  means  so  rare  as  was  formerly 
believed;  at  all  events,  primary  cancer  of  the  gall-bladder  is  much  more 
frequent  than  carcinoma  of  the  biliary  passages.  Approximately,  cancer 
is  found  in  females  5  to  7  times  more  frequently  than  in  males.    Whether, 


NEOPLASMS   OF  THE   GALL-BLADDER  401 

besides  cholelithiasis,  the  clothing  worn  by  women  (lacing)  exerts  a  pre- 
disposing influence  cannot  be  determined.  Carcinoma  of  the  gall-bladder 
usually  occurs  between  the  40th  and  70th  (or  possibly  the  80th)  years  of 
life.  In  the  majority  of  cases  it  develops  after  the  age  of  50.  Frerichs 
mentions  a  case  of  cancer  of  the  gall-bladder  in  a  patient  aged  26. 


SYMPTOMS 

The  symptoms,  unfortunately,  are,  in  the  main,  very  vague,  and  the 
clinical  picture  of  carcinoma  of  the  gall-bladder  is  by  no  means  typical. 

In  a  certain  number  of  cases,  at  most  in  \,  we  will  learn  from  the 
history  that  cholelithiasis  has  preceded.  But  the  frequent  absence  of  this 
proof,  naturally,  does  not  disprove  the  theory  that  cancer  of  the  gall- 
bladder has  developed  from  the  irritation  of  stones.  As  is  well  known, 
concrements  in  the  gall-bladder  do  not  always  cause  subjective  and  ob- 
jective diagnostic  symptoms,  and  cases  of  this  kind,  particularly,  show  a 
tendency  to  the  development  of  carcinoma.  Among  the  subjective  symp- 
toms in  60  per  cent,  of  the  cases,  pain  in  the  gastric  and  hepatic  regions 
(gall-bladder)  is  mentioned,  partly  paroxysmal,  partly  of  a  spasmodic 
character  ("gastric  pain"),  partly  continuous  and  then  less  severe.  Tho 
hepatic  region,  as  a  rule,  is  markedly  susceptible  to  pressure.  There  i^ 
loss  of  appetite,  frequently  absence  of  free  hydrochloric  acid  in  the  gastric 
contents,  usually  constipation,  rarely  diarrhea.  Jaundice  of  varying  de- 
gree occurs  in  about  f  of  all  cases.  Enlargement  of  the  liver  develops  in 
consequence  of  stasis  of  bile  or  metastasis.  Enlargement  of  the  spleen, 
particularly  in  long  existing  jaundice,  is  not  very  rare.  Ascites  is  com- 
paratively frequent ;  its  varying  appearance,  the  jaundice,  and  the  successive 
parallelism  and  divergence  of  biliary  and  portal  vein  stasis,  I  shall  con- 
sider later.  Jaundice  is  observed  more  than  twice  as  frequently  as  ascites. 
Moderate  or  even  decided  fever,  invariable  emaciation,  muscular  weakness, 
cachectic  appearance,  insomnia,  and,  with  decided  jaundice,  the  hemor- 
rhagic diathesis  as  well  as  comatose  conditions,  are  often  observed. 

Following  Courvoisier,  the  symptoms  are  designated  as  "  uncertain 
ones  " ;  they  might  also  be  called  "  inconstant  ones."  In  contrast  to  these, 
alone  or  combined  with  them,  tumor  of  the  gall-bladder  is  a  significant 
sign  which  makes  a  diagnosis  possible. 

Of  all  the  methods  of  examination  employed  in  such  cases,  palpation 
is  the  most  important.  Percussion  usually  gives  us  no  reliable  data.  Rela- 
tive dulness,  at  least,  can  generally  be  determined  over  the  tumor  of  the 
gall-bladder,  and,  passing  upward,  this  is  usually  merged  in  that  of  the 
liver.  If,  however,  the  intestine  covers  the  elongated,  sausage-like  gall- 
bladder between  the  fundus  and  the  border  of  the  liver,  which  sometimes 
occurs,  even  this  relative  dulness  is  absent,  or,  at  least,  its  connection  with 
liver  dulness  is  uncertain.     For  palpation,  the  patient  assumes  the  dorsal 

LI  UK 

COL-LIZ ixll   or   0;^T.E 


402  NEOPLASMS  OF  THE  LIVER  AND  BILIARY  PASSAGES 

decul)itus,  draws  the  knees  up,  and  opens  the  mouth.  The  head  of  the 
patient  should  be  low,  the  respiration  quiet.  The  seat  of  tenderness  is 
si  owl  V  pal]iated,  and  we  become  convinced  that  the  median  region  above 
the  navel  and  the  region  of  the  typhlon  (cecum)  is  not  conspicuously 
sensitive.  To  prevent  muscular  contractions,  we  must  gently  probe  with 
the  tips  of  the  fingers  into  the  deeper  portions,  the  fingers  being  kept 
extended.  Kheinstein  has  recently  called  attention  to  a  method  of  palpating 
the  gall-bladder.  The  best  results  are  obtained  by  bimanual  examination 
with  the  patient  in  the  recumbent  posture,  and,  if  necessary,  also  while  the 
patient  is  in  an  erect  position.  The  physician,  standing  to  the  right  of 
the  patient,  places  his  left  hand  upon  the  right  lumbar  region.  The  index 
finger  rests  upon  the  twelfth  rib,  the  tips  of  the  fingers  being  directed 
toward  the  vertebral  column.  The  right  hand  is  placed  upon  the  anterior 
abdominal  wall  of  the  patient,  the  ulnar  border  being  about  parallel  with 
the  linea  alba.  The  tips  of  the  fingers  palpate  toward  the  lower  border  of 
the  ninth  rib,  which  brings  the  second  finger  to  a  point  corresponding  with 
tlie  parasternal  line.  With  the  left  hand  strong  pressure  is  made  upon  the 
lumbar  region  internally  and  anteriorly,  the  right  hand  exerting  pressure 
at  the  same  time  so  that  the  liver  is  simultaneously  forced  somewhat  down- 
ward, and  the  gall-bladder  presses  upon  the  lower  half  (also  presses  in- 
wardly) of  the  right  kidney,  where  it  may  be  palpated.  If  the  patient 
is  standing,  the  right  hand  of  the  physician  passes  below  the  anterior 
l)order  of  the  liver,  so  that  the  four  fingers  press  the  fundus  of  the  gall- 
bladder downward,  while  the  thumb  exerts  pressure  anteriorly  and  the  left 
hand  grasps  and  helps  to  immobilize  the  liver.  The  latter  method  is 
])articularly  satisfactory  if  the  gall-bladder  be  but  little  or  not  at  all 
enlarged.  In  Wijnhoff's  method  of  examining  the  liver,  the  patient  sits 
upon  a  chair,  flexes  the  legs,  and  bends  the  upper  portion  of  the  body 
anteriorly.  The  physician  is  seated  at  the  right  of  the  patient,  and  pal- 
])ates  the  anterior  region  of  the  liver,  grasping  it  from  behind.  Palpation 
of  the  gall-bladder  is,  of  course,  greatly  facilitated  by  anesthesia.  Accord- 
ing to  Xaunyn,  if  we  occasionally  fill  the  stomach  with  gas,  we  may  be 
convinced  that  the  tumor  in  question  corresponds  to  the  gall-bladder;  in 
this  case  it  moves  decidedly  to  the  right,  sometimes  also  upward;  it  is 
also  forced  more  in  the  direction  of  the  abdominal  walls,  may  be  more 
icadily  palpated,  and  even  becomes  visible.  A  renal  tumor,  on  the  other 
hand,  disappears  when  the  stomach  and  intestine  are  filled  with  air  (water). 
Exploratory  puncture,  of  which  Harley,  in  particular,  made  imprqper  use, 
is  no  longer  employed. 

In  about  one-fourth  of  all  the  cases,  even  in  the  later  course  of  the 
disease,  the  carcinomatous  gall-bladder  cannot  be  palpated.  It  is  then 
either  covered  by  the  enlarged  liver,  or  has  become  adherent  to  the  stomach 
and  small  intestine,  deep  in  the  abdominal  cavity,  or  is  markedly  contracted. 
The  tumor  present  is  not  always  actually  situated   in  the  gall-bladder 


NEOPLASMS   OF  THE   GALL-BLADDER  403 

region;  its  site  varies  decidedly  (hypochondrium  and  also  epigastrium, 
right  mesogastrium,  and  rarely  it  is  low  down  at  the  level  of  the  crest 
of  the  ilium).  Taylor  believed  that  the  enlarged  gall-bladder  was  always 
situated  close  to  a  line  drawn  from  the  normal  position  of  the  fundus  of 
the  gall-bladder  (from  the  anterior  end  of  the  cartilage  of  the  tenth  rib) 
obliquely  to  the  left  and  downward  so  that  the  median  line  is  crossed 
somewhat  below  the  navel.  This  "  diagnostic  "  line  is  of  no  value.  The 
typical  form  of  a  tumor  of  the  gall-bladder  is  oval,  but  it  may  also  be 
cylindrical,  and  a  globular,  a  sausage,  or  cucumber  form  is  also  observed. 
The  upper  border  of  the  tumor  is  usually  difficult  to  define;  sometimes, 
it  is  true,  we  may  perceive  distinctly  that  the  tumor  protrudes  below  the 
border  of  the  liver;  that  is,  we  may  trace  it  to  the  right  and  to  the  left 
sharply  up  to  the  tumor,  and  also  inward  from  the  periphery.  The  tumor 
follows  the  expiratory  excursion,  and  may  be  displaced  laterally;  where 
there  is  connective  tissue  fixation,  the  mobility  is  lost.  Sometimes  only 
dilatation  of  the  gall-bladder  is  apparently  present,  although  a  carcinoma 
of  the  wall  (neck  of  the  gall-bladder)  may  exist.  The  determination  of 
an  uneven,  nodular,  tough  composition  of  the  tumor  is  significant.  Fluc- 
tuation, particularly  with  a  "  smooth ''  tumor,  is  frequently  found. 


DIAGNOSIS,   DURATION,   AND   PROGNOSIS 

The  duration  of  the  disease,  from  the  onset  of  positive  symptoms  until 
death,  is  scarcely  more  than  from  6  to  8  months,  and  in  about  one-half 
of  all  cases  is  less  than  4  months. 

It  is  often  difficult  or  quite  impossible  to  recognize  carcinoma  of  the 
gall-bladder,  even  in  advanced  stages  of  the  disease;  but,  in  the  majority 
of  cases,  by  repeated  careful  examinations,  and  a  minute  weighing  of  all 
the  conditions  present,  it  may  be  correctly  diagnosticated.  The  tumor  of 
the  gall-bladder  is  occasionally  looked  upon  as  a  wandering  kidne}^  a  tumor 
of  the  omentum,  as  a  corset  lobe  of  the  liver,  and  even  as  cancer  of  the 
pylorus.  Such  errors  are  caused  by  the  deviating  position,  the  unusual 
form,  consistency,  etc.,  of  the  tumor.  Of  much  greater  practical  importance 
is  the  fact  that  comparatively  often  operation  is  performed  for  a  supposed 
cholelithiasis,  and  laparotomy  discloses  a  more  or  less  well-advanced  cancer. 
In  a  differentio-diagnostic  respect  it  is  here  of  the  utmost  importance  that, 
as  well  as  a  hard  tumor,  we  may  find  no  sharply  circumscribed  tumor  of 
the  gall-bladder  but  only  a  more  diffused  enlargement  (resistance)  of  the 
entire  gall-bladder  region  including  the  adjacent  liver,  and  thus  the  growth 
of  the  tumor  can  be  recognized.  Inversely,  sometimes  enlargement  of  the 
gall-l)ladder  from  other  causes  (the  presence  of  stones  or  a  mere  thickening 
of  the  walls  of  the  gall-bladder)  has  been  mistaken  for  a  malignant  growth. 
In  cases  in  which  a  tumor  in  this  region  cannot  be  determined  with  cer- 
tainty, the  liver  may  be  definitely  shown  to  have  undergone  carcinomatous 


404  NEOPLASMS   OF  THE   LIVER   AND   BILIARY   PASSAGES 

degeneration;  if  no  primary  carcinomatous  disease  can  be  found  in  other 
regions  of  the  body,  and  there  is  decided  pain  upon  pressure  in  the  region 
of  the  gall-bladder,  and  the  patient  is  a  woman,  carcinoma  of  the  gall- 
bladder should  be  thought  of  as  the  underlying  affection.  If  ascites  be  a 
complication,  splenic  enlargement  is  an  important  diagnostic  factor;  if 
cirrhosis  can  be  excluded,  ascites  and  enlargement  of  the  spleen  favor  a 
neoplasm  upon  the  concave  surface  of  the  liver.  Often  the  course  is  cal- 
culated to  facilitate  the  recognition'  of  the  affection.  Examination  of  the 
urine  and  of  metabolism  does  not  enable  us  to  form  an  early  conclusion 
as  to  the  presence  of  cancer.  In  carcinoma  of  the  gall-bladder,  however,  a 
degree  of  cachexia  soon  appears  such  as  is  observed  in  cholelithiasis  only 
late  or  after  permanent  occlusion  of  the  common  gall-duct.  Incarceration 
from  stone  may  occasionally  last  for  years;  a  case  of  carcinoma  of  the 
gall-bladder  usually  terminates  in  less  than  six  months.  If,  however,  we 
wait  for  the  time  when  a  hard,  oval,  nodular  tumor  appears  in  an  area 
corresponding  to  the  gall-bladder,  and  follows  the  respiratory  excursions, 
and  swelling,  a  hardening,  and  a  nodular  consistence  of  the  liver  as  well 
as  jaundice  and  ascites  have  been  superadded,  the  autopsy  will  then  rarely 
reveal  an  error  in  diagnosis,  but  the  time  for  professional  aid  will  always 
(or  almost  always)  have  passed! 

After  these  statements,  the  fact  that  the  prognosis  of  carcinoma  of  the 
gall-bladder  is  always  exceedingly  grave  needs  no  explanation. 


TREATMENT 

The  only  radical  treatment  is  extirpation  of  the  gall-bladder,  and,  as  a 
rule,  simultaneously  more  or  less  extensive  resection  of  the  liver.  Chole- 
cystectomy was  first  performed  by  Langenbuch  in  1880,  and  since  that 
time  there  have  been  numerous  reports  from  surgeons  who  have  studied 
the  indications  for  this  operation.  The  controversies  concerning  this  point 
do  not  belong  here;  but  they  express  the  unanimous  opinion  that  extirpa- 
tion of  the  gall-bladder  for  carcinoma,  with  or  without  simultaneous  re- 
section of  the  liver,  up  to  the  present  time  has  been  absolutely  unsuccessful. 
In  so  far  as  reports  are  at  hand,  almost  all  the  cases  operated  upon  suc- 
cumbed to  early  relapse,  to  metastases,  or  other  complications  (Tait,  Czerny, 
Riedel,  Bardenheuer,  Hochenegg,  v.  Winiwarter,  Socin,  Heidenhain,  v.  Mi- 
kulicz, Lobker,  and  others).  Kehr  is,  therefore,  of  the  opinion  that  if 
cancer  of  the  gall-bladder  has  been  determined  with  certainty  (exploratory 
incision),  it  is  wise  to  refrain  from  any  attempt  at  a  radical  cure.  Cys- 
tostomy  may,  under  such  circumstances,  bring  about  transitory  amelioration 
of  the  condition;  with  drainage  of  the  gall-bladder  the  pain  ceases;  but, 
on  the  other  hand,  in  consequence  of  the  cancer  attacking  the  cystic  duct, 
a  distressing  mucous  fistula  develops.  Lobker  attempted  in  4  cases  to 
relieve  the  pain  caused  by  a  simultaneously  present  empyema  of  the  car- 


NEOPLASMS   OF  THE   GALI^BLADDER  •  405 

cinomatous  gall-bladder  by  performing  cholecystostomy  with  a  possible 
removal  of  the  stones.  All  of  these  patients  died  soon  afterward,  two  of 
them  directly  in  consequence  of  the  operation,  and  sooner  than  would 
otherwise  have  been  the  case. 

If,  therefore,  we  wait  for  the  time  when  the  diagnosis  can  be  positively 
made,  a  successful  radical  therapy  is  impossible,  because  the  disease  is  no 
longer  confined  to  the  gall-bladder  alone,  or  to  its  immediate  vicinity,  but 
has  extended  to  neighboring  organs,  where  it  has  led  to  the  formation  of 
metastases,  to  perforation,  etc.  Heddaeus,  therefore,  proposes  that  we  regard 
the  symptoms  designated  by  Courvoisier  as  "  uncertain  ones  "  as  indications 
for  exploratory  laparotomy,  and  that  in  the  given  case  we  make  an  ex- 
ploratory incision  into  the  gall-bladder  to  determine  the  condition  of  the 
mucous  membrane.  Thus  he  would  attack  the  evil  at  its  root,  would  arrest 
the  development  of  new  formations,  and  thus  avoid  the  danger  of  too 
extensive  an  operation,  which  inevitably  and  rapidly  leads  to  death.  As 
in  many  cases,  we  refer  the  onset  of  the  carcinoma  to  the  fundus,  he 
hopes  in  this  way,  even  by  a  partial  resection  of  the  gall-bladder,  to  arrest 
the  further  advance  of  the  carcinoma.  In  all  cases  in  which  the  neoplasm 
originates  from  the  cystic  duct  or  from  the  neck  of  the  gall-bladder,  this 
later  method  would,  a  priori,  be  excluded,  but  the  resection  of  an  impli- 
cated portion  of  the  liver  would  not  cause  insurmountable  difficulty.  The 
question  whether  it  is  justifiable  in  cholelithiasis,  and  under  certain  cir- 
cumstances, to  undertake  an  exploratory  incision  may  be  answered  by  every 
physician  in  the  affirmative,  as  the  danger  of  this  operation  is  in  no  sense 
commensurate  with  the  ultimate  advantage  gained  or  with  the  damage 
which  might  ensue  from  neglecting  it.  Exploratory  laparotomy  is  justifi- 
able when  we  have  long-continued  and  severe  pain,  when  the  patient  is 
unable  to  follow  his  occupation,  when  there  is  loss  of  strength  and  decided 
emaciation,  when  internal  treatment  is  futile,  when  there  are  negative  or 
entirely  obscure  findings  in  the  liver  and  gall-bladder,  and  those  symptoms 
are  excluded  which  make  occlusion  of  a  common  gall-duct  by  a  tumor 
very  likely.  Patient  and  physician  will  be  much  less  willing  in  the  fre- 
quent cases  in  which  carcinoma  has  led  to  the  development  of  a  determi- 
nable tumor  with  but  slight  subjective  difficulties.  I  doubt,  therefore,  that 
the  proposition  of  Heddaeus  will  largely  reduce  the  number  of  persons 
succumbing  to  cancer  of  the  gall-bladder. 

The  difficulties  which  attend  a  late  operation  for  carcinoma  of  the  gall- 
bladder may  be  met  by  considering  all  of  the  practical  consequences  of 
the  previously  described  etiology  of  cancer,  and  by  directing  the  treatment 
chiefly  to  the  removal  of  the  cholelithiasis.  No  practitioner,  at  the  present 
time,  can  escape  the  conviction  that  in  numerous  types  of  cholelithiasis  in 
regard  to  which  physicians  and  surgeons,  fortunately,  have  recently  more 
nearly  approached  unanimity  of  opinion,  the  surgeons  are  the  ones  most 
likely  to  afford  relief,  and  are,  therefore,  the  proper  therapeutists.     The 


406  NEOPLASMS  OF  THE   LIVER   AND   BILIARY   PASSAGES 

operative  method  which  is  accompanied  by  comparatively  slight  immediate 
danger  to  the  patient,  which  demands  the  sacrifice  of  an  organ  not  abso- 
lutely necessary  to  life,  and  which  is  by  far  the  most  important  seat  of 
gall-stone  disease,  which  removes  the  first  germs  of  carcinomatous  forma- 
tion in  the  wall  of  the  bladder  irritated  by  the  stone,  is  cholecystectomy. 
Performed  at  the  proper  time,  not  only  for  the  threatening  carcinoma  but 
also  for  general  curative  and  prophylactic  purposes,  an  extension  of  the 
indications  for  extirpating  the  gall-bladder  in  the  cases  in  which  chole- 
lithiasis is  limited  to  this  organ  is  desirable.  At  all  events,  even  chronic 
inflammatory  conditions  of  the  gall-bladder  with  a  thickened  wall  and 
those  anatomical  changes  of  the  epithelium  which  may  be  looked  upon  as 
precursors  of  carcinoma,  should  be  included  in  these  indications.  Natu- 
rally these  points  must  be  left  for  the  surgeons  to  decide;  it  seems  to  me 
that  in  this  respect  their  opinions  are  at  present  undergoing  a  change.  Two 
cases  in  which  Lobker  undertook  to  perform  cholecystectomy  on  account 
of  supposed  empyema,  while  tissue  suspiciously  resembling  tumor  was  un- 
noted by  the  operator,  and  in  which  Grawitz  showed  microscopically  a 
beginning  carcinoma,  should  increase  the  number  of  advocates  of  early 
cholecystectomy  more  than  it  has.  Whether  we  shall  in  this  way  succeed 
in  diminishing  the  percentage  of  patients  with  gall-stone  disease  who 
acquire  carcinoma  of  the  gall-bladder,  future  experience  will  alone  decide. 
One  point  must  certainly  be  touched  upon.  It  has  been  explained  above 
that  in  those  cases  in  which  stones  remain  encysted  in  the  gall-bladder 
for  years,  there  is  a  tendency  to  the  development  of  cancer  of  the  gall- 
bladder producing  actual  spasmodic  paroxysms  without  inflammatory  proc- 
esses. The  law  still  operative  with  many  surgeons :  "  Quiescent  gall-stones 
are  not  subjects  for  treatment,"  must  therefore  be  construed  with  ^ome 
limitations.  Enlarged  gall-bladders  tensely  filled  with  stones,  particularly 
where  there  is  a  hereditary  predisposition  of  the  patient  to  cancer,  should 
be  extirpated  on  principle.  The  question  is  simply  this:  How  does  the 
physician  observe  this  except  quite  incidentally,  and  now  are  we  to  ob- 
tain the  patient's  consent  to  an  operation  if  we  tell  him  that,  in  proportion 
to  cholecystitis  which  is  very  frequent,  cancer  is  a  very  rare  disease? 


2.  OBSTRUCTIONS    OF   THE    COMMON    GALL-DUCT    BY   TUMORS 

CLINICAL  FORMS 

In  clinical  study  it  is  difficult  to  separate  the  consideration  of  carcinoma 
of  the  hiliary  passages  external  to  the  liver  from  that  of  obstructions  of 
the  common  bile-duct  and  of  the  hepatic  duct  in  general. 

Occlusion  of  the  ductus  choledochus  may  result  primarily  from  an 
anaiomical,  abnormal,  duodenal  insertion  and  twining  of  this  passage  at 
its  entrance  into  the  intestine,  whereby,  in  exceedingly  rare  cases,  even  in 


OBSTRUCTIONS   OF  THE  COMMON  GALL-DUCT   BY  TUMORS       407 

youthful  individuals,  a  valve-like  closure  and  consequent  extreme  cystic 
dilatation  occurs  (Konitzky).  This  colossal  dilatation  of  the  gall-duct 
may  then  form  a  resistant  tumor  in  the  right  half  of  the  abdomen,  and 
the  bulging  wall  of  the  passage  in  itself  causes  an  increasing  compression 
from  without  upon  the  end  of  the  gall-duct  extending  into  the  intestinal 
wall.  In  a  child  aged  2  months,  with  decided  jaundice,  an  exploratory 
laparotomy  was  performed  (by  Witzel),  and  the  subsequent  autopsy  showed 
a  congenital  marked  narrowing  of  the  cystic  and  common  ducts,  as  well  as 
the  absence  of  the  hepatic  duct.  Congenital  ohliteration  of  the  ductus 
choledochus,  probably  as  the  result  of  fetal  syphilis,  is  somewhat  more 
frequent.  Soon  after  birth  such  children  are  decidedly  jaundiced  without 
fever  and  rapidly  perish.  This  has  sometimes  repeatedly  occurred  in  the 
same  family  (Donop,  Binz,  Glaister,  Schiippel). 

Chronic  occlusion  of  the  ductus  choledochus  by  stone  (incarceration  of 
calculi)  and  the  infrequent  cicatricial  obliteration  of  the  same  in  conse- 
quence of  cholelithiasis  are  of  far  greater  practical  importance.  The  very 
rare  adhesions  due  to  propagated  (  ?)  inflammations  from  the  intestine  in 
enteric  fever  (Lebert),  in  enteritis  (Musser),  in  the  puerperium,  chronic 
peritonitis  (Andral),  and  in  benign  pyloric  stenosis  (Richard)  at  least  de- 
serve brief  mention  here.  The  greatest  interest  attaches  to  neoplasms  of 
the  common  bile-duct.  We  must  also  mention  occlusion  by  foreign  bodies 
other  than  stones,  and  by  parasites  (echinococcus  cysts,  ascarides,  and 
varieties  of  distoma).  Hydatid  cysts  always  develop  in  the  liver,  from 
which  they  penetrate  to  the  larger  biliary  passages.  Years  ago  a  patient 
of  mine  was  operated  upon  by  v.  Eiselsberg  for  echinococcus  of  the  liver. 
On  account  of  extreme  chronic  jaundice  which  was  simultaneously  present 
I  diagnosticated  a  closure  of  the  common  gall-duct  by  daughter-cysts; 
hepatic  echinococcus  cysts  and  a  cholesterin  stone  were  found  in  the  gall- 
duct  and  were  at  the  same  time  removed.  Besides  occlusion  from  stones 
the  hepatic  duct  is  sometimes  occluded  by  callous  cholangitis  (rare),  by 
neoplasms,  by  fetal  syphilis  and  by  parasites. 

In  addition  to  the  obstructions  to  the  permeability  of  the  large  biliary 
passages  which  have  been  mentioned,  there  are  numerous  "  vinculo  quasi 
injecto  "  which  compress  the  lumen  (or  simultaneously  compress  and  in- 
filtrate it).  These  are  either  actual  neoplasms,  or  tumors  in  the  widest 
sense  of  the  word,  and  connective  tissue  proliferations.  These  obstructions 
may  originate  in  the  porta  hepatis:  hydatids,  aneurysms  of  the  hepatic 
artery  (Niewerth),  of  the  abdominal  aorta  (Stokes),  of  the  superior 
mesenteric  artery  (Wilson,  Gairdner),  enlarged  tuberculous,  carcinomatous, 
lympliomatous,  amyloid  glands  of  the  porta  hepatis,  along  the  hepato- 
duodenal ligament,  and  near  the  mouth  of  the  common  gall-duct,  circum- 
scribed adhesive  perihepatitis  at  the  hilus  in  affections  of  the  liver,  syphilis 
ad  basin,  ulcers  of  the  stomach  and  duodenum,  mediastinitis  after  carci- 
noma of  the  breast  (Smolenski),  and  carcinohiata.     Besides  compression. 


408  NEOPLASMS   OF  THE   LIVER  AND  BILIARY   PASSAGES 

cicatrices  in  the  region  of  the  porta  hepatis  also  cause  torsion  of  the  com- 
mon gall-duct,  so  that  it  is  bent  and  follows  an  irregular  course.  We 
must  also  consider  changes  in  the  size  of  the  pancreas  (cystic  dilatation 
of  the  duct  of  Wirsung  (Wyss  and  others),  suppurative  pancreatitis  (Fri- 
son),  sclerosis  (Dejerine),  principally,  however,  carcinoma  of  the  head 
of  the  organ,  and,  finally,  malignant  disease  and  cicatricial  stricture  of 
the  duodenum.  Primary  carcinoma  of  the  gall-hladder  may  by  continuity 
creep  through  the  cystic  duct  to  the  common  duct  and  the  hepatic  duct, 
and,  besides  producing  angiocholitis,  may  cause  compression  and  stenosis. 
Occasionally  the,  enlarged  tensely  filled  gall-bladder  (in  consequence  of 
occlusion  of  the  cystic  duct  by  stones),  or  dropsy  (empyema)  of  the  gall- 
bladder without  concrements,  may  compress  the  common  duct  (Ramskill, 
Socin,  Kiimmel).  Stones  embedded  in  the  cystic  duct  may  also  occlude 
the  common  duct  (Wilson,  Bardenheuer).  Even  the  relaxed  gall-bladder 
whose  tonus  is  impaired  by  long-continued  distention  due  to  inspissated 
bile,  or  by  a  condition  of  fulness  of  the  common  gall-duct,  may  cause  com- 
pression loading  to  biliary  stasis  (Petit,  Jacob  and  Cyr).  Occasionally 
such  a  gall-bladder  may  be  expressed.  Adhesions  of  the  gall-bladder  to 
the  duodenum  and  colon  may  cause  a  volvulus  of  the  ductus  choledochus, 
and  the  duodenum,  in  particular,  is  drawn  to  the  right  and  upward.  Such 
twisted  stenoses  are  often  increased  by  the  simultaneous  presence  of  stones. 
It  is  also  possible  that  a  wandering  kidney  by  its  tense  ligaments  may 
cause  a  volvulus  of  the  common  bile-duct,  a  possibility  which  Weisker  de- 
nies, but  which,  nevertheless,  exists.  On  the  other  hand,  tumors  of  the  right 
kidney  may  cause  obstruction  (Schiippel).  Even  tumors  of  the  colon,  the 
omentum,  the  retroperitoneum,  and  of  the  ovary  and  uterus,  must  be  con- 
sidered as  possible  obstructions  to  the  flow  of  bile. 

If  we  discuss  only  the  cases  in  which  occlusion  of  the  common  gall- 
duct  develops  an  actual,  extensive  (absolute),  biliary  stasis,  we  find  aneu- 
rysms and  enlargement  of  the  glands  of  the  porta  hepatis,  as  well  as  cysts 
of  the  pancreas,  comparatively  rare.  Perihepatitic  and  pancreatic  indura- 
tions are,  as  Courvoisier  states,  more  important.  Of  most  serious  import 
in  this  connection  are  concrements  and  neoplasms  in  the  ductus  chole- 
dochus, carcinoma  of  the  head  of  the  pancreas  and  of  the  duodenum  in 
the  region  of  the  plica  Vaterii.  Secondary  malignant  infiltrations  of  the 
biliary  passages  by  carcinoma  of  the  gall-hladder  must  also  be  included  here. 
The  most  significant  causes  of  obstruction  of  the  choledochus  are  also  the 
most  frequent,  and,  therefore,  of  the  greatest  clinical  interest.  The  ductus 
choledochus  in  its  passage  to  the  duodenum  burrows  for  itself  a  furrow  in 
the  head  of  the  pancreas,  or  it  perforates  the  same,  and  unites  with  the 
ductus  Wirsung  near  its  mouth.  The  upper  horizontal  portion  of  the  duo- 
denum, as  well  as  the  two^  other  portions,  are  reached  from  the  head  of 
the  pancreas  with  which  the  two  duodenal  areas  closely  unite  and  form 
a  bow-shaped  intestinal  portion.     The  point  where  the  common  gall-duct 


OBSTRUCTIONS   OF  THE  COMMON   GALI^DUCT   BY  TUMORS       409 

enters  the  duodenum  is  the  left  concave  surface  of  the  pars  descendens 
duodeni.  If  the  ductus  choledochus  does  not  penetrate  the  head  of  the 
pancreas  it  passes  behind  it,  and  enters  the  substance  of  the  pancreas  just 
before  its  junction  with  the  pancreatic  duct.  The  two  passages  run  along- 
side each  other  for  a  short  distance,  then  perforate  obliquely  into  the 
longitudinal  musculature,  continuing  their  course  for  some  time  below 
the  mucosa,  and  finally,  by  a  common  orifice,  pass  into  the  diverticulum 
of  Vater.  Sometimes,  however,  they  terminate  separately.  Compression 
is  most  likely  to  occur  when  the  ductus  choledochus  passes  through  the 
head  of  the  pancreas;  but  these  topical  relations  explain  why  a  tumor 
which  has  developed  in  the  ductus  choledochus  furnishes  a  picture  so 
nearly  analogous  to  that  of  a  tumor  at  the  head  of  the  pancreas,  or  of 
a  carcinoma,  or  even  of  a  cicatricial  stricture  in  the  region  of  the  diver- 
ticulum Vateri  duodeni.  From  an  anatomical  standpoint  the  question  has 
arisen  (Pic)  whether  carcinoma  of  the  diverticulum  of  Vater  should  not 
be  referred  to  the  pancreas  rather  than  to  the  duodenum.  No  matter 
what  the  conditions  are,  the  obstructions  which  obliterate  or  compress  the 
ductus  choledochus  must  also  mechanically  implicate  the  pancreatic  pas- 
sage, which  is  not  infrequently  subject  to  dilatation  (cystic). 

In  practice  the  question  usually  resolves  itself  as  follows :  Jaundice 
(stasis)  reaches  its  acme  of  development  either  rapidly  or  gradually;  if  it 
does  not  disappear  after  a  short  time,  it  merges  into  a  chronic  icterus. 
In  prolonged  "catarrhal"  jaundice  (lasting  2,  5  or  even  9  months),  when 
the  symptoms  of  gastrointestinal  catarrh  have  subsided  and  the  signs  of 
pure,  chronic,  biliary  stasis  have,become  prominent,  particularly  a  disturb- 
ance of  the  general  condition,  with  weakness  and  emaciation,  the  clinical 
picture  of  biliary  occlusion  from  other  causes  (incarceration  of  stone  com- 
pressing or  occluding  neoplasms)  may  resemble  it  so  closely  that  the  diag- 
nosis is  made  clear  only  by  the  further  course  of  the  affection  (final, 
complete  and  permanent  restitution  of  permeability  of  the  biliary  passages). 
Certain  diagnostic  support  will  be  found  in  the  fact  that  the  onset  of  the 
disease,  according  to  our  o%vn  observation,  or  after  obtaining  a  history  of 
the  cause  and  clinical  behavior,  coincides  fully  with  that  of  catarrhal  jaun- 
dice; that  the  occlusion  of  the  biliary  passages  is  incomplete,  having 
been  only  partial  for  a  time,  or  even  continuously;  and  that,  finally,  the 
liver  and  spleen  have  permanently  presented  only  a  sign  of  biliary  stasis. 
But  in  catarrhal  jaundice  the  hemorrhagic  diathesis  may  also  develop! 
Neusser  and  Toelg  report  the  case  of  a  man.  aged  39,  who  was  attacked 
by  jaundice  after  partaking  of  sausages,  and  who  succumbed  in  the  eighth 
week  of  the  disease  after  hemorrhage  from  the  urinary  passages.  The 
autopsy  showed  catarrhal  cholangitis,  with  complete  impermeability  of  the 
ductus  choledochus.  The  hemorrhages  began  during  the  seventh  week. 
Nowadays,  under  similar  circumstances  (probably,  however,  before  the 
appearance  of  the  cholemic  hemorrhages)   an  operation   (cholecystotomy) 


410  NEOPLASMS   OF  THE   LIVER  AND  BILIARY   PASSAGES 

would  be  resorted  to.  As  in  simple  "  catarrhal "  swelling,  a  diphtheritic, 
a  typhoid^  and  a  variolous  enlargement  of  the  ductus  choledochus  may 
remain  for  a  long  time.  I  observed  a  case  of  scarlatina  with  jaundice  and 
decided  extension  of  the  gall-bladder.  Apart  from  such  cholangitic  con- 
ditions as  produce  the  syndrome  of  chronic  jaundice,  there  are  certain 
pathologic  processes  in  the  liver  itself  which  must  be  considered  in  diag- 
nosis: Echinococcus,  abscess,  syphilis  (peripylephlebitis  syphilitica),  pri- 
mary and  secondary  carcinomata,  all  at  least  under  the  supposition  of  a 
corresponding  localization,  an  especial  development,  or  in  combination  with 
other  (secondary)  disease  of  the  tissue  (biliary  cirrhosis),  also  hypertrophic 
hepatic  sclerosis  (Todd-Hanot)  in  which  latter  disease  the  jaundice  at  first 
recurs,  later  becomes  permanent,  and  varies  periodically  in  intensity.  Par- 
ticularly in  hypertrophic  hepatic  cirrhosis,  which  among  the  previously 
mentioned  processes  with  by  far  the  greatest  frequency  runs  its  course  with 
most  decided  chronic  jaundice,  the  discoloration  of  the  skin  is  rarely  as 
green  as  in  complete  biliary  stasis,  and,  except  during  the  time  of  the 
so-called  poussees,  a  sufificient  amount  of  bile  enters  the  intestine  to  color 
the  feces.  A  comprehensive  description  of  the  differential  diagnosis  of 
all  the  hepatic  affections  which  have  been  mentioned  (besides  Hanot's 
cirrhosis,  primary  cancer  of  the  liver  and  echinococcus  multilocularis  re- 
quire special  consideration)  cannot  be  given  in  the  framework  of  this 
article.  All  these,  however,  must  first  be  excluded  before  we  can  definitely 
conclude  in  a  given  case  that  the  chronic  icterus  is  due  to  a  definite  (quasi 
definite)  occlusion  of  the  extra-hepatic  ducts,  and  observation  of  the  fur- 
ther course  will  determine  which  of  the  many  diseases  named  is  the  cause. 
It  must,  nevertheless,  be  casually  mentioned  that,  especially  to  these  pri- 
mary affections  of  the  liver,  extra-hepatic  complications  are  usually  added 
which  may  in  themselves  cause  chronic  jaundice  (inflammatory  swelling; 
suppuration  of  periportal  lymph  nodes  in  liver  abscess,  the  affection  having 
previously  run  its  course  without  jaundice;  circumscribed  adhesive  peri- 
hepatitis at  the  porta  hepatis  in  gummatous  syphilis  of  the  liver;  carci- 
nomatous infiltration  of  the  periportal  glands  in  cancer  of  the  liver  or 
gall-bladder). 

Much  more  important  than  the  exclusion  of  primary  disease  of  the 
liver  is  the  diagnosis  of  the  situation  of  an  extra-hepatic  constriction  of 
the  common  bile-duct  in  the  special  cases  in  which  jaundice  develops  with 
more  or  less  rapidity  and  intensity,  and  culminates  in  the  serious  condition 
known  as  icterus  gravis.  The  color  of  the  skin,  even  when  the  jaundice 
varies  or  even  occasionally  becomes  intermittent,  is  greenish,  olive  color 
(melasicterus),  of  the  urine  dark  brown  (greenish-brovm),  of  the  stools 
absolutely  acholic.  In  other  cases,  particularly  in  the  later  stages,  the  dis- 
coloration of  the  skin  is  less  intense,  revealing  a  peculiar  tint  (a  dirty, 
yellowish-  or  brownish-red),  the  urine  also  appears  conspicuously  changed 
fo  a  brownish-red   (ictere  hemapheique  of  Gubler,  metapigmented  icterus 


OBSTRUCTIONS  OF  THE  COMMON  GALI^DUCT  BY  TUMORS      411 

of  Debove  and  Achard,  previously  called  by  us  "  urobilin  icterus  ").  What 
pigments  produce  the  staining  in  the:e  cases  is  not  known  with  absolute 
certainty.  The  French  declare  the  principal  coloring  agent  of  metaicterus 
to  be  urobilin  and  its  chromogens.  The  former  they  believe  to  be  exclu- 
sively produced  in  the  liver,  and  its  appearance  to  denote  a  serious  affection 
of  the  liver  cells.  In  specially  prolonged  cases  the  icteroid  discoloration 
later  loses  its  intensity  simply  by  loss  of  function  of  the  liver  cells  and 
the  consequent  insufficient  production  of  bile.  The  general  nutrition  suf- 
fers to  the  highest  degree  because  of  various  digestive  disturbances  and 
marked  cardiac  asthenia;  not  rarely  there  is  a  tendency  to  capillary,  but 
often  very  decided,  even  fatal,  hemorrhages,  or  to  those  which  may  cause 
a  fatal  termination,  such  as  hemorrhage  into  the  stomach,  the  intestine, 
the  abdominal  cavity,  the  retroperitoneal  cellular  tissue,  from  the  urinary 
passages,  the  uterus,  the  nose,  the  gums,  the  skin,  and  from  operative 
wounds  (Leyden,  Feltz  and  Bitter).  Toward  the  end  there  are  frequently 
paroxysms  of  disturbances  which  usually  terminate  fatally  in  a  short  time 
(dizziness,  coma,  or  a  state  of  excitement,  delirium  or  convulsions,  and 
which  are  at  present  designated  hepatic  autointoxication  or  hepatargy 
[Quincke]).  Rupture  of  the  biliary  passages  which  are  dilated  to  an 
extreme  in  consequence  of  the  absolute  closure  of  the  common  bile-duct 
is  exceedingly  rare,  but  more  frequent  if,  at  the  same  time,  suppuration  of 
the  biliary  passages  or  abscess  of  the  liver,  or,  exceptionally,  trauma  occurs 
in  connection.  Distributed  infectious  processes  in  the  biliary  passages  are 
more  frequent  in  occlusion  of  the  common  gall-duct  by  stone  or  tumor. 
Ulcerative  perforation  of  the  biliary  passages  is  observed  almost  exclusively 
in  incarceration  from  stones.  Peculiar  to  cholelithiasis  also  is  spontane- 
ous recovery  by  the  formation  of  a  fistula  (between  the  biliary  passages 
and  the  intestine,  especially  the  duodenum  and  colon,  or  between  the  gall- 
bladder and  abdominal  walls).  By  direct  chemical  action  of  the  engorged 
bile  upon  the  liver  substance,  biliary  cirrhosis  ensues  (which  must  not  be 
confounded  with  cirrhosis  cholangica  [hypertrophica]  Hanot).  Marked 
tissue  proliferation  and  consequent  induration,  with  occlusion  of  the  com- 
mon duct  by  stones,  occurs  more  often  than  in  occlusion  of  the  ductus 
choledochus  by  carcinoma  or  cicatricial  stricture  of  the  duodenum  in  the 
region  of  the  diverticulum  of  Vater.  With  biliary  stasis  due  to  incar- 
ceration of  calculi,  an  infection  of  the  biliary  system  is  attributed  to 
intestinal  bacteria  which  appears  to  be  substantiated  by  the  frequent  com- 
plication of  marked  purulent  inflammation,  and  this  circumstance  chiefly 
causes,  that  is  to  say,  favors,  the  interstitial  proliferation  of  connective 
tissue.  Evidently,  however,  the  French  designation  of  cirrhose  biliaire  as 
"  calculaire  "  is  much  too  narrow.  If  an  obstruction  by  stone  leads  to  true 
granulation,  even  to  contraction  of  the  liver,  to  enlargement  of  the  spleen 
and  ascites,  the  condition  is  due,  in  addition  to  the  causes  that  have  been 
enumerated,  to  the  prolonged  course  of  the  disease  (sometimes  two  to  three 


412  NEOPLASMS  OF  THE  LIVER  AND  BILIARY  PASSAGES 

years).  As  a  rule,  this  cirrhosis  is  without  decisive  importance  for  the 
decursus  morhi. 

\i,  however,  in  consequence  of  any  occlusion  of  the  common  bile-duct, 
marked,  higli-graded  icterus  stasis  develops,  there  are  also  quite  isolated, 
paradoxical  cases  in  which  this  condition  does  not  follow.  Such  a  case, 
for  example,  was  observed  by  Hanot  and  Gombault.  In  consequence  of 
"  chronic  gastritis  with  submucous  sclerosis  and  callous  retroperitonitis," 
cirrhosis  of  the  hilus  of  the  liver  had  formed  and  completely  obstructed  the 
ductus  choledochus,  but  there  was  no  jaundice,  and  merely  partial  occlusion 
of  the  hepatic  artery  and  portal  vein.  Hanot  and  Gombault  assumed  that 
the  succeeding  disturbance  of  circulation  had  limited  the  quantity  of  bile 
formation  and,  synchronous  with  the  hindrance  by  occlusion,  absorption 
was  suspended  so  long  as  even  the  smallest  quantity  of  bile  passed  into  the 
intestine;  later  the  secretion  ceased  entirely,  so  that  even  complete  occlu- 
sion of  the  common  bile-duct  did  not  produce  jaundice.  From  a  deficiency 
in  formation  products,  the  secretion  of  bile  ceased,  and  this  caused  the 
death  of  the  patient.  In  this  case,  the  important  factor  was  the  simultane- 
ous strangulation  of  the  hepatic  vessels.  However,  I  believe  it  more  likely 
in  such  exceptional  cases  that  an  auxiliary  system  of  biliary  canals,  which 
is  also  present  under  normal  conditions  and  serves  the  purposes  of  anas- 
tomosis, intervenes  and  permits  the  vicarious  emptying  of  an  auxiliary 
brancli  of  the  ductus  choledochus  and  the  like. 

Among  the  previously  mentioned  pathological  processes  which  with 
comparative  frequency  cause  obstruction  of  the  choledochus  the  following' 
must  be  mentioned:  Chronic  impaction  hy  stone,  carcinomata  of  the  com- 
mon bile-duct,  of  the  head  of  the  pancreas  and  duodenum,  as  well  as 
cicatricial  stricture  in  the  region  of  the  diverticulum  of  Voter,  circum- 
scribed perihepatitis  at  the  hilus  of  the  liver,  and,  possibly,  also  enlarge- 
ment of  the  periportal  lymph  nodes.  In  so  far  as  a  gastric  cancer,  or  a 
primary  carcinoma  of  the  gall-bladder,  attacks  the  ductus  choledochus  and 
the  hepatic  duct,  the  resulting  stasis  of  bile  must  be  ascribed  to  the  tumor 
of  the  choledochus  provided  a  fundamental  diagnosis  cannot  be  made.  It 
is  of  the  utmost  importance  for  the  physician  to  know  with  certainty 
that  an  occlusion  of  the  biliary  passages  by  stone  or  some  other  cause 
(tumor)  has  occurred.  If  we  feel  assured  that  a  stone  is  present  in  the 
coiiimon  duct,  and  in  case  intermittent  fever  sets  in  soon  after  the  first 
colic  which  is  accompanied  by  jaundice,  choledochotomy  is  to  be  per- 
formed. In  chronic  obstructive  jaundice  due  to  carcinoma,  much  less  is 
to  bo  hoped  for  from  operative  interference;  even  exploratory  laparotomy, 
according  to  experience,  is  badly  borne!  Causes  purely  mechanical  also 
favor  the  conception  of  these  two  groups  of  cases:  Calcareous  occlusion 
and  occlusion  of  the  biliary  passages  from  other  causes.  For,  as  will  be 
shown  in  the  following,  a  series  of  other  factors  may  be  recognized  by 
which,   aside   from  numerous,  not  rarely  insurmountable,   diflficulties   in 


OBSTRUCTIONS  OF  THE  COMMON   GALI^DUCT  BY  TUMORS       413 

individual  observations,  the  differentiation  between  chronic  occlusion  of 
the  ductus  choledochus  by  calculus  and  tumor  may  be  indicated;  as  a  rule 
it  is  almost  impossible  to  distinguish  the  different  cases  of  occlusion  not 
due  to  stones.  The  course  is  most  favorable,  as  was  first  indicated  by 
Courvoisier,  Leube,  and  others,  and  corroborated  by  Neusser  in  the  diag- 
nosis of  obstruction  of  the  choledochus  from  pressure  in  the  porta  hepatis. 
Probably  in  most  of  the  cases  belonging  to  this  group,  but  by  no  means 
exclusively,  there  is  a  determinable,  characteristic  factor,  that  is,  the  paral- 
lelism between  biliary  stasis  and  portal  vein  stasis  evidently  caused  by  the 
anatomical  situation  referred  to.  As  symptomatic  expressions  of  the  latter, 
besides  ascites  and  enlargement  of  the  spleen,  we  must  consider  diarrhea, 
gastric  and  intestinal  hemorrhages,  and  a  visible  collateral  circulation. 
An  intense  and  almost  simultaneous  stasis  in  the  portal  vein  and  biliary 
system  (after  excluding  ordinary  hepatic  cirrhosis)  would  lead  us  to  think 
of  enlarged  glands  at  the  hilus  of  the  liver  and  circumscribed  perihepatitis 
ad  hasin.  Apart  from  carcinoma  and  syphilis,  the  clinical  interest  of  these 
processes  is  comparatively  slight.  Naturally  there  are  tumors  also  upon 
the  under  surface  of  the  liver,  as,  for  instance,  in  the  case  of  Quincke,  in 
which  a  large  fibroma  was  present,  but  which,  on  account  of  its  position, 
merely  occluded  the  choledochus  without  causing  ascites.  On  the  other 
hand,  in  the  much  more  frequent  cases  in  which  the  greatest  pressure  is 
on  the  duodenum,  this  is  a  variable  condition.  Usually  jaundice  is  present 
for  a  long  time  before  ascites  appears,  or  the  latter  symptom  does  not 
occur  at  all  (it  is  most  readily  produced  in  carcinoma  of  the  ductus 
choledochus  and  of  the  duodenum  itself),  that  is,  during  the  entire  course 
of  the  disease  it  is  very  slight.  Whether  the  peritoneal  effusions  of  the 
tumors  which  we  have  an  opportunity  of  observing,  and  which  are  due 
to  the  very  small  tumors  of  the  intestinal  portion  of  the  biliary  passages, 
actually  depend  upon  purely  mechanical  obstruction  of  the  circulation  in 
the  portal  vein,  I  believe  to  be  very  questionable.  In  carcinoma  of  the 
head  of  the  pancreas  and  the  upper  end  of  the  duodenum,  as  well  as  in 
cancer  of  the  gall-bladder  which  extends  in  the  direction  of  the  porta 
hepatis,  at  least  occasionally  and  in  certain  stages  of  the  course,  the  ductus 
choledochus  and  the  portal  vein  sustain  almost  equal  pressure. 

As  is  shown  by  the  statistics  of  surgeons  up  to  the  most  recent  times, 
in  tumors  which  occlude  the  distal  portion  of  the  choledochus,  a  positive, 
diagnostic  recognition  in  the  individual  case  prior  to  the  operation  (that 
is,  during  the  life  of  the  patient)  was  frequently  impossible;  if,  indeed,  a 
correct  opinion  with  a  special  localization  of  the  tumor  could  be  given 
at  any  time.  On  the  contrary,  the  operation  was  usually  performed  be- 
cause, diagnostically,  the  disease  was  supposed  to  be  present,  but,  at  the 
same  time  it  was  often  erroneously  presumed  to  be  a  ease  of  occlusion 
of  the  biliary  passages  by  stones.  I  shall,  therefore,  utilize  a  somewhat 
extensive  and  original  experience  in  regard  to  obstruction  of  the  chole- 


414  NEOPLASMS   OF  THE  LIVER   AND  BILIARY   PASSAGES 

dochus  by  tumor  to  criticize  the  differential  diagnostic  factors  which  have 
up  to  the  present  time  been  proposed.  Since  1887  I  have  collected  24 
autopsy  reports  of  occlusion  of  the  choledochus  not  due  to  stone  (in 
Prague,  Vienna,  Graz).  In  another  case,  metastases  due  to  sarcoma  were 
present,  which,  starting  from  a  large,  visible  and  palpable  tumor  of  the 
left  ilium,  compressed  the  biliary  passage.  Twenty-two  cases  were  due  to 
obstruction  from  carcinoma,  the  two  other  cases  were  attributed  respect- 
ively to  an  echinococcus  cyst  upon  the  concave  surface  of  the  liver  and 
to  a  cicatricial  stenosis  of  the  duodenum  after  rupture  from  a  stone.  In 
13  cases  we  were  dealing  with  cancer  of  the  biliary  passages,  in  7  with 
carcinoma  of  the  head  of  the  pancreas,  and  in  2  with  a  duodenal  tumor. 
To  this  must  be  added  2  cases  (with  section)  of  tumor  of  the  pancreas 
without  Jaundice,  and  3  others,  not  confirmed  by  autopsy,  of  occlusion  of 
the  ductus  choledochus,  in  which  the  diagnosis  of  carcinoma  was  made 
with  at  least  great  probability  and  which,  in  certain  respects,  may  here 
be  utilized.  In  contrast  with  these  reports  of  occlusion  of  the  choledochus 
not  duo  to  stone  are  11  original  cases  in  which,  by  autopsy  or  opera- 
tion, incarceration  due  to  stone,  to  cicatricial  stricture  of  the  biliary 
passages  following  cholelithiasis  or  abscess,  but  without  a  complicating 
carcinoma,  could  be  determined.  From  the  literature  at  hand  it  is  diffi- 
cult to  form  a  conclusive  opinion  as  to  the  frequency  of  chronic  occlusion 
by  stone  compared  with  that  due  to  pressure  from  malignant  tumors. 
Hilton  Fagge,  after  an  experience  extending  over  years,  states  that  per- 
manent biliary  stasis  with  all  of  its  sequelae  occurs  twice  as  often  in 
consequence  of  malignant  disease  causing  pressure  as  in  pressure  from 
stones.  ]\Iurchison  knew  of  only  two  cases  of  fatal,  uncomplicated,  chronic 
jaundice  due  to  stone,  and  Glover  believes  every  case  of  this  kind  worth 
publishing  on  account  of  its  great  rarity.  Robson  cautions  us  in  general 
against  operations  for  obstructive  jaundice,  since,  as  a  rule,  carcinoma  of 
the  biliary  passages  is  found.  Fiedler  found  this  condition  only  twice 
among  800  to  900  autopsies  in  cases  of  gall-stone  disease  (that  is,  among 
10,000  general  mortalities).  In  343  cases  of  cholelithiasis  (among  4,313 
autopsies)  Schloth  (in  Erlangen)  found  a  stone  in  the  ductus  choledochus 
9  times,  therefore, . in  0.2  per  cent,  of  all  autopsies,  and  in  2.6  per  cent. 
of  all  the  cases  of  gall-stones.  According  to  Courvoisier,  the  proportions 
are  oven  greater  in  Basle:  In  2,520  autopsies  and  255  cases  of  cholelithia- 
sis, stone  was  found  10  times  in  the  choledochus,  i.  e.,  in  0.4  per  cent,  of 
all  autopsies  and  3.9  per  cent,  of  all  gall-stone  cases.  The  rarity  of  pure 
eases  coming  to  autopsy  does  not  certainly  prove  the  rarity  of  the  condi- 
tion; occlusion  due  to  stone  need  not,  as  such,  be  absolutely  fatal,  for,  in 
a  largo  number  of  cases,  the  calculus  eventually  finds  its  way  out.  Of 
n  non-operative  cases  collected  by  W.  Braun  (Pringle,  White,  Copeman, 
^lioliaiix.  Riedol,  Thornton)  the  outcome  was  fatal  in  5,  and  in  the  patient 
of  the  last  named  author  a  spontaneous  passage  of  the  stone  occurred  and 


OBSTRUCTIONS  OF  THE  COMMON  GALL-DUCT  BY  TUMORS      4l5 

was  followed  by  cure.  Important  complications  may  set  in.  That  chronic 
jaundice  due  to  a  calculus  permanently  incarcerated  in  the  ductus  chole- 
dochus  is  not  absolutely  rare  is  proven,  in  the  first  place,  by  the  experi- 
ences of  surgeons  who  are  specialists  in  this  line.  Nevertheless,  according 
to  my  own  experience,  if  the  physician  does  not  observe  "  selected  "  cases, 
even  allowing  due  weight  for  the  intermissions  in  the  jaundice,  he  must 
be  familiar  with  the  fact  that  the  severest  (fatal)  cases  of  chronic  biliary 
stasis  are  due  far  more  frequently  to  obstruction  of  the  choledochus  which 
is  not  due  to  calculi.     In  this  opinion  Schiippel  coincides. 


PATHOLOGY 

In  regard  to  the  special  pathology  of  adhesive  perihepatitis  in  the 
porta  hepatis  and  in  affections  of  the  periportal  lymph  nodes,  I  shall  not 
at  this  point  enter*  into  details.  In  syphilitic  hepatitis  marked  icterus 
from  compression  of  the  biliary  passages  is  much  rarer  than  ascites.  Car- 
cinomatous metastases  of  the  portal  glands  are  peculiar  to  primary  and 
secondary  cancer  of  the  liver,  and  cause  decided  swelling.  Primary  cancer 
of  the  gall-bladder  leads  to  the  development  of  cancer  in  the  glands  of 
the  hilus  and  in  the  porta  hepatis,  by  which  the  outflow  of  bile  is  impeded 
and  the  portal  vein  is  compressed.  Ascites  is  found  here  much  more 
frequently  than  enlargement  of  the  spleen.  Intestinal  hemorrhage,  even 
dilatation  of  the  collateral  venous  trunks,  is  observed  in  this  condition. 
It  must  be  borne  in  mind  that  the  portal  vein  may  also  be  occluded  and 
ascites  result  from  complicating  cirrhotic  changes  (carcinomatous  cirrho- 
sis) or  from  obstruction  (compression)  of  the  veins  of  the  liver.  In 
leukemic  and  lymphomatous  tumors,  the  portal  lymph-glands  are  also 
frequently  enlarged.  But  if  the  liver  is  not  correspondingly  changed  from 
other  causes  (for  example,  in  certain  cases  of  pseudo-leukemia  with  chronic 
relapsing  fever)  decided  jaundice  is  very  rarely  present,  and  ascites  usually 
occurs  late.  (Chronic  peritonitis  of  leukemia  belongs  to  another  category.) 
In  the  diagnosis  of  these  conditions,  therefore,  aside  from  the  relation 
between  the  biliary  and  portal  vein  stasis,  it  is  necessary,  above  all,  that 
we  find  in  some  part  of  the  body  the  primary  organic  affection  which 
would  produce  secondary  carcinomatous  disease  of  the  glands  of  the  hilus, 
or  the  proof  of  an  analogous  affection  of  other  peripheral  lymph-glands 
(leukemia,  pseudo-leukemia),  or  that  we  discover  signs  of  constitutional 
syphilis,  etc. 

The  case  mentioned  above  of  compression  of  the  biliary  passages  upon  the  lower 
concave  surface  of  the  liver  by  an  echinococctis  cyst  may  be  here  briefly  quoted. 

A  woman,  aged  30,  wife  of  a  meat-chopper    (butcher),  who  had  previously  suf- 
fered from  enlargement  of  the  liver  and  ascites,  and  afterward  from  gradually  in- 
creasing jaundice,  subsequently  noted  a   more  rapid  and  more  decided  enlargement 
of  the  abdomen  with  slight  swelling  of  the  feet.    Severe  abdominal  pains  were  added. « 
28 


416  NEOPLASMS   OF  THE   LIVER  AND  BILIARY   PASSAGES 

On  June  8th,  1888,  she  was  visibly  emaciated,  markedly  jaundiced,  her  color  brown- 
ish-gray, her  temperature  between  100°  F.  and  102.9°  F.  Upon  the  right  side  of 
the  neck  a  mass  of  partly  isolated,  partly  connected,  lymph-glands  of  the  size  of 
a  small  apple;  in  the  left  supraclavicular  fossa  isolated  intumescent  lymph-glands 
from  the  size  of  a  millet  seed  to  the  size  of  a  bean.  Left-sided  pleurisy.  Over  both 
lungs  piping  rales,  occasionally  crepitation.  Free  fluid  in  the  peritoneal  sac.  The 
liver  enlarged,  of  coarse  consistence,  its  surface  smooth;  the  border,  which  may  be 
readily  palpated,  is  dull.  Gall-bladder  not  palpable.  On  percussion,  at  least,  en- 
largement of  the  spleen.  Urine  very  dark,  yellowish,  foamy;  chlorids  in  normal 
amount. 

Pain  in  the  right  hypochondrium  continues.  The  temperature  rises  each  evening 
above  102.2°  F.,  early  in  the  morning  it  falls  below  100.4°  F.  Feces  not  entirely 
devoid  of  bile,  very  rich  in  fat.  No  bacilli  in  the  expectoration.  June  18th:  Peri- 
carditis. Jime  19th:  Complete  absence  of  bile  from  the  feces.  Hemorrhagic  diathesis, 
hemorrhages  into  the  skin,  from  the  nose,  hemorrhage  of  the  gums.  June  23rd: 
Marked  loss  in  strength.     June  25th:   Subnormal  temperature.     June  26th:    Death. 

Autopsy:  Echinococcus  cysticus  multiplex  cum  compressione  ductus  hepatici  et 
cystici,  subsequente  ictero  gravi. — Tuberculosis  chron.  gld.  lymphaticar.  colli.  Peri- 
carditis, pleuritis  sin.  tuberculosa  cum  exsudato  fibrinoso-haemorrhagico.  Perito- 
nitis tub.  The  liver  appeared  enlarged  to  l^/g  times  its  normal  size;  upon  the 
upper  border  of  the  right  lobe  between  the  gall-bladder  and  the  hepato-umbilical 
ligament  an  uneven  tumor  of  the  size  of  a  man's  fist  was  noted,  and  at  the  vault 
of  the  liver,  under  the  capsule,  a  whitish  tumor  the  size  of  a  hen's  egg  was  found. 
The  first  mentioned  tumor  bulged  decidedly  downward,  so  that  around  it  the  hepatic 
duct  and  the  beginning  portion  of  the  common  duct  were  found  empty  and  pressed 
flat.  Owing  to  this  dragging,  previously  mentioned,  it  was  difficult  for  the  sound 
to  pass  the  biliary  passages.  The  cystic  duct  also  encircled  the  lower  border  of 
the  tumor,  and  this,  too,  markedly  dragged.  The  walls  of  the  distended  biliary 
passages  were  decidedly  atrophic.  The  gall-bladder  contained  but  little  bile.  A  third 
tumor  of  the  same  character  was  found  deeply  embedded  in  the  right  lobe  of  the 
liver ;  the  liver  tissue  showed  an  increased  consistence.  A  brownish-green  icteroid 
condition  was  observed.  The  distended  intrahepatic  biliary  passages  contained  much 
mucoid,  watery,  yellow  bile.  The  enlargement  of  the  spleen  was  very  considerable. 
The  tumor  presented  the  characteristic  features  of  echinococcus  cysts. 


As  is  well  known,  compression  of  the  large  biliary  passages  upon  the 
concave  surface  of  the  liver  combined  with  jaundice  in  consequence  of 
the  stasis  of  bile  is  rare,  particularly  in  echinococcus  cysts  of  the  liver; 
according  to  Finsen  it  occurred  only  7  times  in  167  cases,  according  to 
Xcisser  20  times  in  388  cases.  An  analogous  effect  upon  the  portal  vein 
or  vena  cava  is  infrequent.  Damaschino  once  found  a  large  echinococcus 
sac  in  the  right  lobe  of  the  liver,  pressing  upon  the  ductus  choledochus 
in  the  porta  hepatis;  in  this  case  another  small  hydatid  lay  along  the 
longitudinal  fold  of  the  bile  ducts.  In  my  case  the  complete  closure,  the 
icterus  gravis,  the  hemorrhagic  diathesis,  the  hepatargy,  as  well  as  the 
preceding  ascites  (apparently  the  peritonitis  occurred  late),  were  most 
remarkal)le. 

I  have  seen  no  case  in  which  enlargement  of  the  pancreas  other  than 
from  carcinoma  could  give  rise  to  complete  occlusion  of  the  common  bile 


OBSTRUCTIONS   OF  THE  COMMON   GALI^DUCT   BY  TUMORS       417 

duct.  Evidently  obstructions  from  cystic  dilatation  of  the  duct  of  Wirsung 
(Wyss)  from  purulent  pancreatitis,  and  even  from  sclerosis,  are  rarities. 
On  the  other  hand,  tumors  of  the  head  of  the  pancreas  with  actual  tumors 
of  the  choledochus  may  in  their  frequency  enter  into  competition  (in  this 
relation  cancer  is  first,  lymphosarcoma  is  rare).  Many  authors  regard 
cancer  of  the  pancreas  as  even  the  usual  cause  of  obstruction  of  the  common 
bile  duct.  In  my  own  observations,  as  has  been  mentioned,  there  are  13 
cases  of  cancer  of  the  choledochus  (among  these  8  positive  primary  neo- 
plasms), and,  in  contrast,  7  of  primary  carcinoma  of  the  head  of  the 
pancreas.  No  doubt  primary  cancer  of  the  duodenum  beginning  at  the 
diverticulum  of  Vater  is  much  more  uncommon.  One  of  my  patients 
with  cancer  of  the  pancreas  was  only  25  years  old,  the  age  of  the  others 
varied  between  47  and  70.  In  regard  to  sex  my  experience  was  uniform 
with  that  of  all  other  observers,  in  that  among  my  cases  there  were  but 
two  women.  Of  the* etiology  of  carcinoma  of  the  pancreas,  we  know  as 
little  as  of  the  cause  of  cancer  in  general.  Anatomically,  the  epithelioma 
starting  from  the  epithelium  of  the  glands  as  well  as  from  the  cells  of 
the  ducts  usually  presents  itself  as  scirrhus,  more  rarely  as  a  medullary 
tumor,  and  most  rarely  as  a  colloid  cancer.  Most  often  (in  over  60  per 
cent,  of  all  cases)  the  seat  is  in  the  head,  and  the  tail  of  the  gland  is 
usually  exempt.  The  growing  neoplasm  of  the  pancreas  much  more  fre- 
quently proliferates  to  the  duodenum  (also  to  the  stomach)  than  the  duo- 
denal (pyloric)  cancer  to  the  pancreas  (in  spite  of  Olivier's  conclusions). 
The  head  of  the  pancreas  attacked  by  cancer  *is  often  decidedly  enlarged, 
up  to  the  size  of  a  child's  fist  or  larger;  during  the  life  of  the  patient, 
however,  even  to  the  end,  the  tumor  is  not  palpable  (this  was  true  of  6 
out  of  7  of  my  cases),  which  is  in  contrast  to  the  view  of  Leichtenstern, 
who  maintained  that  it  was  very  frequently  palpable.  Sometimes  the 
pancreatic  duct  is  occluded,  and  if  the  resisting  tissue  still  secretes  fluid, 
stasis  of  the  secretion  with  cyst-like  dilatation  of  the  duct  occurs  (Bolds). 
As  may  be  readily  surmised  from  the  previous  description,  the  ductus 
choledochus  with  very  rare  exceptions  meets  the  same  fate,  but  the  mode 
of  implication  of  the  biliary  passage  varies.  If  this  reaches  the  intestine 
without  entering  the  substance  of  the  pancreas  itself,  under  some  circum- 
stances compression  alone  occurs.  The  common  bile  duct  remaining  free 
may,  however,  be  actually  surrounded  or  infiltrated  by  the  carcinoma.  If 
it  permeate  the  head  of  the  pancreas,  a  malignant  growth  develops  in  its 
walls,  perforates  it,  and  occludes  the  lumen.  Under  these  varying  condi- 
tions decided  stenosis  of  different  grades  is  found  rather  than  absolute 
closures.  Dilatation  of  the  biliary  passages  is  the  rule,  dilatation  of  the 
gall-bladder  is  found  in  at  least  70  per  cent,  of  all  cases  that  have  been 
observed,  in  all  of  my  own  cases  with  the  exception  of  one  (Classen, 
Arcelet,  Krieger,  Legendre,  Rotch,  Lachmann,  Wyss,  Frerichs,  Murchison). 
Besides  cancer  of  the  pancreas,  I  saw  one  case  of  chole(cysto)lithiasis. 


418  NEOPLASMS  OF  THE  LIVER  AND  BILIARY  PASSAGES 

The  large  blood-vessels  in  the  vicinity  and  the  solar  plexus  are  also  impli- 
cated in  cancer  of  the  pancreas,  and  not  rarely,  as  is  the  case  with  the 
duodenum ;  in  my  7  cases  perforation  of  its  wall  was  found  3  times.  Even 
the  ureters  may  be  compressed;  this  is  partly  due  to  pressure,  partly  to 
continued  carcinomatous  growths,  and,  in  some  measure,  to  the  develop- 
ment of  tough,  strand-like  thickenings,  with  volvulus  of  portions  of  the 
intestine,  etc.  Apart  from  the  mesenteric  lymph-glands  and  the  peri- 
toneum, extensive  metastases  in  distant  organs  are  said  to  be  rare ;  I  found 
several  quite  isolated  ones  and  even  general  carcinosis.  In  three  instances 
I  saw  numerous  secondary  cancerous  nodules  in  the  liver.  At  the  autopsy 
of  one  of  my  cases  a  tough  blood  clot  was  found  which  had  been  lodged 
behind  the  stomach  and  correspondingly  presented  the  shape  of  a  half- 
filled  stomach.  The  blood  originated  from  the  malignant  pancreas,  upon 
the  posterior  wall  of  which  and  adjoining  the  blood  focus,  two  lacerations 
were  found,  more  than  3  cm.  in  length  and  running  a  zig-zag  course 
through  the  serosa  and  the  sub-serous  connective  tissue. 

At  least  briefly,  both  observations  of  carcinoma  of  the  pancreas  are  to 
be  mentioned  in  which  the  ductus  choledochus  remained  free. 

The  first  of  these  cases  occurred  in  a  cheese-maker,  aged  59,  who  was  repeatedly 
the  subject  of  trauma  of  the  abdomen.  Upon  muscular  exertion  the  patient  suf- 
fered from  pain  of  a  neuralgic  character  in  the  upper  abdominal  region,  deeply  local- 
ized between  the  pit  of  the  stomach  and  the  navel,  and  radiating  toward  the  back. 
For  four  months  he  had  severe  diarrhea,  and  there  was  great  emaciation  (loss  of 
13  kilograms).  Upon  the  5th  of  November,  1898,  there  was  no  fever,  no  jaundice, 
no  palpable  abdominal  tumor,  no  ascites.  Liver  enlarged  and  permeated  with 
nodules.  Gall-bladder  not  palpable.  Spleen  of  normal  size.  Except  in  the  inguinal 
region,  no  enlarged  glands.     No  edema.     Four  hemorrhagic  stools  daily. 

By  the  administration  of  two  test-meals  the  amount  of  free  HCl  in  the  gastric 
contents  was  proven.  The  stomach  was  not  dilated.  The  diarrhea  was  somewhat 
improved  (milk  diet).  No  butter  stools;  no  marked  alimentary  glycosuria.  Up  to 
the  time  of  death    (November   19th)    a  further  loss  in  weight  of  5  kilograms. 

Autojjsy :  Carcinoma  of  the  body  of  the  pancreas,  the  head  remaining  free.  Begin- 
ning rupture  into  the  stomach.     Hepatic  metastases. 

The  second  case  was  that  of  a  locksmith's  apprentice,  aged  18,  who,  after  quite 
prolonged  constipation,  was  attacked  toward  the  end  of  May,  1900,  by  celiac  neu- 
ralgia and  vomiting.  The  patient  observed  a  rapidly  growing  tumor  in  the  upper 
abdominal  region;  some  portions  of  the  feces  (after  purgatives)  were  said  to  be 
"  white  like  bacon."  Upon  the  7th  of  June,  the  patient  was  still  well  nourished  and 
without  jaundice.  There  was  no  fever,  no  edema.  Bilaterally  upon  the  neck  and 
also  in  the  right  axilla  small  coarse  lymph-glands  were  palpable.  A  little  to  the 
right  of  the  epigastrium,  between  the  median  line  and  the  arch  of  the  rib,  was  a 
prominence  about  8  cm.  in  diameter,  coarse,  globular,  but  nowhere  fluctuating,  and 
insensible  to  pressure.  The  tumor  was  deeply  adherent,  situated  in  front  of  the 
abdominal  aorta  behind  the  stomach,  readily  displaced  laterally,  and  also  somewhat 
movable  upon  change  of  position  and  with  inspiratory  excursions.  Liver  and  spleen 
not  enlarged.  The  colon  which,  on  account  of  inflation  with  gas,  could  be  readily 
seen  and  palpated,  surrounded  the  tumor  from  below,  and  in  front  the  stomach  ap- 
peared to  be  forced  upward.     The  latter  organ  was  not  dilated. 


OBSTRUCTIONS  OF  THE  COMMON   GALI^DUCT   BY  TUMORS       419 

Constipation  continues.  The  stools  are  stained  with  bile;  they  contain  numerous 
unchanged  muscular  fibers  and  starch  granules,  and  are  apparently  rich  also  in  fat, 
(Fat-splitting  not  investigated.)  The  urine  contains  no  indican.  The  gastric  con- 
tents (2  test-meals)  show  absence  of  free  HCl;  the  total  acidity  varies  between 
1.1  to  2.1  to  the  thousand  HCl.  As  the  filtered  gastric  contents  have  a  brownish 
appearance,  the  absence  of  free  acid  is  probably  due  only  to  regurgitated  bile.  De- 
cided alimentary  glycosuria  cannot  be  proven.  The  tumor  grows  rapidly.  On  account 
of  the  torturing  attacks  of  neuralgia  coeliaca,  and  at  the  urgent  entreaty  of  the 
patient,  exploratory  laparotomy  was  performed  (Prof.  Nicoladoni).  This  demon- 
strated that  the  duodenum  had  been  considerably  narrowed  by  the  tumor.  Death 
upon  June  28th. 

Autopsy:  The  tumor  to  the  left  reaches  to  the  duodeno- jejunal  flexure  which 
appears  to  be  forced  to  the  left  and  upward.  The  duodenum  also  appears  to  be 
displaced  to  the  right.  The  permeable  ductus  choledochus  runs  its  course  upon  the 
right  surface  of  the  tumor.  The  right  portion  of  the  pancreas  is  granular,  tough, 
and  shows  a  whitish  discoloration;  the  tumor  extends  across  this  portion  of  the 
head,  and  includes  a  portion  of  the  retained  tail  of  the  gland.  Two-thirds  of  the 
pancreas  has  been  oblitertlted  by  the  neoplasm,  the  duct  of  Wirsung  is  markedly 
dilated.     In  the  vena  lienalis  is  a  non-obstructing  thrombus  from  the  tumor. 

I  believe  it  is  not  too  much  to  declare  in  these  two  cases,  in  the  first 
on  account  of  the  typical  pains,  the  diarrhea  and  the  normal  gastric  func- 
tion, in  the  second  from  the  topical  relations  of  the  tumor  and  the  fact 
that  biliary  stasis  did  not  occur,  that  a  probable  diagnosis  is  possible. 
Furthermore,  in  both  cases  the  reason  for  the  absence  of  obstruction  of  the 
choledochus  is  quite  obvious;  the  carcinoma  did  not  develop  from  the  head 
of  the  pancreas.  No  explicit  and  unanimous  reports  are  found  in  litera- 
ture to  show  how  frequently  persistent  impermeability  of  the  duct  occurs 
in  cancer  of  the  pancreas  involving  the  body  of  the -gland,  but  the  most 
reliable  reports  are  furnished  by  Wyss. 

Similarly  as  in  the  vessels,  a  carcinoma  of  the  liver  may  directly  im- 
plicate the  biliary  passages,  forming  a  tumor  mass  extending  into  the  large 
biliary  passages  and  the  intrahepatic  ducts,  and  leading  to  occlusion  of 
the  same,  thence  to  biliary  stasis.  Benign  neoplasms  arising  from  the 
ductus  choledochus  and  the  hepatic  duct  were  early  mentioned  in  literature 
(the  reports  of  Courvoisier  are  not  complete,  Alexander  Benedictus,  1508, 
Marcellus  Donatus,  1588).  Valuable  descriptions  have  been  published 
since  1840  ( Durand-Fardel,  W.  Stokes,  van  der  Bye).  Among  the  forms 
described  were  "fibroids"  (Albers),  "fatty  tumors,"  i.e.,  presumably 
lipomatous  tumors  (Wardell,  Bouisson),  fibrosarcomata  (metastatic.  Schiip- 
pel),  adenomata,  myoadenomata  (Calzavara),  cystoadenomata  (Hippel). 
As  in  the  bile  organs  in  general,  here  also  carcinomata  are  far  the  most 
important  tumors,  and  the  ones  most  frequently  found.  In  a  number  of 
cases,  it  was  microscopically  proven  that  they  originated  in  the  glands 
of  the  bile  ducts.  The  large  bile  ducts,  particularly  the  central  portions, 
are  well  supplied  with  glands.  These  are  found  in  profusion  in  the 
hepatic  duct,  are  less  plentiful  in  the  upper  portion  of  the  ductus  chole- 


420  NEOPLASMS   OF  THE  LIVER  AND  BILIARY  PASSAGES 

dochiis,  and  in  its  lower  portion  least  numerous.  The  body  of  the  gland, 
constructed  of  acini,  lies  like  the  crown  of  a  stone  pine  in  the  connective 
tissue  walls  (Riess).  A  mucoid  secretion  is  ascribed  to  it,  but  it  is  still 
doubtful  whether  it  contains  true  mucin.  After  enlargement  of  the  gland 
vesicles,  perhaps  by  coalescence,  the  cylindrical  epithelium  proliferates 
markedly,  and  permeates  the  lumen  in  the  form  of  tubes.  Connected  with 
this  is  a  proliferation  into  the  stroma,  and  the  gland  vesicles  are  trans- 
foimcd  into  microscopically  small,  cancerous  nodules  (M.  Howald).  Usu- 
ally the  stroma  is  profuse,  and  the  cancer  shows  the  characteristics  of 
scirrhus  (Dieckmann).  In  rare  cases  the  conditions  are  those  of  colloid 
cancer.  The  neoplasm  first  filtrates  the  wall  of  the  biliary  passage  which 
it  narrows  and  later  occludes.  The  mucous  membrane  above  the  infiltrate 
may  for  a  long  time  remain  wholly  or  partially  intact.  The  neoplasm 
assumes  the  shape  either  of  a  ring  or  a  polypus;  occasionally  its  formation 
rosoiiil)lcs  that  of  villi.  Throughout  the  course  the  tumors  are  almost 
always  of  small  size.  Often  their  diameter  does  not  amount  to  more  than 
1  cm.,  and  in  length  they  are  comparatively  short;  some  appear  to  attack 
the  wall  only  to  an  extent  of  5  cm.  Nevertheless,  tumors  from  the  size 
of  a  walnut  to  that  of  a  fist  have  been  observed.  Their  concealed  position 
and  small  size  almost  invariably  make  palpation  of  tumors  of  the  chole- 
dochus  impossible.  In  accordance  with  the  well-known  laws  of  localiza- 
tion for  cancer  in  general,  carcinomata  of  the  bile  passages  are  found 
chiefly  in  the  most  narrowed  areas  of  the  canal  (at  the  mouth  of  the  com- 
mon bile  duct,  at  the  confluence  of  the  cystic  and  hepatic  duct,  at  the 
point  of  bifurcation  of  the  hepatic  duct).  At  the  autopsy  of  my  cases, 
7  times  a  tumor  was  found  in  the  vicinity  of  the  diverticulum  of  Vater, 
or,  at  least,  below  the  middle  of  the  course  of  the  common  duct,  which 
was  about  8  cm.  in  length;  in  3  cases  carcinoma  near  the  junction  of  the 
hepatic  duct  and  the  cystic,  and  once  only  in  the  hepatic  duct.  In  an- 
other case,  there  was  a  contact  carcinoma  of  the  ductus  choledochus  con- 
joined to  a  primary  tumor  of  the  gall-bladder,  in  another  a  projecting 
cancer  of  the  cardia  ventriculi  attached  to  the  gastrohepatic  ligament,  and 
another  of  the  common  bile  duct  and  cystic  duct.  In  passing  it  may  be 
ri^markcd  that  metastatic  cancerous  nodules  are  also  found  isolated  in  the 
ductus  choledochus.  Clinically  it  is  of  little  significance  whether  the  car- 
cinoma be  primary  or  secondary,  since  the  prognosis  of  a  cancer  of  the 
gall-bladder,  for  example,  one  which  by  proliferating  occludes  the  chole- 
dochus. is  in  any  case  still  more  serious  than  that  of  a  primary  tumor 
in  the  bile  duct.  The  exact  localization  of  the  origin  of  the  neoplasm,  as 
may  be  readily  understood,  sometimes  is  difficult.  In  two  of  the  seven 
cases  of  carcinoma  of  the  ductus  choledochus  which  have  been  referred 
to,  the  lowest  portion,  corresponding  to  the  diverticulum  of  Vater,  rup- 
tured into  the  duodenum;  in  one  there  was  simultaneous  proliferation  to 
the  pancreas.     Inversely,  primary  carcinoma  of  the  duodenum  may  not 


OBSTRUCTIONS   OF  THE  COMMON   GALL-DUCT   BY  TUMORS       421 

only  include  the  mouth  of  the  choledochus,  but,  invading  deeply,  may  also 
occlude  the  bile  duct.  The  ductus  choledochus,  below  the  insertion  of  the 
cystic  duct,  may  also  be  occluded  by  the  tumor  mass  which  burrows  through 
the  latter  to  the  gall-bladder,  where,  in  the  narrow  portion  which  is  imme- 
diately connected  with  the  cystic  duct,  it  may  be  of  very  small  size.  That 
the  neoplasms  actually  originate  in  these  small  masses  may  be  readily 
recognized  from  the  fact  that  the  secondary  growth  permeates  the  entire 
wall  of  the  gall-bladder  and  also  attacks  the  substance  of  the  liver  in  its 
immediate  vicinity.  I  have  never  seen  a  neoplasm  of  the  cystic  duct  which 
was  not  connected  with  carcinoma  of  the  gall-bladder  or  of  the  ductus 
choledochus  (hepaticus).  According  to  some  statistics  (Courvoisier),  in 
19  cases  of  cancer  of  the  choledochus  the  origin  of  the  neoplasm  was  9 
times  in  the  beginning  of  the  duct  near  the  junction  of  the  cystic  and 
hepatic  ducts,  3  times  in  the  middle,  7  times  in  the  pars  intestinalis,  that 
is,  in  the  ostium.  Carcrnomata  of  the  gall-ducts  are  evidently  rarer  than 
those  of  the  gall-bladder.  Among  the  causes  of  obstruction  of  the  chole- 
dochus by  tumors,  carcinoma  of  the  pancreas,  from  its  frequency,  can  alone 
be  considered.  Etiologically,  heredity  here  appears  to  play  no  role.  Of 
my  13  cases  7  were  males.  The  women  who  were  attacked  had  almost 
all  borne  children  (one  13  times).  A  predominant  implication  of  the 
male  sex  has  been  frequently  emphasized,  and  this  preponderance  perhaps 
had  too  much  weight  attached  to  it  in  comparison  with  the  previously 
mentioned  implication  in  cancer  of  the  gall-bladder,  in  which  disease 
females  unquestionably  show  by  far  the  greater  number  of  cases.  The 
importance  of  the  question  consists  in  the  intimate  relation  of  carcinoma 
of  the  gall-bladder  to  cholelithiasis.  In  opposition  to  the  views  of  Naunyn, 
Leichtenstern,  G.  Hoppe-Seyler  and  others,  this  etiologic  factor,  however, 
quite  apart  from  the  consideration  of  the  implication  of  either  sex,  does  not 
appear  to  occur  to  quite  the  same  extent  in  cancer  of  the  ductus  choledochus 
and  hepaticus  as  the  material  at  hand  seems  to  warrant  us  in  concluding. 
In  the  autopsy  reports  of  my  own  cases,  only  once  do  we  find  mention  of 
a  stone  in  the  biliary  passages  (gall-bladder)  and  once  in  the  intestines 
(appendix).  Positive  proof  of  cholelithiasis  could  be  determined  at  most 
in  only  three  of  the  histories  of  my  patients;  in  some  of  the  cases  in  prior 
and  more  recent  literature  the  stone  was  found  directly  in  the  region 
of  the  neoplasm,  that  is,  in  the  carcinomatous  structure.  Twice  in  my 
cases  abdominal  trauma  was  assumed  to  be  the  cause  of  the  disease. 
The  frequent  seat  of  carcinoma  of  the  choledochus  in  the  lowest  portion 
of  the  duct  appears  to  me  at  least  to  favor  the  view  that  deleterious  ac- 
tion of  the  intestinal  contents  may  be  a  cause.  In  regard  to  age,  only  one 
of  my  patients  was  under  50;  seven  were  past  60,  the  oldest  was  72. 
In  no  case  was  the  anatomical  extension  of  the  disease  limited  to  the 
biliary  organs.  Secondary  metastatic  carcinoma  was  found  five  times  in 
the  liver,  twice  in  the  lung,  twice  in  the  duodenum,  once  in  the  pancreas, 


422  NEOPLASMS   OF  THE   LIVER  AND  BILIARY   PASSAGES 

once  in  the  kidney,  once  in  the  uterus,  and  frequently  in  the  peritoneal 
glands.  In  regard  to  the  implication  of  the  proliferal  lymph-glands,  later 
reports  must  be  used  for  comparison.  In  opposition  to  the  general  view 
that  this  rarely  occurs  on  account  of  the  absolute  stasis  of  bile  and  the 
early  death  ( Leichtenstern  counts  it  among  the  greatest  exceptions!),  in 
my  experience  the  development  of  metastases  was  quite  invariable  and  pro- 
fuse. The  liver  was  always  enlarged  and  its  tissues  coarser;  well  developed 
biliary  cirrhosis  developed  in  3  cases.  The  portions  of  the  ductus  chole- 
dochus  and  ductus  hepaticus  above  the  obstruction  showed,  without  excep- 
tion, more  or  less  extreme  dilatation.  In  7  cases  the  gall-bladder  was 
markedly  distended  to  the  size  of  a  fist.  We  find  in  literature  some 
mention  of  biliary  passages  thus  dilated  from  which,  by  puncture,  almost 
a  liter  of  fluid  was  obtained.  In  cases  of  decided  enlargement  of  the 
gall-bladder,  the  tongue-like  elongation  of  the  liver,  corresponding  to 
the  gall-bladder  (Riedel's  lobe),  was  noted.  In  4  of  my  cases  dilatation 
of  the  gall-bladder  was  not  present,  yet  there  was  no  apparent  reason  for 
this  absence;  twice  in  the  autopsy  reports  the  gall-bladder  is  mentioned 
as  small  and  showing  a  simultaneous  long-existing  cholelithiasis  and  chole- 
cystitis. Cholangitis  (cholecystitis)  with  a  purulent  exudate  was  present 
in  4  cases;  traces  or  remains  of  inflammation  of  the  biliary  passages  were 
much  more  common.  Diffuse  purulent  cholangitis  of  the  finer  branches 
of  the  hepatic  duct  (Ely)  ^  have  not  seen.  A  few  isolated  cases  of  multiple 
abscess  of  the  liver  are  mentioned  in  literature  (van  Gieson).  The  adhe- 
sions (and  ulcerations)  observed  by  me  are  of  such  a  character  as  to  require 
no  detailed  description.  None  of  my  patients  succumbed  directly  to  per- 
foration, formation  of  fistula,  or  rupture  of  the  biliary  passages.  Dilata- 
tion of  the  pancreatic  duct  and  connective  tissue  proliferation  in  the  head 
of  the  pancreas  I  saw  repeatedly.  In  the  majority  of  cases  (even  without 
other  complications)  the  spleen  was  distinctly  enlarged.  Ascites  as  well 
as  anasarca  is  mentioned  expressly  six  times  in  the  autopsy  findings;  in 
reality  it  is  probably  more  frequent.  Hemorrhage  from  the  neoplasm  itself 
I  have  observed  only  once;  the  hemorrhagic  diathesis  is  mentioned  in  4 
cases.  Appendicitis  was  diagnosticated  in  one  case  and  the  abscess  was 
opened.  At  the  autopsy  the  necrosis  of  the  appendix  was  discovered  to 
be  due  to  a  gall-stone  (cholesterin).  In  3  cases  sepsis  of  the  oral  cavity 
(tonsillar  abscess,  parotitis)   was  a  sequel. 

Pr'unary  cancer  of  the  duodenum  is,  as  already  stated,  extremely  rare 
(we  are  here  only  interested  in  that  form  with  a  periampullar  seat;  the 
parnptjloric  form  (Nothnagel),  that  is,  cancer  situated  above  the  divertic- 
ulum of  Vater,  I  shall  not  describe  at  all).  The  former  may  develop  upon 
the  base  of  a  peptic  ulcer.  This  is  either  the  round  form  of  ulcer  about  the 
size  of  a  silver  quarter  of  a  dollar  with  medullary  infiltrated  borders  near 
the  mouth  of  the  ductus  choledochus,  or  the  same  base,  in  the  center  of 
which  a  polypus-like  protruding  portion  of  mucous  membrane  is  still  pre- 


OBSTRUCTIONS   OF  THE  COMMON   GALI^DUCT   BY  TUMORS       423 

served  which  carries  the  ostium  of  the  duct.  Such  carcinomatous  growths, 
naturally,  do  not  form  palpable  tumors.  The  constriction  of  the  ductus 
choledochus  and  Wirsung's  duct,  under  these  circumstances,  is  extreme. 
Extending  further,  the  tumor  mass  may  directly  occlude  the  ducts.  The 
choledochus  is  dilated  to  the  size  of  the  small  intestine,  the  hepatic  duct 
to  the  diameter  of  the  thumb,  and  the  gall-bladder  attains  the  size  of 
two  fists.  The  duct  of  Wirsung  is  similarly  dilated,  so  that  it  stands 
forth  prominently,  and  the  smaller  lobes  of  the  ducts  resemble  cysts.  In 
contrast  to  this  there  are  also  cauliflower-like  and  submucous  duodenal 
cancers,  which,  on  account  of  their  size,  may  be  palpated  during  the  life 
of  the  patient.  These  latter  tumors  are  prone  to  necrosis  and  hemorrhage. 
As  long  as  the  growth  does  not  rupture,  there  is  occlusion  of  the  ostia; 
later,  the  bile  and  pancreatic  juice  may  find  an  outlet.  The  mouth  of 
Wirsung's  duct  is  dilated  and  surrounded  by  shreddy,  secondary  growths; 
the  same  is  true  of  the  nTbuth  .of  the  common  bile  duct.  The  biliary  pas- 
sages and  the  pancreatic  duct  appear  to  be  only  moderately  dilated.  The 
mesocolon  is  drawn  toward  the  growths,  the  intestinal  wall  is  perforated. 
The  head  of  the  pancreas  is,  as  a  rule,  inseparably  attached  to  the  base 
of  the  growth. 

A  case  of  cicatricial  duodenal  stenosis  which  I  have  observed  is  as 
follows : 

A  day  laborer,  aged  40,  who,  since  his  20th  year,  had  suflFered  from  digestive 
difficulty  and  vomiting.  In  October,  1896,  he  was  suddenly  seized  with  chills  and 
spasmodic  pains  in  the  right  hypochondrium,  and  immediately  after  there  was  a 
yellow  discoloration  of  the  skin  as  well  as  a  brown  color  of  the  urine.  After  a  brief 
period  the  jaundice  cleared  up.  Two  months  later  he  had  another  attack,  and  at 
the  end  of  December  a  third  and  severe  attack  lasting  10  days.  Since  the  2d  of 
February,  1897,  his  condition  has  been  stationary.  He  now  has  pain  in  the  right 
hypochondrium;  the  feces  show  no  bile.  Occasionally  there  is  vomiting.  Fever  (up 
to  102.2°  F. )  until  the  12th  of  February;  later  it  disappeared  entirely.  Marked 
emaciation.  Extreme  jaundice.  No  edema;  abdomen  occasionally  shows  meteorism. 
No  collateral  circulation.  Ascites  absent  during  the  entire  course.  Liver  is  indu- 
rated, border  readily  palpated,  surface  smooth.  Gall-bladder  not  palpable.  Feces 
show  no  bile  and  are  rich  in  fat.  Urine  contains  profuse  amounts  of  bile.  Attacks 
of  pain  constantly  recur. 

March  10th,  epistaxis.  March  14th,  right-sided  pneumonia.  March  17th,  vomit- 
ing of  brownish -black  masses;   sub-normal  temperature.     March  23rd,  death. 

Autopsy:  Stenosis  cicatricosa  duodeni  cum  occlusione  ostiorum  d.  choledochi  et 
Wirsungiani  accidente  cholestasi  et  ictero.  Perforatio  vesicae  felleae  supra  hepar. 
Abscess,  chron.  choliferus.     Dilatatio  et  hypertrophia  ventriculi.     Peritonitis  diflFusa. 

The  stricture  had  established  itself  at  the  site  of  an  old  fistula  from  gall-stones. 
Stones  were  still  present  in  the  common  bile  duct.  This  case  illustrates  drastically 
the  natural  cure  of  incarceration  from  stone. 


424  NEOPLASMS   OF  THE   LIVER   AND   BILIARY  PASSAGES 

DIAGNOSIS;   DIFFERENTIAL   DIAGNOSIS 

After  having  studied  the  special  pathology  of  circumscribed  adhesive 
perihepatitis  in  the  porta  hepatis,  and  the  affections  of  the  periportal 
h'niph-glands,  carcinomata  of  the  head  of  the  pancreas,  primary  and 
secondary  tumors  of  the  biliary  passages,  as  well  as  cancer  of  the  duo- 
denum, we  shall  now  turn  to  the  differential  diagnosis;  first,  of  occlu- 
sion of  the  ductus  choledochus  due  to  stone  and  to  tumor  (of  the 
biliary  passages  themselves  and  of  the  neighboring  organs).  In  enumer- 
ating and  describing  the  individual  diagnostic  factors,  I  shall  utilize  the 
most  recent  literature  of  the  subject  (the  earlier  literature  is  of  little 
value),  and,  on  account  of  numerous  contradictions,  I  shall  base  these 
remarks  upon  my  own  experience.  A  special  classification  of  the  differ- 
eiiiial  symptoms  is  hardly  possible,  nor  is  it  necessary;  the  simplest 
division  appears  to  me  to  be  indicated  by  the  method  of  clinical  ex- 
amination. On  account  of  the  rarity  of  obstruction  of  the  choledochus, 
not  only  the  usual  diagnostic  factors  must  be  considered,  but  the  ex- 
ceptions also  must  be  carefully  noted;  we  must  guard  against  schematic 
force ! 

Let  us  begin  with  the  history.  In  the  diagnosis  of  cancer  of  the 
choledochus,  Leichtenstern  lays  special  stress  upon  the  fact  that  the  affec- 
tion is  prone  to  occur  in  women.  This  coincides  with  the  reports  of 
numerous  authors,  but  even  Courvoisier  has  disproven  it.  My  own  experi- 
ences (see  above)  also  conflict  with  this  statement.  Cancer  of  the  pancreas 
probably  attacks  men  more  frequently  than  women.  Bohnstedt  maintains 
that  while  those  persons  affected  by  incarcerated  stones  usually  attribute 
their  malady  to  a  definite  trauma  which  they  have  sustained,  patients  with 
cancer  report  nothing  of  the  kind.  This  does  not  coincide  with  my  ex- 
perience. The  majority  of  my  patients  with  obstruction  due  to  tumor  have 
attributed  the  sudden  appearance  of  the  affection  to  some  error  in  diet,  a 
trauma,  or  something  similar.  Courvoisier  has  proposed  a  diagnostic  law: 
Preceding  colic,  particularly  if  combined  with  jaundice,  is  sufficient  evi- 
dence for  assuming  an  occlusion  of  the  ductus  choledochus  due  to  stone. 
The  repeated  and  frequent  appearance  for  years  of  one,  usually  brief, 
atlmk  of  jaundice,  especially  if  it  be  accompanied  by  colic,  or  have  pre- 
ceded colic  by  a  short  time,  is  one  of  the  most  infallible  signs  of  chole- 
lithiasis. The  previous  passage  of  small  stones  occurs  only  in  occlusion 
duo  lo  calculi.  Colic  was  a  symptom  in  80  cases  of  stone  in  the  common 
duct,  and  in  51  of  the  cases  collected  by  Courvoisier;  in  26  cases  of  pre- 
ceding, repeated,  brief  attacks  of  jaundice,  colic  was  noted  22  times;  in 
74  cases  of  obstruction  of  the  choledochus  due  to  other  causes,  colic  was 
rejiorted  only  4  times  (in  two  of  these  last  mentioned  cases  the  previous 
passage  of  calculi  must  be  considered).  Naunyn  also  declares  it  to  be 
the  rule  that  incarceration  of  stone  is  preceded  by  many  attacks  of  colic. 


OBSTRUCTIONS  OF  THE  COMMON  GALL-DUCT  BY  TUMORS       426 

According  to  my  observation,  typical  chronic  occlusion  of  the  choledochus 
due  to  stone  certainly  develops  after  prolonged  gastric  difficulty  (epigastric 
pressure,  spasm  of  the  stomach)  sometimes  lasting  for  years;  attacks  of 
pain  without  jaundice  first  occur,  then  well-developed  colic  with  fever  and 
violent  vomiting,  but  still  without  jaundice.  This  is  then  followed  by 
jaundice,  the  intensity  of  which  varies  decidedly,  and  which,  after  a  longer 
or  shorter  period,  may  show  complete  intermissions.  Chronic  gall-stone 
jaundice,  therefore,  originates  in  an  attack  of  colic.  Colic  recurs,  but, 
with  every  attack,  it  becomes  less  severe,  the  pains  decrease,  and  only 
chills  and  jaundice,  or  the  latter  alone,  remain.  Many  patients  declare 
that  with  the  appearance  of  well-developed  chills  and  of  permanent  jaun- 
dice the  character  of  the  pain  changes.  Exceptionally,  however,  the  pain 
and  the  other  signs  of  an  attack  of  cholelithiasis  in  occlusion  due  to  stone 
may  be  entirely  absent  (in  Courvoisier's  cases  their  absence  is  expressly 
mentioned  10  times),  and  ^'aundice  may  appear  without  any  indication  of 
colic.  Various  subjective  symptoms  may  then  have  preceded,  but  this  is 
not  necessarily  so.  I  saw  a  case  (confirmed  by  autopsy,  which  will  be 
again  mentioned)  in  which  the  patient  (Rvi.),  without  prodromes,  some 
time  prior  to  his  admission  to  the  hospital,  and  in  consequence  of  an  error 
in  diet,  was  attacked  with  vomiting,  diarrhea  and  chills;  this  was  followed 
in  four  days  by  moderate  sensitiveness  to  pressure  in  the  right  hypo- 
chondrium  and  permanent  jaundice.  If  we  ask  whether  pain,  and  of  what 
nature,  usually  accompanies  the  development  of  tumors  leading  to  occlu- 
sion of  the  common  gall-duct,  Leichtenstern  maintains  that,  as  a  rule, 
especially  in  cancer  of  the  biliary  passages,  cholelithiasis  (colic),  which 
may,  perhaps,  have  preceded  for  years,  is  a  factor.  This  does  not  agree 
with  the  experience  of  other  authors  nor  with  my  own.  Undoubtedly  there 
are  cases  of  obstruction  due  to  tumor  in  whose  history,  even  during  the 
entire  course  of  the  affection,  pain  was  scarcely  ever,  if  at  all,  present; 
that  is,  there  was  at  most  only  tenderness  on  pressure  in  the  gastrohepatic 
region.  In  my  cases  the  absence  of  pain  or  attacks  of  pain  only  prior  to 
the  appearance  of  jaundice  is  mentioned  in  8  cases;  in  the  remaining 
course  of  the  disease  in  5  cases.  Among  these,  unquestionably,  there  must 
have  been  cases  of  primary  neoplasm  of  the  ductus  choledochus.  Among 
my  24  cases  cholecystolithiasis  is  proven  by  autopsy  five  times,  and  by 
typical  attacks  of  colic  (exclusive  of  actual  tumors  in  the  biliary  passages) 
three  times.  Therefore,  pain  of  a  varying  character  is  generally,  as  I 
believe,  much  more  frequent  than  its  entire  absence,  particularly  at  the 
height  of  the  disease.  If  Kehr  maintains  that,  in  occlusion  of  tumors, 
colic  is  rare,  much  depends  upon  what  is  included  under  the  term  "  colic." 
The  intensity  of  these  subjective  difficulties,  before  and  during  the  perma-* 
nent  jaundice,  naturally  varies  greatly,  and  shows  all  the  degrees  between 
an  indefinite,  disagreeable  sensation  of  pressure  in  the  gastrohepatic  re- 
gion, and  boring,  lancinating  and  spasmodic  pains  of  intolerable  severity 


4'2G  NEOPL.'VSMS   OF  THE  LIVER   AND  BILIARY   PASSAGES 

which  rob  the  patient  of  his  sleep,  make  every  position  he  may  assume 
unbearable,  compel  him  to  cry  aloud  and  to  long  for  operative  relief,  etc. 
There  are  cases  in  which  continuous  pain  predominates;  in  many  others 
exacerbations  are  conspicuous,  the  pain  comes  in  paroxysms,  and  the  at- 
tacks are  of  varying  duration.  Not  infrequently  nausea  is  combined  with 
the  pain.  An  error  in  diet  may  produce  the  first,  which  is  then  followed 
by  jaundice,  and  gastric  difficulties  not  rarely  introduce  the  series  of  symp- 
toms ;  subsequently  the  paroxysms  may  follow  meals.  Vomiting  (vomiting 
of  bile)  is  mostly  absent,  that  is,  such  as  would  correspond  to  typical 
gall-stone  colic  at  the  height  of  the  attack.  Severe,  frequent  vomiting, 
often  bilious  in  character,  which  persists  for  long  periods  during  the 
course,  is  invariably  found  in  duodenal  and  also  in  pancreatic  cancer  when 
stenosis  of  the  duodenum  takes  place.  The  deep-seated,  neuralgic  pain, 
chiefly  localized  in  the  region  between  the  pit  of  the  stomach  and  the  navel, 
radiating  toward  the  bach,  and  usually  referred  to  the  solar  plexus,  is  an 
important  diagnostic  factor  only  in  certain  cases  (compare  the  history  of 
the  two  cases  quoted  above).  The  pains  arising  from  the  biliary  passages 
themselves  also  usually  radiate  to  the  gastric  region,  to  the  back,  and  espe- 
cially to  the  shoulder.  I  am  inclined  to  attach  especial  value  to  this 
shoulder  pain  in  the  diagnosis  of  affections  in  the  region  of  the  biliary 
passages,  but  I  have  never  succeeded  in  making  a  positive  differentiation 
between  occlusion  of  the  choledochus  by  a  neoplasm  of  this  duct  or  by  a 
pancreatic  cancer  from  this  sign  alone.  I  attach  a  certain  significance  to 
the  circumstance  that,  in  cancer  of  the  duodenum,  the  pains  increase  after 
the  ingestion  of  food.  But  this  is  a  differentio-diagnostic  factor  of  but 
relative  importance,  in  that  pains  in  obstruction  due  to  tumors  of  the 
ductus  choledochus  only  exceptionally  correspond  to  typical  colic  (pains 
and  vomiting)  of  gall-stone  (in  which,  of  course,  I  leave  entirely  out  of 
consideration  secondary  carcinoma  of  the  ductus  choledochus  in  primary 
cancer  of  the  gall-bladder). 

In  the  diagnosis  of  cholelithiasis,  Neusser  and  Ortner  attach  great  im- 
portance to  the  jaundice  which  in  a  brief  time  becomes  marked,  that  is, 
soon  reaches  its  maximum.  A  villous  cancer  growing  rapidly  may  also 
in  a  short  time  give  rise  to  extreme  icterus.  In  carcinoma  of  the  duo- 
denum, the  appearance  of  jaundice  is  said  to  be  much  more  gradual. 
In  a  scries  of  cases  of  carcinomata  of  the  pancreas  Leichtenstern  found 
that  icterus  appeared  in  an  acute  form  and  in  a  few  days  reached  its 
maximum.  I  attach  but  little  weight  to  the  statements  of  the  patient, 
wliich  are  often  quite  vague,  as  to  the  manner  in  which  the  permanent 
jaundice  appeared.  I  know  of  undoubted  cases  of  incarceration  of  stones 
in  which  jaundice  developed  gradually;  this  seems  most  apt  to  occur  in 
cases  in  which  the  stone  is  partly  in  the  cystic  duct,  and  partly  in  the 
common  duct.  Among  my  own  eases  of  obstruction  due  to  tumor, 
5    times   the   history   showed   that   jaundice   had   appeared   "suddenly," 


OBSTRUCTIONS  OF  THE  COMMON  GALI^DUCT  BY  TUMORS      427 

in   a   few  hours  or  in  a   night,   and   this   was   also   true   in   cancer   of 
the  pancreas. 

Another,  perhaps  significant,  diagnostic  difference  between  the  develop- 
ment of  permanent  jaundice  from  obstruction  due  to  calculi  contrasted 
with  occlusion  from  tumor  is  the  timely  extension  of  the  same.  This 
factor  is  naturally  considered  with  the  history,  and  in  the  further  observa- 
tion of  the  case.  Here  again  Courvoisier  was  foremost  with  the  definite 
statement  that  permanent  jaundice  lasting  several  years  generally  indi- 
cated stone  and  excluded  any  other  form  of  obstruction.  He  mentions 
cases  of  obstruction  due  to  stone  lasting  2  to  5  years,  and  even  longer. 
Kehr  operated  upon  and  cured  a  patient  who,  for  12  years,  suffered  from 
the  symptoms  of  occlusion  by  stone.  Schiippel,  as  well  as  Neusser  and 
Ortner,  on  the  other  hand,  exclude  cancer  in  general  (except,  possibly, 
primary  carcinoma  of  the  gall-bladder)  if  the  jaundice  persists  longer  than 
6  months.  This  latter  pemd,  however,  appears  to  me  to  be  entirely  too 
limited.  In  my  cases  of  primary  cancer  of  the  biliary  passages,  the  total 
duration  of  the  course  from  the  onset  of  chronic  jaundice  up  to  the  time 
of  death  was  7  to  9  months ;  in  one  case  only  was  it  less  than  6  months ;  in 
my  cases  of  cancer  of  the  pancreas,  3  lasted  less  than  6  months,  and  in  all 
the  others  the  duration  was  8  to  11  months;  in  duodenal  cancer  the  course 
was  somewhat  longer  than  6  mouths.  Perhaps  the  average  duration  in 
cancer  of  the  head  of  the  pancreas  is  slightly  less  than  in  cancer  of  the 
choledochus.  With  Naunyn  and  others,  I  think  it  wiser  to  estimate  the 
duration  of  jaundice  which  excludes  cancer  at  about  one  year.  In  prac- 
tice, however,  there  is  no  absolute,  precise  law.  For,  in  occlusion  due  to 
stone,  death  may  occur  also  after  a  brief  duration  of  the  jaundice,  often 
a  few  months,  often  only  weeks  or  days !  In  most  of  the  known  cases, 
death  was  preceded  by  symptoms  of  hepatic  autointoxication  from  the  6th 
to  the  12th  month;  therefore,  chronic  gall-stone  jaundice  rarely  lasts 
longer  than  one  year.  The  reason  why  occlusion  of  the  coinmon  duct 
by  a  tumor  produces  jaundice  which  lasts  such  a  short  time  is,  accord- 
ing to  Courvoisier,  simply  this, — that  here  the  underlying  disease  in  some 
other  manner  early  causes  death.  But  I  do  not  believe  this.  I  am  inclined 
to  agree  with  Kehr,  and  admit  a  chronic  closure  of  the  common  duct  by 
stone  in  the  supraduodenal  portion,  and  one  due  to  calculus  in  the  vicinity 
of  the  duodenal  papilla.  In  the  latter  case,  and  under  severe  circumstances, 
the  jaundice  is  at  once  intense,  and  varies  but  little  from  that  observed 
in  most  obstructions  due  to  carcinoma.  In  these  later  cases,  however, 
provided  a  choledocho-duodenal  fistula  does  not  bring  relief,  or  if  a  chole- 
dochotomy  is  not  performed,  a  fatal  termination  is  just  as  certain  and  as 
rapid  as  in  carcinoma  of  the  common  duct  and  pancreas,  and  with  the 
same  symptoms  of  severe  inanition  and  hepatargy.  In.no  less  than  14 
of  my  own  cases,  without  regard  to  the  focus  for  the  development  of  the 
cancer,  this  was  absolutely  demonstrated  (often  by  prolonged  coma  with 


428  NEOPLASMS   OF  THE   LIVER  AND  BILIARY   PASSAGES 

or  without  the  liemorrhagic  diathesis).  Among  auxiliary  causes  of  death 
suppuration  was  found  in  four  cases,  an  old  syphilis  in  one,  portal  vein 
stasis  in  another,  and  in  a  few,  metastases. 

Jaundice,  as  a  cardinal  symptom,  occupies  a  leading  position  in  the 
status  and  course  of  the  clinical  history.  It  may  be  assumed  from  the 
onset  that  a  stone  with  its  changeable  form,  or  even  a  great  number  of 
stones,  will  not  completely  occlude  the  lumen  of  the  bile  ducts,  as  would, 
for  instance,  be  the  case  with  a  soft  tumor  which  perfectly  adjusts  itself 
to  the  lumen  and  the  wall  of  the  canal,  and  entirely  occludes  the  former. 
Even  Cruveilhier  attempts  to  base  this  theory  of  constriction,  a  priori, 
upon  the  comparison  of  the  pathologico-anatomical  changes  which  occur 
in  incarceration  from  stone.  Behind  the  stone  arrested  in  the  common  bile 
duct  stasis  of  bile  occurs,  whereupon  the  passage  dilates,  the  lumen  in- 
creases to  the  circumference  of  a  finger,  or  even  that  of  the  small  intestine. 
Then  the  bile  rises  to  the  stone,  floats  in  the  dilated  common  duct,  and 
passes  it.  The  jaundice  may  then  entirely  disappear.  But  the  stone 
invariably  floats  along  to  lower  parts  of  the  gall-duct  toward  the  intestine. 
Clinical  experience  confirms  the  opinion  that  in  chronic  occlusion  of  the 
common  bile  duct  by  stone,  a  decided  variation  in  the  intensity  of  the 
jaundice,  even  its  complete  disappearance,  is  very  characteristic.  Under 
these  circumstances  the  urine  likewise  shows  variations  in  color  between 
dark  and  light,  and  only  in  rare  cases  are  the  feces  permanently  free  from 
bile.  Tn  cases  of  obstruction  due  to  tumor,  the  jaundice  is  usually  intense, 
and  does  not  vary  so  manifestly.  The  feces  are  persistently  acholic.  In 
contrast  to  the  usual  conditions,  however,  we  must  bear  in  mind  that  also 
in  incarceration  from  stone  (in  the  papilla  of  the  duodenum)  the  complete 
exclusion  of  bile  from  the  intestine,  with  all  its  serious  consequences 
(hepatic  intoxication,  the  hemorrhagic  diathesis,  and  death  in  from  6  to 
12  months)  is  quite  possible,  and  this  may  occasionally  occur  even  when 
permanent  jaundice  has  been  the  first  alarming  symptom  of  a  cholelithiasis 
previously  latent.  An  example  of  this  kind  is  my  case  before  referred  to 
(Ku.).  Here  for  a  short  time  only  the  jaundice  was  moderate,  the  feces 
slightly  tinged  with  bile,  but  the  symptoms  rapidly  became  more  intense, 
and  the  feces  subsequently  and  during  the  7  months  of  the  protracted 
course  of  the  disease  were  absolutely  acholic;  the  course  was  that  severe 
form  just  indicated.  Moreover,  in  my  experience  it  is  the  rule  that  also 
in  cases  of  obstruction  due  to  tumor,  variations  in  the  intensity  of  the 
jaundice  are  quite  manifest,  but  they  are  never  very  decided  ones.  Par- 
ticularly at  the  onset  of  the  affection,  paroxysmal  aggravation  of  all  the 
subjective  symptoms,  produced  by  a  still  more  marked  impediment  to 
the  flow  of  bile,  brings  about  a  renewed  staining  of  the  visible  mem- 
branes. Haarmann  believed  that  a  complete  but  temporary  disappearance 
of  jaundice  in  obstruction  from  tumor  could  be  explained  by  the  destruc- 
tion, and  its  recurrence  by  the  renewed  proliferation,  of  a  soft  tumor 


OBSTRUCTIONS   OF  THE  COMMON    GALL-DUCT   BY  TUMORS       429 

which  in  his  case  was  situated  at  the  ostium.  Courvoisier  admits  the 
probability  of  similar  conditions  from  analogous  observations  by  Bour- 
ceret  and  Bradbury,  Neusser  and  Ortner  designate  as  a  decisive  factor 
in  the  diagnosis  of  carcinoma  of  the  common  bile  duct  the  circumstance 
that,  in  the  course  of  a  jaundice  which  has  developed  to  its  maximum 
intensity  combined  with  acholia  of  the  feces  (usually  after  a  duration  of 
from  2  to  3  weeks)  a  full,  even  abnormally  profuse,  biliary  staining  of 
the  feces  may  again  occur;  this  may  happen  once  or  repeatedly,  suddenly 
or  at  least  rapidly,  occasionally  with  fulminant  symptoms;  there  may  be 
a  slight  admixture  of  blood  to  the  dejecta  or  to  the  vomitus;  in  a  brief 
time,  the  condition  gives  place  to  a  new  period  of  acholia.  I  have  reason 
to  believe  that  instances  of  this  kind  frequently  occur.  In  one  of  my  own 
cases  of  primary  cancer  of  the  choledochus  (at  the  onset  of  permanent 
jaundice)  the  previously  intensely  yellow  discoloration  of  the  skin  decidedly 
diminished,  and  the  white, "clay-l ike  stools  again  became  tinged  with  bile; 
this  change  lasted  for  only  8  days,  and  was  followed  by  an  aggravation 
and  permanent  acholia  which  was  unyielding.  Hemorrhages  from  cancer 
of  the  common  bile  duct,  even  to  a  marked  extent  (black  feces),  are  not 
uncommon.  One  of  my  cases  of  cancer  of  the  duodenum  also  exhibited 
the  condition  described  by  Neusser,  and  an  anatomical  preparation  satis- 
factorily explained  it  as  due  to  decided  ulceration.  Naunyn  also  mentions 
a  case  of  Coupland's  of  neoplasm  in  the  duodenal  wall  at  the  diverticulum 
of  Vater,  in  which  a  disappearance  of  the  jaundice,  biliary  staining  of  the 
feces,  and  a  simultaneous  decrease  in  the  size  of  the  distended  gall-bladder 
could  be  repeatedly  recognized.  In  two  of  my  cases  of  occlusion  of  the 
choledochus  from  tumor  of  the  pancreas,  besides  a  manifest  and  very  vary- 
ing jaundice  of  the  skin,  there  was  long-continued  diarrhea,  and  feces 
containing  bile,  some  showing  deficiency  of  bile,  and  completely  acholic 
stools  alternated.  Finally,  cases  of  obstruction  from  tumor  exist  (two 
among  my  own)  in  which  the  feces  up  to  the  time  of  death  show  only  a 
feebly  feculent  character.  Somewhat  diiferent  from  the  variations  in  the 
intensity  of  the  jaundice  in  incarceration  from  stone  and  occlusion  from 
tumor,  which  have  been  described,  is  a  clearing  of  the  skin  and  urine  after 
a  long  continuance  of  the  jaundice  without  the  feces  losing  their  clay 
color.  The  significance  of  this  prognostically  unfavorable  sign  is  evident 
from  the  foregoing  descriptions. 

In  the  opinion  of  different  investigators  the  diagnostic  importance  of 
fever  varies.  By  many  the  presence  of  fever  preceding  and  during  the 
permanent  jaundice,  and  especially  the  repeated  occurrence  of  chills  at 
regular  or  atypical  periods,  combined  with  attacks  of  pain,  with  sudden 
rises  of  temperature,  and,  later,  also  the  remittent  or  continuous  rises  of 
temperature  in  chronic  obstructive  jaundice  are  referred  either  to  gall- 
stones, that  is,  to  suppuration,  to  ulceration,  etc.,  in  the  biliary  passages 
(the  liver)   or  to  a  superadded  pyemia.     Courvoisier  reports  that  in  80 


430  NEOPLASMS   OF  THE   LIVER   AND  BILIARY   PASSAGES 

cases  of  occlusion  by  stone  19  (therefore  about  ^),  and  of  74  obstructions 
due  to  other  causes  7  (about  ^),  were  accompanied  by  fever.  I  must 
emphasize  here  that  I  also  know  of  cases  of  impacted  stone  which,  in  certain 
j)hases  of  the  ajffection,  showed  jaundice  only  some  time  after  the  attacks 
of  fever  (previously  frequent)  had  ceased  entirely,  Leichtenstern  main- 
tains that  as  soon  as  cancer  of  the  gall-bladder  or  of  the  biliary  passages 
appears  the  preceding  inflammatory  phenomena  due  to  gall-stones  cease 
entirely.  High  fever  or  chills  are  said  categorically  to  contraindicate  the 
presence  of  cancer  although  numerous  other  symptoms  may  be  present 
which  favor  it.  According  to  Kehr,  in  occlusion  by  tumor  fever  occurs 
in  exceptional  cases,  particularly  in  the  last  stages  of  carcinoma.  In  the 
case  of  scirrhus  of  the  pancreas  this  author  has  observed  multiple  abscesses 
in  the  liver  and  perihepatic  suppuration.  Naunyn  emphasizes  the  fact 
that  fever  combined  with  chills  is  observed  with  especial  frequency  in 
neoplasms  of  the  liver  (even  those  due  to  metastases).  In  15  of  my  cases 
of  occlusion  due  to  carcinoma,  there  was  fever  lasting  a  long  or  short  time. 
Only  5  times,  either  clinically  or  at  the  autopsy,  was  it  possible  to  attribute 
it  to  a  complication  outside  of  the  biliary  passages  themselves  (parotitis, 
tonsillar  abscess  and  pyemia,  cystopyelitis,  suppuration  of  the  glands  of 
the  neck,  gall-stone  appendicitis).  Fever,  with  either  a  moderate,  inter- 
mittent or  remittent  course  or  (not  so  frequently)  with  decided  rises  in 
temperature  to  101,3°  F.  and  103.1°  F.,  was  present.  In  the  late  stages 
of  the  disease  (leaving  out  of  consideration  the  closing  days  of  life,  when 
lobular  pneumonias,  etc.,  developed)  the  fever  usually  but  not  invariably 
l)ecame  more  marked.  Periodically  recurring  or  even  isolated  chills  I  have 
never  observed  (except  in  a  case  of  lithogenous  cancer  of  the  gall-bladder 
which  proliferated  into  the  biliary  passages),  I  am  unable  to  decide  whether 
fever  is  more  frequent  in  that  form  in  which  there  is  proliferation  into 
the  duodenum  leading  to  destruction,  which  is  particularly  the  case  in 
carcinoma  of  the  head  of  the  pancreas,  or  in  primary  cancer  of  the  biliary 
passages.  As  will  be  observed,  I  can  take  only  a  middle  position  in  regard 
to  tlio  differentio-diagnostic  value  of  fever;  all  the  more  so  since,  in 
literature,  I  note  that  chills  also  occur  in  occlusion  due  to  carcinoma. 

The  degree  of  inanition  and  the  loss  of  weight  in  all  of  my  cases  of 
tuinor  obstruction  have  been  very  considerable;  cachexia  developed  with 
exceeding  rapidity.  I  have  not  observed  that  cachexia  praecox  is  peculiar 
to  cancer  of  the  pancreas ;  nor  have  I  noted  subnormal  temperature  in  such 
cases  (the  syndrome  of  Bard  and  Pic).  In  my  cases  the  N-excretion  in 
comparison  to  the  intake  was  not  determined.  In  doubtful  cases,  among 
otlier  signs,  light  was  occasionally  shed  on  the  diagnosis  by  the  estimation 
of  N  and  NaCl  in  the  urine  (diminished  excretion  of  chlorin  in  cancer). 
1  liave  no  personal  experience  of  the  proportions  of  N  and  PoO^  in  the 
excretion  of  persons  suffering  from  obstruction  of  the  choledochus  by 
tumor,  nor  in  regard  to  the  increase  of  ammonia  and  the  separation  of 


OBSTRUCTIONS  OF  THE  COMMON   GALI^DUCT   BY  TUMORS       431 

the  total  nitrogen  into  the  various  N-containing  products  of  the  urine. 
In  all  of  my  cases  of  obstruction  by  tumor  in  which  an  examination  was 
made,  deviations  from  the  normal  blood  were  noted,  although  not  very 
decided:  decrease  of  hemoglobin  to  75-65  per  cent,  (Fleischl),  decrease 
of  the  red  blood-corpuscles  to  5,800,000,  4,100,000,  or  3,900,000;  the  num- 
ber of  white  corpuscles  (not  directly  due  to  the  fever)  varied  between 
5,800  and  16,400.  In  one  case  (carcinoma  of  the  pancreas  with  enteritis 
and  fever)  very  decided  oxyphilia  of  the  blood  was  observed.  Finally,  we 
should  be  most  cautious  in  drawing  far-reaching  differentio-diagnostic 
conclusions  from  the  miserable  appearance  of  the  patient  and  his  loss 
of  weight ! 

In  discussing  biliary  stasis  due  to  obstruction  of  the  choledochus  I  have 
not  minutely  considered  the  dilatation  of  the  biliary  canal.  In  the  first 
place,  experience  shows  that  dilatation  occurs  in  the  common  and  hepatic 
ducts.  Particularly  in  casQg  of  closure  near  the  opening  of  the  ducts  into 
the  intestine  do  dilatation  and  elongation  occur,  and  these  ducts  may 
enlarge  to  the  size  of  a  thumb  or  a  coil  of  the  small  intestine.  The  com- 
mon duct  occasionally  forms  a  sort  of  cyst,  protruding  from  under  the 
liver,  containing  from  one  to  several  liters  of  bile,  and  has,  in  fact,  been 
confounded  with  the  gall-bladder  upon  which  operation  has  been  attempted. 
The  dilatation  of  the  final  branches  of  the  hepatic  duct  extends  usually 
to  the  periphery  of  the  liver,  and  may  produce  fluctuating  protuberances  on 
the  surface  of  this  organ,  or,  upon  a  uniform  dilatation  of  the  intrahepatic 
canals,  the  liver  in  toto  becomes  enlarged,  but,  as  a  rule,  it  shortly  after 
again  decreases  in  size.  In  chronic  obstruction  of  the  common  duct  dila- 
tation of  the  gall-bladder  and  of  the  cystic  duct  does  not  occur  with  the 
same  frequency.  As  we  were  inclined  to  believe  from  the  reports  mentioned 
in  text-books,  Courvoisier  found  the  tissue  changes  in  the  gall-bladder 
different  and  more  complicated.  Previously  it  was  the  general  opinion 
that  permanent  closure  of  the  choledochus  invariably  led  also  to  a  dilata- 
tion of  the  gall-bladder.  Courvoisier  found,  however,  that  among  109  fully 
described  cases  of  dilatation  of  the  gall-bladder,  17  only  were  due  to  occlu- 
sion by  stone;  all  other  obstructions  of  the  ductus  choledochus  were  due 
to  different  causes  (10  to  tumors  in  the  interior,  8  to  obliterations,  74  to 
external  compressions).  Furthermore,  the  dilatation  of  the  gall-bladder 
in  obstruction  from  stones  was  usually  of  only  moderate  extent,  and  in 
but  a  few  cases  was  the  organ  stated  to  be  enormously  enlarged.  On  the 
other  hand,  dilatation  due  to  other  causes  of  occlusion  was  often  very 
decided,  and  in  some  cases  colossal  tumors  were  formed.  In  contrast  to 
these  dilatations  are  78  cases  also  collected  by  Courvoisier,  in  which,  in 
spite  of  occlusion  of  the  common  duct  and  a  patulous  cystic  duct,  the 
gall-bladder  was  not  enlarged  but  atrophic.  Of  these,  70  (i.  e.,  90  per 
cent.)  were  cases  of  impaction  of  stone  in  the  common  duct,  8  only 
(i.  e.,  10  per  cent.)  were  due  to  other  causes  (in  5  of  the  last-mentioned 
29 


432  NEOPLASMS   OF  THE   LIVER  AND   BILIARY  PASSAGES 

cases  the  gall-bladder  also  contained  stones).  Courvoisier  separates  his 
187  cases  into  two  groups,  one  containing  87  cases  due  to  obstruction  from 
stone  and  100  from  other  causes  of  occlusion.  With  incarceration  of 
calculi,  atrophy  of  the  gall-bladder  occurred  in  80.4  per  cent.,  dilatation, 
which  was  found  in  19.6  per  cent,  of  the  cases,  being  much  rarer.  The 
other  causes  of  obstruction,  on  the  contrary,  much  less  often  ran  their 
course  with  atrophy  (8  per  cent.),  dilatation  being  much  more  frequently 
present  (92  per  cent.).  In  impaction  of  stone  in  the  common  duct,  there- 
fore, dilatation  of  the  gall-bladder  is  rare,  the  organ  being  previously 
contracted  by  connective  tissue  (chronic  cholecystitis,  atrophic  effect  of 
adhesion).  In  occlusion  of  the  cholcdochus  of  other  nature,  however, 
dilatation  is  the  usual  result.  Courvoisier  collected  35  cases  of  obstruction 
of  the  common  duct  in  which  operation  had  been  performed;  in  17  cases 
due  to  stone  4  only  showed  dilatation,  and  in  18  due  to  pressure  from 
tumor,  from  stricture,  etc.,  dilatation  was  found  in  16;  of  the  first  17 
there  were  13,  and  of  the  last-mentioned  18  only  2,  without  enlargement 
of  the  gall-bladder.  Of  the  20  cases  of  dilatation  of  the  gall-bladder, 
4  only  were  due  to  obstruction  by  stone,  16  being  from  other  causes. 
The  correctness  of  this  view  has  been  confirmed  in  a  large  number  of 
cases  by  subsequent  investigation.  Encklin  (1896),  in  a  total  of  172 
cases  of  occlusion  due  to  stone,  found  contracted  gall-bladder  present 
in  64  per  cent.;  in  19.7  per  cent,  the  organ  had  retained  its  normal  size, 
and  in  only  16.25  per  cent,  was  it  dilated.  On  the  contrary,  in  129  cases 
of  occlusion  from  other  causes  (stricture  of  the  cholcdochus,  compression 
of  the  duct  by  enlarged  lymph-glands,  tumors  of  the  common  duct  and  of 
the  pancreas)  the  gall-bladder  was  found  dilated  in  87  per  cent.,  and 
contracted  or  normal  in  only  6.5  per  cent.  Courvoisier  regarded  this 
incontestable  contraction  of  the  gall-bladder  from  the  presence  of  stone 
in  the  common  duct  a  particularly  valuable  point  of  support  in  the  differ- 
ential diagnosis.  Naunyn,  Kehr,  Langenbuch,  Bohnstedt,  and  others  con- 
curred with  him.  This  diagnostic  point  is  referred  to  (particularly  in 
French  literature)  as  Courvoisicr-Tcrrier's  symptom.  Terrier,  however, 
only  followed  Courvoisier's  teaching.  G.  Hoppe-Seyler  maintains  a  con- 
servative position.  Leichtenstern,  "  naturally,"  does  not  conform  to  the 
Courvoisier  rule  in  deciding  the  question  whether  occlusion  of  the  common 
(Uiet  due  to  stone  or  cancer  of  the  biliary  passages  is  present,  the  latter 
of  which  he  declares  to  be  lithogenous;  he  maintains  absolutely  that  in 
|)ritnary  carcinoma  of  the  cholcdochus  there  is  no  enlargement  of  the 
ual  I -bladder,  while,  in  contrast  to  this,  in  cancer  of  the  pancreas  a  well- 
lilled  gall-bladder  can  be  determined.  Neusser  and  Ortner  declare  in  the 
diagnosis  of  primary  cancer  of  the  ductus  cholcdochus  that  a  distinctly 
enlarged  gall-bladder  is  of  "  little  importance."  Quenu  also  maintains  that 
ilie  Courvoisier  system  is  not  absolutely  decisive,  and  reports  some  mistakes 
in  diai^nosis. 


I 


OBSTRUCTIONS  OF  THE  COMMON  GALI^t)UCT  BY  TUMORS      433 

I  have  already  briefly  alluded  to  the  results  obtained  in  my  autopsies. 
In  my  opinion,  in  a  diagnostic  respect  (I  am  considering  only  the  diag- 
nosis prior  to  operation),  and  without  weighing  the  autopsy  findings,  the 
question  is  as  follows :  Are  the  cases  with  a  non-palpable  gall-bladder  in 
obstruction  due  to  tumor,  and  the  cases  with  an  enlarged  palpable  gall- 
bladder in  occlusion  due  to  stone,  actually  so  rare  that  Courvoisier's  sign 
may  be  looked  upon  as  pathognomonic,  and  that,  in  each  individual  case, 
a  decision  may  be  made  from  this?  In  my  8  cases  of  primary  carcinoma 
of  the  choledochus,  during  the  entire  course  of  the  disease  the  gall-bladder 
was  4  times  non-palpable,  and  in  my  7  cases  of  cancer  of  the  head  of 
the  pancreas  with  occlusion  of  the  common  duct,  this  was  the  case  3  times. 
In  one  instance  of  primary  cancer  of  the  gall-bladder  with  subsequent 
cancer  of  the  choledochus,  the  gall-bladder  could  not  be  felt.  In  one  case 
of  duodenal  carcinoma  the  gall-bladder  was  visible,  in  the  second  case  it 
could  never  be  seen.  The  gall-bladder  was  observed  to  be  anatomically 
dilated  in  some  cases  in  which  the  enlargement  could  not  be  discerned 
clinically.  The  largest  tumor  of  the  gall-bladder  which  was  found  during 
life  in  my  cases  was  about  the  size  of  an  apple.  The  tumor  invariably 
had  the  characteristics  of  the  tumors  of  the  gall-bladder  which  have  been- 
described.  Fluctuation  at  the  top  of  the  tumor  was  never  absent.  In  two 
cases  with  particularly  well-developed  Kiedel's  lobes  it  was  readily  per- 
ceived that  a  neoplasm  had  formed  at  the  point  of  transition  into  the 
coarser  liver.  In  a  clinical  history  pain  upon  pressure  of  the  tumor  is 
sometimes  emphasized,  sometimes  absent.  The  growth  of  the  tumor  and 
its  variation  in  size  have  been  occasionally  mentioned.  In  4  positive  cases 
of  obstruction  due  to  stone  I  remember  that  the  gall-bladder  was  more  or 
less  enlarged  to  palpation.  In  one  of  these  cases,  we  were  able  during 
the  life  of  the  patient  to  determine  that  the  gall-bladder  was  not  absolutely 
smooth  and  freely  movable,  as  is  the  rule  in  occlusion  due  to  carcinoma. 
In  my  opinion,  in  cholelithiasis  much  depends  upon  how  and  when  the 
impaction  of  stone  takes  place.  In  a  case  repeatedly  mentioned  (Ru.), 
in  which  permanent  jaundice  was  the  first  alarming  symptom  of  chole- 
lithiasis, and  the  cystic  duct  was  not  obliterated,  the  gall-bladder  was  very 
markedly  dilated,  yet  no  stone  was  present  in  the  cystic  duct,  and,  there- 
fore, in  addition  to  the  obstruction  of  the  choledochus,  there  was  neither 
dropsy,  empyema  of  the  gall-bladder,  nor  obliteration  of  the  duct.  Cour- 
voisier  collected  13  cases  from  literature  in  which  the  last-named  accident 
supervened.  Kehr  also  calls  attention  to  the  diagnostic  difficulties  when 
we  have  a  combination  of  dropsy  or  purulent  cholecystitis  of  the  gall- 
bladder with  chronic  occlusion  of  the  choledochus.  He  operated  on  5 
cases  of  this  kind.  In  the  differential  diagnosis  between  occlusion  of  the 
choledochus  due  to  stone  and  to  tumor,  after  all  that  has  been  said,  and 
apart  from  the  fact  that  the  exceptions  also  must  be  considered  (on 
accoimt  of  the  rarity  of  the  cases)  no  actual  pathognomonic  importance 


434  NEOPLASMS   OF  THE   LIVER   AND  BILIARY   PASSAGES 

can  be  attributed  to  the  Courvoisier  symptom,  the  value  of  which,  I 
believe,  is  often  exaggerated. 

According  to  Naunyn,  there  is  often  no  marked  enlargement  of  the 
liver  in  chronic  gall-stone  jaundice.  With  obstructing  carcinoma  of  the 
common  duct  and  of  the  pancreas,  also,  the  liver  is  usually  small  (for 
cancer  of  the  gall-bladder.  Bard  and  Pic  hold  similar  views),  while  in  can- 
cer of  the  gall-bladder,  as  a  rule,  decided  enlargement  and  nodular  consist- 
ence of  the  liver  are  never  long  absent.  In  my  clinical  histories  of  tumor 
occlusion,  enlargement  of  the  liver  is  frequently  and  particularly  empha- 
sized. In  5  cases,  metastatic  cancerous  nodules  could  be  palpated  on  the 
surface  of  the  liver  during  the  life  of  the  patient;  anatomically,  metastases 
of  this  organ  have  been  even  more  frequently  proven;  upon  examination, 
the  liver  may  appear  smooth  although  carcinomatous  nodules  have  already 
formed.  Considering  our  previous  remarks  on  this  subject  a  minute  ex- 
amination of  the  liver  for  secondary  cancerous  nodules  (and  also  palpa- 
tion of  the  cavum  Douglasii)  should  never  be  omitted.  When  carcinoma 
of  the  liver  is  absent,  the  consistence  of  the  organ  is,  as  a  rule,  moderately 
increased.  Biliary  cirrhosis  was  twice  anatomically  determined  with  cer- 
tainty during  the  life  of  the  patient. 

Most  authors  agree  that,  in  the  majority  of  cases,  the  tumor  which 
causes  obstruction,  as  such,  notwithstanding  exact  and  repeated  investiga- 
tions, is  not  palpable.  I  was  able  to  palpate  it  in  only  one  of  my  cases 
of  carcinoma  of  the  pancreas  and  in  one  of  my  two  cases  of  cancer  of  the 
duodenum  (the  latter  only  occasionally).  Leichtenstern  describes  a  tumor 
at  the  head  of  th^  pancreas  which  may  generally  be  definitely  palpated; 
carcinoma  of  the  duodenum  below  the  papilla  he  diagnosticates  by  the 
presence  of  a  tumor,  etc.  Moncorge  emphasizes  the  presence  of  a  tumor 
in  the  median  line.  In  the  case  of  tumors  of  the  pancreas  leading  to 
obstructive  jaundice,  I  was  unable  to  confirm  this.  In  malignant  tumors 
which  develop  in  an  area  insusceptible  to  palpation,  G.  Hoppe-Seyler  ex- 
pects results  from  the  X-rays;  but  I  cannot  share  this  hope  because  of 
my  experience  in  other  cases. 

The  consensus  of  opinion  (Naunyn,  Kehr)  is,  that  ascites  is  absent 
in  uncomplicated  jaundice  due  to  stone.  In  my  case  (Ru.)  it  was  present 
as  well  as  anasarca  and  biliary  cirrhosis,  without  peritonitis  and  without 
llirombosis  of  the  portal  vein.  On  the  other  hand,  in  neoplasms  of  the 
l)iliary  canals  and  in  carcinoma  of  the  pancreas,  ascites  is  not  rare.  Ex- 
cej)ting  one  case  of  cancer  of  the  pancreas  in  which  aspiration  was  neces- 
sary, I  found  slight  ascites  10  times,  and  anasarca  6  times. 

Naunyn  reports  that  splenic  tumor  is  rare  in  carcinoma;  on  the  other 
hand  it  is  common  in  chronic  gall-stone  jaundice  (not  merely  in  addition 
to  diffuse  hepatitis!).  In  8  of  my  cases  of  obstruction  due  to  tumor  there 
was  decided  prominence  of  the  spleen,  and  in  4  it  could  be  palpated.  I 
do  not  believe  the  condition  of  the  spleen  of  paramount  significance  in 


OBSTRUCTIONS   OF  THE  COMMON   GALI^DUCT   BY  TUMORS       435 

a  differential  diagnosis.  According  to  my  experience,  in  any  chronic 
jaundice  (even  in  catarrhal  jaundice  apart  from  cirrhosis),  the  spleen 
may  be  enlarged;  and,  moreover,  the  enlargement  of  the  spleen  may  also 
be  explained  by  a  superadded  stasis  of  the  portal  vein  (pressure  of  the 
tumor  upon  the  trunk  or  branches). 

According  to  Leichtenstern,  a  sign  which  is  of  great  importance  in 
the  diagnosis  of  cancer,  although  not  very  frequent,  is  that  the  malignant 
infiltration  causes  a  swelling  of  the  "jugular  gland"  (Virchow's  gland), 
a  lymph-gland  situated  behind  the  clavicular  insertion  of  the  sterno-cleido- 
mastoid.  Laterally  this  swelling  may  often  extend  above  the  muscle,  may 
attain  the  size  of  a  cherry,  a  chestnut,  or,  occasionally,  of  a  hen's  egg; 
it  is  invariably  present  on  one  side,  generally  the  left,  is  occasionally  iso- 
lated, i.  e.,  with  no  other  enlargement  of  glands  in  the  supraclavicular 
region  or  in  the  neck.  Kehr  confirms  Leichtenstern's  observations ;  but  the 
gland  is  found  only  in  advaTlced  stages  of  the  disease  when  the  diagnosis 
is  no  longer  difficult.  My  clinical  histories  contain  exact  reports  of  the 
enlargement  of  peripheral  lymph-glands ;  frequently  of  the  inguinal  glands, 
sometimes  those  of  the  axilla  (particularly  upon  the  right  side) ;  in  the 
neck,  as  a  rule,  the  enlargement  is  multiple  and  bilateral,  and  in  the  supra- 
clavicular regions;  enlargement  of  the  jugular  gland  alone  is  mentioned 
rarely ;  in  one  case  it  was  decidedly  increased  in  size  and  finally  broke  down. 

In  the  preceding,  a  series  of  factors  are  mentioned  which  are  of  varying 
importance,  which,  carefully  combined  and  utilized,  will  facilitate  the  dif- 
ferential diagnosis  between  chronic  impaction  of  stone  and  obstruction  due 
to  tumor.  Incarceration  of  stone  complicated  by  carcinoma  of  the  common 
duct  (lithogenous)  which  occurs  occasionally  (see  above),  scarcely  permits 
a  positive  decision;  in  such  cases,  from  the  standpoint  of  professional 
treatment  only  the  diagnosis  of  cancer  is  necessary.  Stricture  of  the  com- 
mon duct  following  cholelithiasis  is  not  always  characterized  clinically  in 
the  picture  of  the  disease.  In  such  cases,  on  the  assumption  that  stones 
are  present,  I  advise  operation,  and  in  case  no  stones  are  found,  operative 
procedure  is  to  be  limited  to  the  breaking  up  of  adhesions,  etc.,  which  is 
of  marked,  although  only  temporary,  benefit.  Complete  obliteration  of  the 
choledochus,  provided  intense  permanent  jaundice  (with  enlarged  or  non- 
palpable gall-bladder),  repeated  attacks  of  jaundice  of  brief  duration,  or 
typical  colic  with  fever  have  not  preceded,  may  be  referred  to  cholelithiasis ; 
and  in  a  differentio-diagnostic  respect,  ulcer  of  the  duodenum  (cicatricial 
stenosis  of  the  duodenum)  and  obstruction  due  to  cancer  must  be  prin- 
cipally considered. 

Up  to  the  present  time,  the  only  diagrammatic  methods  for  the  group- 
ing of  the  different  forms  of  occlusion  of  the  biliary  passages  not  due  to 
stone  have  been  short  formulas  proposed  by  Xeusser  and  Leichtenstern; 
Nothnagel  also  furnishes  such  for  the  duodenum,  Oser  for  cancer  of  the 
pancreas. 


43G 


NEOPLASMS   OF  THE  LIVER  AND  BILL\JIY  PASSAGES 


SYMPTOMS    IN    FAVOR    OF    PRIMARY 

According  to  Neusser 
A  duration  of  the  disease  beyond 
six  months  excludes  cancer.  Deci- 
sive negative  signs:  Absence  of  tu- 
mor upon  palpation.  Positive  fac- 
tors: Suddenly  during  permanent 
jaundice  and  while  there  is  an  ad- 
mixture of  blood  to  the  feces,  com- 
plete biliary  staining  of  the  feces  is 
seen,  rapidly  changing  again  to 
acbolia.  Eventually  infectious  cho- 
langitis. Prolonged  absence  of  gas- 
tric symptoms.  Less  important :  Dis- 
tinct enlargement  of  gall-bladder. 

SYIMPTOIMS    IN    FAVOR    OF    CARCINOMA    OF    THE    PANCREAS    AS    A    CAUSE    OP 
OCCLUSION    OF    THE    COMMON    BILE    DUCT 


CANCER    OF    THE    COMMON    GALL-DUQT 

According  to  Leichtenstern 
Aged  people,  particularly  women. 
Cholelithiasis,  even  though  years 
previously.  No  palpable  tumor. 
Metastases  extraordinarily  rare.  No 
fever.  Painless  melasicterus  of  long 
duration.  Acholia  of  the  feces. 
Liver  large  and  smooth.  No  tumor 
of  the  gall-bladder.  Cachexia.  Ana- 
sarca. Eventually:  Enlargement  of 
Virchow's  gland. 


According  to  Neusser 
Besides  jaundice:  Celiac  neural- 
gia ;  from  the  onset  decided  aortic 
pulsation  in  the  epigastrium,  and 
the  absence  of  a  localized,  or  at 
most  an  indistinctly  palpable,  tu- 
mor. Later  glycosuria  ( maltosuria) , 
the  absence  of  indicanuria;  profuse 
amounts  of  transverse  striped  mus- 
cular fibers;  undigested  starches,  de- 
ficiency of  fat-splitting  in  the  feces. 

SYMPTOMS    IN    FAVOR    OF    CARCINOMA    OF    THE    SMALL    INTESTINE    BELOW 
THE    DIVERTICULUM    OF    VATER 


According  to  Leichtenstern 
Intense  jaundice,  acholia  of  the 
feces.  Occasionally  a  tensely  filled 
gall-bladder.  Pancreatic  tumor  usu- 
ally distinctly  palpable.  Persistent 
and  severe  gastric  symptoms.  Late 
disappearance  of  free  hydrochloric 
acid  from  the  gastric  contents. 


According  to  Neusser 
Jaundice;  acholia  of  the  stools, 
temporarily  disappearing  and  then 
recurring;  a  gradual  change  in, 
perhaps  even  gradual  first  develop- 
ment of,  the  jaundice.  No  marked 
symptoms  of  pyloric  intestinal  ste- 
nosis, but  other  dyspeptic  symptoms 
witbout  recognizable  disturbances  of 
tlie  gastric  chemism.  Helena  with- 
out luMiiatemesis.  Late:  Lumbar 
pains.  Slow  course.  Carcinomatous 
metastases  often  absent  (liver). 


According  to  Leichtenstern 
Parity  of  this  carcinoma.  Duo- 
denal cancer  early  causes  stenosis 
of  the  intestine,  in  consequence  of 
which  massive  bilious  vomiting  and 
gastrectasis  occur.  Tumor.  Con- 
spicuously acute  development  of  the 
jaundice. 


OBSTRUCTIONS   OF  THE  COMMON    GALI^DUCT   BY  TUMORS      437 

In  regard  to  my  own  views,  in  several  points  I  must  agree,  and  very 
frequently  disagree,  with  these  contradictory  statements,  and  my  position 
may  readily  be  determined  from  the  foregoing  explanations.  One  point 
only  I  shall  briefly  touch  upon.  In  regard  to  the  presence  of  gastrectasis, 
which  is  maintained  by  Leube  in  those  cases  of  duodenal  cancer  in  which 
the  neoplasm  is  situated  in  the  diverticulum  of  Vater,  I  concur  in  the 
opinion  of  Neusser.  Typical,  graphite-like  fatty  stools,  i.  e.,  such  as  are 
about  one-half  composed  of  fatty  acid  needles,  are  mentioned  in  only  one 
of  my  cases.  In  regard  to  fat-splitting  in  the  intestine,  I,  unfortunately, 
undertook  no  special  investigations.  As,  however,  according  to  experi- 
ence, in  carcinomata  situated  at  the  mouth  of  the  ductus  choledochus 
there  is  sometimes  a  simultaneous  occlusion  of  the  duct  of  Wirsung,  and 
in  consequence  an  exclusion  of  the  pancreatic  juice  from  the  intestine 
leading  to  dilatation  of  the  pancreatic  duct  and  even  to  connective  tissue 
proliferation  in  the  tissue  oi^the  pancreas  (I  saw  this  in  two  cases),  I  do 
not  expect  such  examination  of  the  feces  to  aid  us  much  in  the  differential 
diagnosis.  In  all  of  my  cases  there  was  either  constipation  or  diarrhea. 
Glycosuria  upon  ordinary  diet  I  did  not  once  observe  in  my  cases  of  car- 
cinoma of  the  pancreas.  In  my  recent  cases,  including  the  cases  of  cancer 
of  the  pancreas,  the  systematic  test  of  the  patient's  power  of  assimilation 
for  grape  su^ar  never  showed  alimentary  glycosuria  beyond  the  ordinary 
amount;  in  only  one  case  was  there  marked  glycosuria  with  other  signs 
of  diabetes  even  on  an  albumin  diet.  This  was  a  positive  case  of  carci- 
noma of  the  ductus  choledochus,  with  a  metastatic,  malignant  involvement 
of  the  lymph-glands  in  the  concavity  of  the  celiac  plexus,  and  slight  hard- 
ening of  the  pancreas.  Indoxyl  was  sometimes  present  in  the  urine,  some- 
times absent,  but  not  only  in  the  pancreatic  tumors.  Polyuria  was  an  in- 
constant finding  in  my  cases  of  cancer  of  the  pancreas.  Finally,  but  little 
reliance  can  be  placed,  diagnostically,  upon  the  secretory  function  of  the 
stomach:  in  two  instances  of  cancer  of  the  biliary  passages,  and  in  one 
of  cancer  of  the  pancreas,  free  hydrochloric  acid  was  absent  in  the  gastric 
contents.  In  one  of  the  cases  of  duodenal  cancer  the  reaction  for  free  HCl 
was  positive.  The  motor  function  of  the  stomach  was  not  conspicuously 
impaired. 

In.  conclusion,  a  few  words  concerning  the  differential  diagnosis  in  the 
case,  of  the  new-horn.  Here  intense  jaundice,  lasting  longer  than  14  days, 
with  absence  of  bile  from  the  feces,  points  to  a  serious  disease  of.  the 
large  gall-duct.  It  cannot  be  merely  a  case  of  syphilis  of  the  liver,  but  is 
due  to  the  congenital  absence,  that  is,  fetal  occlusion,  of  the  biliary 
passages. 

Our  reason  for  making  an  early  diagnosis  minutely  in  cases  of  chronic 
obstructive  jaundice  is  already  indicated,  but  it  is  by  no  means,  as  Bohn- 
stedt  thinks,  because,  with  the  early  recognition  of  a  cancer  of  the  biliary 
passages,  this  may  be  removed  by  operation.    On  account  of  the  anatomical 


438  NEOPLASMS  OF  THE   LIVER  AND  BILIARY   PASSAGES 

relations  and  the  condition  of  the  patient,  a  radical  cure  is  always  excluded. 
No  reports  are  known  to  me  of  successful  extirpation  of  cancer  of  the 
choledochus,  and  the  tumor  situated  at  the  head  of  the  pancreas  is  particu- 
larly difficult  to  remove  on  account  of  its  nearness  to  the  duodenum  and 
the  excretory  ducts  which  must  be  retained.  Cholecystenterostomy,  accord- 
ing to  my  own  experience  and  that  of  others,  I  believe  to  be  hopeless,  for 
even  successful  anastomoses  between  the  biliary  passages  and  the  intestine 
scarcely  prolong  the  life  of  the  patient  beyond  days  or  weeks.  Anesthesia 
and  its  consequences,  and  an  exploratory  laparotomy,  are  very  badly  borne 
by  patients  suffering  from  obstruction  due  to  cancer.  The  results  of  these 
palliative  operations  in  two  of  my  own  cases  proved  their  uselessness  to 
me  more  conclusively  than  the  reports  of  Reclus,  Regnier,  Terrier,  Socin 
and  others.  Therefore,  while  all  operative  interference  is  to  little  purpose 
(and  is  usually  undertaken  at  the  urgent  request  of  the  patient,  solatii 
causa),  every  practitioner  to  whom  the  dispute  between  the  internal  clini- 
cian and  the  surgeon  as  to  their  special  realm  is  an  artificial  one,  will, 
at  the  present  time,  agree  with  those  surgeons  who  in  chronic  obstruction 
due  to  stone  perform  choledochotomy  according  to  definite  indications. 
For  although  cases  of  chronic  gall-stone  jaundice  may  recover  naturally 
(choledochus-duodenal  fistula)  even  after  months  (or  years),  unquestion- 
ably the  danger  in  an  expectant  treatment  is  greater  than  from  operative 
interference.  But,  not  to  compromise  this  operation  unnecessarily,  ob- 
struction due  to  tumor  must  be  entirely  excluded  from  among  operable 
cases. 

3.  NEOPLASMS  OF  THE  LIVER 

CLINICAL  FORMS 

The  neoplasms  of  the  liver  itself  which  are  important  to  the  practi- 
tioner are  malignant  in  the  overwhelming  majority  of  instances.  Among 
these  we  deal  mostly  with  epitheliomata;  sarcomata  are  much  rarer.  The 
benign  tumors  usually  mentioned  are:  angioma^  lymphangioma  caverno- 
sum,  fibroma,  and  non-parasitic  cysts. 

Most  fibromata  are  not  dangerous  to  life  and  cause  no  difficulty. 
Quincke,  however,  mentions  a  case  in  a  child  in  which  jaundice,  acholia 
of  the  feces,  enlargement  of  the  circumference  of  the  abdomen,  a  large, 
hard  tumor  of  the  right  lobe  of  the  liver,  demonstrable  dilatation  of  the 
gall-bladder  and  fever  were  observed;  finally  death  occurred  after  a  dura- 
tion of  the  disease  for  9  months.  Larger  fibromata  were  also  seen  by 
Chiari  and  Lanceraux.     In  the  latter's  case  the  neoplasm  was  multiple. 

It  is  at  least  conceivable  that,  under  particularly  favorable  circum- 
stances, and  when  the  diagnosis  has  been  made  early  (perhaps  by  the  aid 
of  an  exploratory  laparotomy)  the  fibroma  may  be  removed  by  operation. 
Sklifosowski  (1890)  successfully  removed  a  fibromyoma,  lipomatodes  pe- 


NEOPLASMS   OF  THE   LIVER  439 

diculated,  the  size  of  a  man's  head,  which  was  supposed  to  be  a  tumor  of  the 
omentum.  When  the  tumor  is  centrally  situated  at  the  time  of  diagnosis, 
the  conditions  for  the  removal  of  the  neoplasm  are,  as  a  rule,  not  nearly 
so  favorable. 

In  spite  of  the  fact,  everywhere  emphasized,  that  angiomata  have  no 
clinical  importance,  it  nevertheless  occurs  now  and  then  that,  by  the  devel- 
opment of  such  a  tumor  in  the  liver,  changes  in  its  size  and  volume  take 
place.  During  the  life  of  the  patient  the  diagnosis  is  only  possible  by 
exploratory  laparotomy  if,  on  account  of  a  large  tumor  due  to  cavernous 
formation,  which  is  rare,  serious  conditions  are  produced  which  require 
operative  interference.  Here  we  are  principally  concerned  with  the  rare 
congenital  form,  which,  according  to  Virchow,  depends  upon  hypergenesis 
and  dilatation  of  the  hepatic  vessels,  and,  according  to  Pilliet,  presents 
fetal  inclusions  of  meso-chymic  tissue  similar  to  the  naevi  vasculosi  of  the 
skin  and  the  fissured  angiomaiSn.  Steffen  describes  a  solitary  angioma,  the 
size  of  an  apple,  in  the  right  lobe  of  a  child.  Schuh  and  Maier  saw  two 
similar  structures.  Chervinsky  found  in  the  markedly  enlarged  liver  of 
a  girl  7  months  old,  such  enormous  cavernous  tumors  that  the  upper 
surface  of  the  organ  was  covered  with  nodular  prominences,  similar  to 
the  condition  in  carcinoma.  In  this  class  probably  belong  the  cases  of 
V.  Eiselsberg,  Eosenthal  and  Hagedorn.  The  first  author  extirpated  from 
a  woman,  aged  5(5,  a  carcinoma  situated  upon  the  border  of  the  liver  of 
the  size  of  two  fists  which  had  distressed  the  patient  for  fifteen  years. 
The  case  was  one  of  slowly  but  steadily  growing  tumor  in  the  right  hypo- 
chondrium;  it  was  occasionally  very  sensitive  and  hard  to  the  touch;  it 
had  a  small,  nodular  surface  which  could  be  somewhat  displaced  laterally, 
and  which  was  connected  with  the  liver  by  a  demonstrable  bridge.  Prior 
to  the  successful  operation  it  was  questionable  whether  it  was  a  tumor 
of  the  liver  or  of  the  kidney.  Monneret  and  Fleury  are,  therefore,  not 
correct  when  they  report  that  angiomata  which  are  susceptible  to  palpation 
differ  from  carcinomatous  nodules  by  softness  and  elasticity,  while  indis- 
tinct fluctuation  and  the  absence  of  the  hydatid  thrill  permit  a  differentia- 
tion from  abscess  and  from  echinococcus  cysts.  Rosenthal's  patient,  aged 
41,  had  observed  a  tumor  in  the  abdomen  for  only  a  few  weeks,  and  had 
become  debilitated.  A  hard,  slightly  movable  tumor  about  the  size  of  a 
child's  head,  situated  below  the  navel,  and  the  connection  of  which  with 
the  liver  could  not  be  determined,  was  observed;  laparotomy,  however, 
showed  that  it  was  joined  to  Spiegel's  lobe.  The  hepatic  angioma,  partially 
removed  by  Hagedorn,  filled  the  abdominal  cavity,  having  about  the  cir- 
cumference of  a  gravid  uterus.  Only  such  isolated  tumors  as  the  last 
named  (which  are,  besides,  encapsulated  by  connective  tissue)  may  be 
reckoned  among  those  to  be  treated  surgically  with  success.  In  considering 
the  prognosis  it  may  be  briefly  remarked  that,  according  to  Hanot  and 
Gilbert,  there  are  cavernomata  which  become  infiltrated  with  black  pig- 


440  NEOPLASMS   OF  THE   LIVER  AND  BILIARY  PASSAGES 

ment  (melanoangiomata) ;  this,  however,  does  not  permit  the  assumption 
that  a  tumor  of  this  kind,  or  angiomata  in  general,  will  become  carci- 
nomatous. 

Non-parasitic  cysts  of  the  liver  must  be  included  with  the  neoplasms 
because,  at  least  in  part,  they  originate  from  new  structures,  newly  formed 
biliary  passages;  they  may  all  be  regarded  as  originating  from  the  vasa 
aberrantia  or  from  the  intrahepatic  biliary  passages  (related  to  the  ade- 
nomata). We  usually  differentiate  solitary,  congenital,  isolated  cysts 
from  multiple  cysts  of  the  liver  developing  during  postuterine  life.  The 
congenital  cysts,  as  a  rule,  do  not  reach  great  size;  in  certain  cases,  how- 
ever, they  become  important  on  account  of  their  decided  volume,  that  is, 
in  consequence  of  the  ascites  they  produce,  or  by  an  obstruction  to  the 
birth  of  the  child  in  question  (Witzel,  Bagot,  Sanger,  and  Klopp).  Mul- 
tiple cystomata  or  cystic  liver  (cystic  degeneration  of  the  liver  and  kidney) 
may  fre<iucntly  but  not  invariably  be  combined  with  cirrhosis  of  the 
organ  (also  being  in  causal  connection  [?]).  Besides  those  the  size  of 
a  pin's  head,  there  are  others  which  contain  as  much  as  a  liter  of  fluid; 
upon  section,  a  liver  of  this  kind  shows  a  collection  of  cavities,  the  smallest 
of  the  size  of  a  pin's  head,  and  upon  the  surface  of  the  organ  larger  and 
smaller  protuberances  form.  The  liver  varies  in  size ;  usually  it  is  enlarged. 
Biliary,  portal  vein,  and  even  vena  cava  stasis  may  be  the  consequence. 
In  com])ination  with  those  of  cystic  liver,  analogous  changes  occur  also 
in  the  kidneys,  to  which  the  symptoms  of  chronic  nephritis  may  be  added. 
More  rarely  there  are  simultaneous  cysts  of  the  ovary,  the  uterus,  the 
seminal  vesicles,  and  of  the  thyreoid  gland.  Occasionally,  multiple  cysts 
of  the  liver  cause  no  symptoms  during  the  life  of  the  patient.  Sometimes 
such  a  liver  may  be  palpated  (nodular  surface  of  the  organ,  fluctuation 
of  the  cysts).  Puncture  of  the  latter  for  diagnostic  purposes  should  never 
be  performed,  as  this  induces  suppuration;  besides,  it  furnishes  no  positive 
facts.  The  rarer,  simpler  (that  is,  isolated)  serous  or  biliary  cysts  of  the 
liver  usually  form  in  advanced  age  (after  the  40th  year  of  life),  sometimes 
earlier  than  this,  and,  as  it  appears,  more  frequently  in  women.  Their 
scat  is  usually  the  upper,  occasionally,  however,  the  lower  surface  of  the 
liver,  immediately  beneath  the  capsule.  Their  shape  is  globular  or  oval, 
hut  there  is  a  variation  in  size  which  may  even  attain  that  of  a  child's 
head.  The  liver  may  be  distinctly  nodular,  and  sometimes  the  greater 
part  of  the  cystoma  extends  above  the  hepatic  mass;  in  rare  cases  the  cyst 
may  develop  at  the  expense  of  the  parenchyma  to  such  an  extent  that 
llic  capsule  and  scant  remains  of  tissue  form  only  a  thin  sac.  Suppura- 
tion has  been  observed.  Operation  upon  such  hepatic  cysts  (the  cases  in 
(|uestion  are  congenital  cystomata  and  cystic  degeneration)  have  been  per- 
form ed  by  llueter.  North,  Terillon,  Winckler,  Kaltenbach,  Berg,  Bayer. 
and  others. 

In  passing  to  the  malignant  neoplasms,  we  must  first  devote  a  few 


NEOPLASMS   OF  THE   LIVER  441 

words  to  sarcomata  which  up  to  the  present  time  have  unfortunately  pos- 
sessed greater  pathologico-anatomical  than  practical  interest.  The  occur- 
rence of  primary  sarcomata  was  for  a  time  denied;  but  some  quite  positive 
observations  (Podrouzek)  have  been  recently  reported.  The  focus  of  the 
disease  is  principally  the  region  of  the  branches  of  the  portal  vein,  and 
particularly  the  wall  of  the  smallest  vessels,  as  these  are  most  apt  to  show 
the  characteristic  proliferation  of  sarcomatous  tissue.  At  the  autopsy  of 
an  undoubted  case  of  Kahlden's  which  may  be  positively  looked  upon  as 
primary,  in  a  man,  aged  32,  who  had  suffered  from  ascites,  the  liver  was 
found  permeated  by  circumscribed,  multiple,  medullary  nodules,  the  sur- 
face of  which  in  many  areas  was  umbilicated,  so  that  they  closely  resem- 
bled malignant  metastases.  Microscopic  examination  revealed  their  size, 
the  older  cirrhotic  changes,  the  sarcomatous  nature  of  the  tumors,  and 
permitted  the  recognition  of  a  distinct  tendency  to  alveolar  structure.  The 
number  of  cell  forms,  as  shoWn  by  the  microscopic  examination,  also  in 
sarcoma  of  the  liver  (primary  and  secondary),  is  a  very  varying  one. 
Clinically,  the  question  of  the  cell  type  of  sarcoma  of  the  liver  is  scarcely 
of  importance;  the  malignity  of  the  change  shows  only  slight  gradations. 
Melanosarcoma,  although  very  rarely,  also  occurs  primarily  in  the  liver 
(Block,  Belin  and  others).  But  the  majority  of  sarcomata  of  the  liver 
are,  as  a  rule,  secondary  growths,  and,  as  is  readily  conceivable,  metastatic 
sarcomata  of  the  liver  are  not  as  frequent  as  those  of  the  lungs;  why  this 
condition  is  reversed  in  carcinomata,  we  shall  see  later  on.  Often  the 
primary  sarcoma  which  secondarily  infects  the  liver  is  situated  in  an  area 
of  the  body  which  may  be  reached  by  the  physician  (in  the  muscles,  bones, 
breast,  etc.) ;  sometimes,  however,  a  careful  autopsy  shows  only  a  small 
primary  tumor  situated,  for  example,  in  the  apple  of  the  eye.  In  the 
case  of  melanornata  the  original  neoplasm  is  usually  in  the  choroid  or  in 
the  skin  ( sarcomatously  degenerated  naevi  pigmentosi).  After  the  enu- 
cleation of  the  diseased  bulb,  years  may  sometimes  pass  without  the  liver 
being  attacked.  The  fact  is  of  practical  significance  that  the  skin  may  also 
be  secondarily  diseased.  All  secondary  sarcomata  in  the  liver  cause  either 
an  extensive  formation  of  nodular  tumors  or  a  more  diffuse  infiltration. 
The  particularly  malignant  melanomata  may  be  the  cause  of  extremely 
large  tumors  of  the  liver,  by  far  exceeding  in  size  the  non-pigmented 
growth.  Occlusion  of  the  capillaries  and  succeeding  thrombosis  of  the 
intrahepatic  portal  branches  produce  ascites. 

Excepting  for  the  longer  period  of  time  which,  at  least  occasionally, 
elapses  between  the  appearance  of  the  primary  neoplasm  and  the  discovery 
of  sarcomatous  metastases  of  the  liver,  the  symptomatology  of  secondary 
sarcoma  of  the  liver  hardly  differs  from  that  of  medullary  cancer,  that  is, 
of  secondary  carcinoma  of  the  liver.  The  sarcomatous  metastases  of  the 
liver  may  remain  latent  during  the  life  of  the  patient  or  may  become 
prominent  in  the  symptomatology.     The  organ  enlarges  decidedly,  its  sur- 


442  NEOPLASMS   OF  THE   LIVER  AND  BILIARY  PASSAGES 

face  is  covered  with  nodules,  ascites  appears  (or  may  also  be  absent), 
Digestive  disturbances,  pain,  and  jaundice  are  frequent. 

Melanomata  of  the  liver  are  sometimes  unrecognized  in  that  they  are 
masked  by  disturbances  due  to  other  and  more  prominent  metastases.  Ir 
other  cases  the  liver  affection  is  the  most  obvious,  that  is,  it  represents 
the  only  secondary  disease.  Then  there  are  digestive  disturbances,  ever 
vomiting,  the  strength  decreases,  the  right  hypochondrium  is  markedly 
sensitive  to  pressure,  dull  or  sharp  pain,  increasing  in  paroxysms,  and 
radiating  to  wide  extent,  appears;  the  volume  of  the  liver  increases  de- 
cidedly. Its  surface  is  by  no  means  always  nodulated;  it  is  probably  so 
only  in  the  majority  of  cases;  often  it  is  smooth  to  the  touch,  and  hard 
as  wood.  The  right  hypochondrium,  the  epigastrium,  and,  eventually,  the 
entire  abdomen  are  correspondingly  distended.  Meteorism  and  ascites  are 
rarely  absent;  the  spleen,  however,  is  not  decidedly  increased  in  size. 
The  stools  may  be  acholic  or  may  contain  bile.  Jaundice  is  very  rarely 
present.  Moderate  fever  is  comparatively  frequent.  In  all  forms  of 
hepatic  sarcomatosis  this  latter  symptom  may  be  most  prominent;  its 
intensity  is  then  considerable,  and,  with  an  intermittent  type,  chills,  etc., 
may  be  added.  The  urine  which,  upon  casual  examination,  is  of  normal 
color,  if  placed  in  the  light,  with  an  addition  of  saltpeter  or  chromic  acid, 
turns  black  (Eiselt).  This  melanuria  is  of  great  diagnostic  significance; 
unfortunately,  however,  the  symptom  is  rarely  present.  The  total  dura- 
tion of  the  disease  after  the  affection  of  the  liver  has  been  determined 
varies  between  1  and  6  months;  on  the  average  it  is  2  to  3  months. 

In  by  far  the  majority  of  cases,  even  with  a  tentative  diagnosis,  for 
the  confirmation  of  which  an  exploratory  incision  may  sometimes  be  neces- 
sary, the  affection  of  the  liver  is  so  diffuse  or  manifold  that  (apart  from 
other  metastases  of  the  neoplasm)  operative  removal  cannot  be  attempted. 
The  question  whether  a  "  malignant  tumor "  in  the  liver  is  solitary  or 
multiple  can  only  be  answered  after  the  abdominal  cavity  has  been  opened. 
Isolated  resections  of  liver  sarcomata  have  been  reported  (J.  Israel  and 
others). 

Tumors  of  the  liver  composed  of  epithelial  elements  are  still  the  subject 
of  controversy  among  pathological  anatomists,  and  particularly  the  rela- 
tion between  adenoma  and  carcinoma,  although,  according  to  the  investi- 
gations of  Hanot  and  Gilbert  as  well  as  of  Siegenbeck  van  Heukelom,  it 
is  very  likely  that  there  is  a  fundamental  difference  between  them;  for 
the  present,  at  least,  the  rare  solitary  tubulous  adenoma  of  the  liver 
is  of  special  clinical  interest  because  large  tumors  of  this  kind  have 
repeatedly  been  successfully  removed  by  operation.  While  I  shall  omit, 
therefore,  the  benign,  solitary,  nodular  hyperplasia  of  the  liver  (Rokitan- 
sky,  Klob,  Mohamed  and  others),  I  shall  briefly  discuss  the  multiple, 
nodular  hyperplasia  (which,  according  to  experience,  has  a  certain  tendency 
to  adenomatous  and  carcinomatous  formation)    as  well  as  the  multiple. 


NEOPLASMS  OP  THE  LIVER  443 

tubular  adenomata  which  I  place  with  the  group  of  hepatic  carcinomata 
( cirrhosis  carcinomatosa ) . 

In  a  case  of  Keen's  an  adenoma  which  was  extirpated  proved  to  be 
a  coccidia  tumor ;  perhaps  this  etiology  really  plays  a  role  (  ?) .  In  rabbits, 
at  least,  there  are  adenoma  cysts  arising  epidemically  in  the  liver  in  the 
papillary  proliferations  of  which  Felsenthal  and  Stumm  have  found  coc- 
cidia in  various  stages  of  development.  As  a  rule,  the  solitary  hepatic 
adenoma  of  man  runs  a  comparatively  benign  course  and  does  not  give  rise 
to  metastases.  In  a  few  cases,  however,  the  proliferation  of  the  tumor 
into  the  portal  veins  and  a  thrombus-like  growth  has  been  described;  in 
a  case  of  Perls,  an  actual  metastasis  with  glandular  tubules  was  found  in 
the  sella  turcica,  and  from  the  lumen  of  the  tubules  a  greenish  mass  was 
excreted  (Schmidt  describes  a  primary  hepatic  cancer  with  metastases, 
and  a  nodule  in  the  sternum  of  similar  structure  to  that  of  the  liver,  in 
which  bile  was  positively  secreted)  ;  in  another  case  secondary  nodules 
were  found  in  the  lungs  and  in  the  mediastinal  glands.  As  the  hepatic 
adenomata  increase  in  size,  regressive  metamorphosis  and  hemorrhage  occur 
(with  the  formation  of  "blood  cysts"),  occasionally  even  to  suppuration. 
In  literature  cystoadenomata  are  reported  with  a  single  layer  of  cylindrical 
epithelium  and  serum-like  or  colloid  contents;  they  are  connected  with  the 
biliary  passages  (compare  what  has  been  stated  regarding  cysts  of  the 
liver). 

The  previously  mentioned  regressive  metamorphosis  and  the  malig- 
nancy occasionally  observed  in  adenomata  of  the  liver  necessitate  their 
extirpation  as  soon  as  practicable.  A  diagnosis  without  opening  the  ab- 
dominal cavity  is,  unfortunately,  impossible.  A  solid  tumor,  small  or 
large,  sometimes  of  the  size  of  a  child's  head,  often  movable,  which  causes 
subjective  difficulties  (pain)  the  existence  of  which  dates  back  "several 
years,"  but  which  evidently  grows,  and  a  diffused  enlargement  of  the  liver 
which  in  a  young  or  older  individual  may  be  marked — this  is  the  usual 
clinical  finding.  The  recognition  is  made  difficult  by  the  circumstance 
that  the  tumor  adheres  to  the  liver,  is  tongue-shaped  or  even  pediculated, 
therefore,  cannot  always  be  definitely  referred  to  this  organ.  (Successful 
operations  have  been  performed  by  Keen,  v.  Bergmann,  Tricomi,  Grube, 
F.  Schmidt  and  others.  Grube's  patient  died  11  months  later  from  cancer 
of  the  liver.) 

The  history  of  carcinomata  hepatis  is  a  comparatively  recent  one.  It 
is  true  that  literature  previous  to  the  nineteenth  century  contains  mention 
of  cancer  of  the  liver  (van  Swieten,  Morgagni,  Euysch,  Stoll),  but  it  is 
not  separable  from  gumma,  abscess,  cirrhosis,  and  other  hepatic  affections. 
Bayle  and  Cayol  (1812)  are  usually  mentioned  as  the  first  who  attempted, 
at  least  pathologico-anatomically,  precise  differentiation  (from  tubercle). 
The  clinical  differentiation  between  primary  and  secondary  carcinoma  of 
the  liver  is  ascribed  to  Monneret.     Prior  to  the  beginning  of  the  sixth 


444  NEOPLASMS  OF  THE  LIVER  AND  BILIARY  PASSAGES 

decade  of  the  last  century  it  was  believed  that  carcinoma  of  the  liver  was 
usually  of  primary  development,  or,  at  least,  was  as  often  primary  as 
secondary.  Bamberger  (1864)  was  the  first  to  state  that  hepatic  cancer 
was  not  only  rarely  a  primary  affection,  but  was  much  more  frequently 
secondary.  Virchow  proved  that  the  liver  is  exceptionally  fertile  soil 
for  the  deposition  of  carcinomata  from  all  parts  of  the  body,  and  that 
insignificant  primary  tumors  give  rise  to  enormous  secondary  neoplasms 
of  the  liver;  following  this,  for  a  brief  period,  the  possibility  of  primary 
cancer  of  the  liver  was  even  denied.  With  increasing  knowledge  of  the 
histologic  structure  of  the  liver  and  its  epitheliomata,  the  view  that  car- 
cinoma may  actually  develop  from  the  liver .  cell  itself  has  again  been 
expressed,  and,  unfortunately,  is  abundantly  confirmed  by  clinical  experi- 
ence. Hanot  and  Gilbert  estimate  that  for  every  8  secondary  cancers  of 
the  liver  there  is  one  primary.  Hansemann  examined  in  this  respect  the 
reports  of  the  Berlin  Pathologic  Institute  from  1870  to  1889,  strictly 
investigating  each  individual  case,  and  found  among  258  carcinomata  of 
the  liver  25  primary  neoplasms  of  the  gall-bladder,  2  primary  cancers 
of  the  large  biliary  passages,  and  only  6  primary  tumors  of  the  liver 
(concerning  2  of  which  he  was  not  positively  certain).  According  to  my 
experience  (which  is  confirmed  by  my  colleague,  Eppinger),  primary  can- 
cer of  the  liver  is  comparatively  more  frequent  in  Graz  than  in  Prague 
or  Vienna.  An  insight  into  the  pathogenesis  and  finer  structure  of  car- 
cinoma of  the  liver  has  been  given  us  by  the  investigations  of  Naunyn, 
Waldcyer,  Schiippel,  Fetzer,  Perls,  Eindfleisch,  Kelsch-Kiener,  Weigert, 
Sabourin,  Simmonds,  Hanot-Gilbert,  Hansemann,  and  v.  Kahlden,  which 
will  not  be  here  minutely  considered.  The  clinical  differentiation  between 
adenoma  and  carcinoma,  in  so  far  as  may  be  seen  from  these  investigations, 
is  still  impossible,  a  view  which  has  been  previously  stated. 

For  a  clear  conception  of  the  forms  of  primary  cancer  of  the  liver, 
not  only  in  a  pathologico-anatomical  but  particularly  in  a  clinical  respect, 
it  is  best  to  follow  the  division  of  Hanot-Gilbert.  They  differentiate  three 
main  types :  First,  the  massive  cancer,  which  appears  alone ;  that  is,  forms 
but  a  few  nodules;  secondly,  the  nodular  cancer  in  which,  as  is  the  rule 
in  metastatic  carcinoma,  the  nodules  are  more  numerous;  and,  thirdly, 
cirrliosis  carcinomatosa,  which  designation  is  based  on  the  simultaneous 
occurrence  of  an  epithelial  neoplasm  and  a  diffuse  cirrhotic  hardening 
of  tlie  hepatic  tissue.  This  last-named  form  included  (at  least  to  the 
greatest  extent)  the  previously  described  primary  epithelial  neoplasms 
called  multiple  hepatic  adenomata  (Kelsch-Kiener,  Simmonds,  Sabourin), 
and  the  diffuse  cancerous  degeneration  also  called  infiltrated  hepatic  car- 
cinoma (Schiippel).  (Ziegler  adds  to  these  a  fourth  variety  of  cancer 
consisting  of  multiple  nodules  which  develop  from  the  periportal  con- 
nective tissue  and  break  into  the  neighboring  hepatic  tissue.)  Finally 
Orth  and  Hansemann  describe  a  form  which  originates  in  the  small  biliary 


NEOPLASMS   OF  THE   LIVER  445 

passages,  and,  tree-like  in  its  course,  spreads  through  the  liver  from  Glis- 
son's  capsule.  Strictly  speaking,  we  are,  at  least,  dealing  with  a  neoplasm 
of  the  biliary  passages,  such  as  primary  carcinoma  of  the  hepatic  duct,  etc. 

The  very  rare  massive  cancer  (Gilbert),  the  carcinoma  "  of  the  nature 
of  a  solitary  tumor"  develops  (preferably  in  the  right  lobe)  as  a  solitary, 
rapidly  growing,  sharply  defined  tumor,  nearly  globular  in  shape,  occa- 
sionally of  very  marked  dimensions,  sometimes  surrounded  by  intact  hepatic 
tissue  (almond  cancer)  which  only  late  in  the  course  causes  metastases 
in  its  adjacent  areas.  The  markedly  enlarged,  diffused  organ  (sometimes 
weighing  10  kilograms)  retains  its  shape,  and  the  surface  either  remains 
smooth  or  only  small  prominences  form.  The  non-implicated  hepatic  tis- 
sue, however,  is  not  cirrhotically  indurated;  numerous  connective  tissue 
branches  envelop  isolated  nodulated  portions  of  the  secondary  mass.  The 
lymph-glands  of  the  hilus,  the  gastrohepatic,  the  peripancreatic,  the  pre- 
vertebral and  the  mediastinal  Jymph-glands  often  show  malignant  infiltra- 
tion. Metastases  external  to  the  liver  are  frequently  absent;  by  continuity 
the  cancer  occasionally  proliferates  into  the  gall-bladder  and  the  right 
kidney;  the  peritoneum  may  also  be  attacked.  Specific  emboli  may  find 
their  way  into  the  hepatic  veins,  and  develop  into  nodules  in  the  lungs. 
Perihepatitis  and  ascites  are  comparatively  rare.  The  spleen  is  usually 
enlarged. 

The  nodulated  carcinoma  forms  numerous  secondary  masses  (occasion- 
ally one  large  and  several  smaller  ones),  varying  in  size  from  the  head 
of  a  pin  to  an  orange,  and  differing  in  consistence  and  color.  The  liver 
in  these  cases  is  often  enormously  enlarged,  its  surface  becomes  nodulated; 
umbilication  is,  however,  rarer  than  in  metastatic  carcinoma  with  the 
same  dissemination.  According  to  the  structure  the  nodules  may  resemble 
the  so-called  nodular  hyperplasia,  the  trabecular  adenoma,  and  true  cancer 
formation.  Distributed  connective  tissue  proliferation  in  some  areas,  with 
induration  of  the  tissue,  and  atrophy  of  the  parenchyma  at  other  points, 
as  well  as  perihepatitis,  is  frequent.  Occasionally  there  is  right-sided 
pleurisy.  Enlargement  of  the  spleen  is  found  in  about  one-half  of  the  cases. 
The  lymph-glands  show  the  same  development,  likewise  the  metastases. 

In  frequency  this  form  corresponds  to  cirrhosis  carcinomatosa,  in  which 
the  nodular  (or  massive)  cancer  is  not  only  in  juxtaposition  with  the 
cirrhosis,  but  there  is  a  genetic  connection  between  the  carcinomatous 
development  and  sclerosis  of  the  liver;  the  latter  is  sometimes  but  slight, 
and,  under  some  circumstances,  may  naturally  also  be  markedly  diffused 
and  the  liver  enlarged;  besides,  we  find  connective  tissue  proliferation 
which  is  uniform,  mostly  annular,  rarely  in  isolated  arrangement;  numer- 
ous trabecular  epitheliomata,  that  is,  adenomata  and  carcinomata,  which 
are  situated  deep  in  the  liver  tissue  (upon  section  these  are  quite  uniformly 
distributed,  and  are  often  surrounded  by  connective  tissue  capsules)  or 
(more  frequently)  upon  the  surface  of  the  organ,  or,  perhaps,  protruding 


446  NEOPLASMS  OF  THE  LIVER  AND  BILIARY  PASSAGES 

beyond  the  latter  in  such  a  way  that  cirrhotic  granula  may  be  found  lying 
beside  cancerous  nodules.  The  volume  of  the  nodules  varies;  they  may 
be  the  size  of  a  millet  seed  or  lentil  to  that  of  a  pea  or  hazel-nut.  This 
carcinomatous  development  rarely  penetrates  into  the  lymph-glands,  but 
it  extends  into  the  venous  system  much  more  frequently  than  any  other 
cancerous  variety;  in  more  than  one-half  of  the  undoubted  cases  the  sec- 
ondary mass  enters  the  large  afferent  and  efferent  veins  of  the  liver. 
Secondary  nodules  are  found  in  the  lungs  (subpleural) ;  more  rarely  in 
the  peritoneum  (Douglas's  sac).  Perihepatitis  is  usually  present;  ascites 
is  almost  invariably  added.  In  more  than  50  per  cent,  of  the  cases  the 
s])leen  is  enlarged  and  hardened,  dilatation  of  the  subcutaneous  veins  of 
the  abdomen  is  frequent,  even  severe  hemorrhages  from  varicose  dilata- 
tions of  the  esophagus  occasionally  appear  (original  observation).  "  In- 
fiUrating  cancer,"  which  this  form,  at  first  sight,  is  called  at  the  autopsy, 
gives  the  impression  of  being  cirrhosis  of  the  highest  grade.  Only  by 
microscopic  examination  do  we  learn  that  the  islands  of  cells  in  isolated 
areas  which  resemble  resistant  hepatic  tissue  really  consist  of  cancerous 
masses. 

Hemorrhages  into  and  from  the  carcinomatous  liver,  which  are  the 
result  of  trauma,  of  erosion,  or  of  acute  congestion  and  venous  hyperemia, 
are  occasionally  of  clinical  importance,  especially  if  the  cancerous  tissue 
itself  is  very  rich  in  vessels,  that  is,  if  cavernous  capillary  dilatations  are 
present.  The  blood  either  enters  the  secondary  mass  and  the  neighboring 
hepatic  tissue,  or  it  flows,  as  I  saw  in  a  particularly  severe  case  (potator 
strenuus),  from  a  portion  of  the  cancer  perforating  Glisson's  capsule  into 
the  abdominal  cavity.  Here  it  is  sacculated  by  previously  formed  adhe- 
sions in  the  bursa  omentalis,  in  Douglas's  sac,  etc. ;  or  it  forms  a  hematoma 
above  the  liver  (Eollett),  or,  finally  (rapidly  fatal),  it  is  freely  effused 
into  the  abdominal  cavity,  and  is  discharged  from  the  peritoneal  sac 
througli  the  inguinal  and  femoral  canals,  then  infiltrating  the  subcutane- 
ous tissue. 

In  regard  to  "recovery"  by  means  of  retrogressive,  fatty,  or  other 
metamorphosis  which  the  cancerous  nodules  of  the  liver  often  anatomically 
present,  and  the  tough,  cicatricial  masses  which  are  formed  thereby,  a 
process  which  Oppolzer,  Bochdalek,  and  Henoch  held  to  be  possible,  scarcely 
anytliing  need  to-day  be  said. 

Both  sexes  appear  to  be  affected  by  primary  cancer  of  the  liver  in 
('(lual  proportions;  but  cirrhosis  carcinomatosa  is  more  frequent  in  men, 
])resumably  on  account  of  its  etiologic  relation  to  the  abuse  of  alcohol ; 
this  appears  as  an  epiphenomenon  to  alcoholic  cirrhosis.  Secondary  car- 
cinonia  of  the  liver  (for  obvious  reasons)  is  more  often  found  in  women. 
'V\\Q  majority  of  cases  occur  between  the  40th  and  45th  years;  naturally, 
])riinary  carcinoma  of  the  liver  also  occurs  in  advanced  age  and,  excep- 
tionally, in  early  life,  even  in  children.     Heredity  and  trauma  are  im- 


NEOPLASMS  OF  THE  LIVER  447 

portant  etiologic  factors.  Malaria  is  said  to  be  a  predisposing  cause. 
Some  authors  believe  there  is  a  significant  relation  to  cholelithiasis,  since 
gall-stones  are  not  rarely  found  besides  carcinoma  of  the  liver  (Biermer). 
The  statement  is  commonly  made  that  the  clinical  history  of  cancer 
of  the  liver  presents  such  a  varpng  picture  that  a  general  description  is 
scarcely  possible.  My  own  experience  leads  me  to  agree  with  Hanot  and 
Gilbert  that,  at  least  in  certain  stages  of  the  course,  the  three  main  ana- 
tomical groups  may  be  clinically  separated  without  discussing  too-far- 
reaching  theories,  although,  naturally,  the  special  diagnosis  is  impossible 
in  some  cases.  Of  massive  cancer  of  the  liver,  I  have  collected  no  indi- 
vidual observations  (Gilbert  mentions  8  cases  with  autopsy) ;  but  I  may 
cite  7  clinical  histories  of  my  own  (including  autopsies),  among  them  3 
cases  of  cirrhosis  carcinomatosa. 


CLIKICAL  TYPES 

1.  Massive  Cancer. — Stages  of  development:  Dyspeptic  symptoms. 
Sometimes  pain,  emaciation,  increasing  muscular  weakness.  Pallor.  At 
the  height  of  the  disease:  Tympanitic  abdomen,  particularly  in  the  upper 
areas.  Enlargement  of  the  entire  liver,  and  extending  below  the  level 
of  the  navel  to  the  anterior  superior  spine  of  the  ilium.  Consistence  of 
the  organ  markedly  firm  and  hard  as  wood.  Surface  remains  smooth. 
Final  stages:  Enlargement  (moderate)  of  the  spleen;  ascites  or  dilatation 
of  the  veins  in  the  abdominal  skin  is  rare.  In  some  cases:  Hypocholia  or 
acholia  of  the  feces.  Jaundice  usually  absent.  Finally,  anorexia;  rarely 
vomiting.  Constipation  (also  sometimes  diarrhea).  Occasionally,  and  in 
paroxysms,  exacerbation  of  the  pain.  In  proportion  to  the  hyponutri- 
tion,  diminished  excretion  of  urine.  Albuminuria  usually  absent.  Fever 
(100.4°-102.2°  F.)  seldom  occurs.  Course  always  progressive,  rapid,  lead- 
ing to  marked  cachexia  with  anasarca.  Frequently  autotoxic  coma.  Total 
duration:  1  to  5,  more  rarely,  6  to  7  months. 

2.  Nodulated  Carcinoma. — At  the  onset:  Digestive  disturbances,  aver- 
sion to  meat,  etc.,  pain  in  the  right  hypochondrium.  Exceptionally,  early 
jaundice.  After  a  few  weeks,  enlargement  of  the  abdomen.  At  the  height 
of  the  disease:  The  enlarged  liver,  under  some  circumstances,  raises  the 
diaphragm  perceptibly,  enlarges  the  right  side  of  the  thorax,  and  causes 
the  hypochondrium  and  epigastrium  to  bulge  more  decidedly.  In  a  down- 
ward direction  the  organ  extends  below  the  arch  of  the  ribs,  its  anterior 
border  below  the  navel,  and  at  the  height  of  the  spine  of  the  ilium  it 
reaches  the  margo  crenatus  lienis.  The  surface  of  the  liver  is  no  longer 
smooth,  the  edge  no  longer  sharp;  these  changes  are  caused  by  multiple 
tumors  which  may  be  small  and  numerous,  protruding  semiglobularly, 
hard  or  soft,  or  may  be  less  in  number,  voluminous,  flat,  sometimes 
even  confluent,  as  if  composed  of  a  single  tumor.    TJmbilications  are  usually 

30 


i 


448  NEOPLASMS  OF  THE  LIVER  AND  BILIARY  PASSAGES 

not  perceptible.  Occasionally  a  very  distinct  "  shadow "  -of  ftie  livet-  is 
seen;  sometimes  peritoneal  friction  in  the  hepatic  region.  Recognizable 
continuous  growth  of  the  liVer  under  the  eyes  of  the  observer.  The  spleen 
is  either  normal  in  size  or  only  moderately  enlarged.  In  advanced  stages 
of  the  disease,  in  more  than  one-half  of  the  cases,  there  is  serous  or  hemor- 
rhagic ascites,  the  amount  of  fluid  often  remaining  small,  and  only  occa- 
sionally necessitating  aspiration.  Sero-fibrinous  effusions  occur  only  in 
secondary  peritoneal  carcinosis.  The  specific  gravity  of  the  ascitic  fluid 
varies  between  1.010  and  1.020.  The  amount  of  albumin  may  be  from  1 
to  4  per  cent.  Pain  is  almost  always  present,  but  varies  greatly  in  degree 
and  character  (radiations  to  the  right  shoulder,  attacks  of  marked  dyspnea, 
similar  to  that  in  diaphragmatic  pleurisy).  In  one-third  of  the  cases 
jaundice  is  absent  during  the  entire  course;  in  another  third,  the  icterus 
is  moderate,  occasionally  only  just  before  death,  and,  in  the  last  third  of 
the  cases,  marked  permanent  jaundice  which  is  not  subject  to  variation 
develops  (by  compression  of  numerous  intrahepatic  biliary  passages,  or  of 
the  common  gall-duct  by  cancerous  hilus  ganglia,  or  by  large  intumescent 
gastrohepatic  and  peripancreatic  lymph-glands).  Constipation.  During 
the  latter  period  there  is  vomiting,  especially  when  there  is  rapid  growth 
of  the  tumor.  Acholia  in  consequence  of  hepatargy  is  rare.  Profound 
anemia,  cardiac  asthenia,  variable  temperature,  usually  normal,  but  toward 
the  end  with  moderate  fever,  may  occur.  Long-continued'  high  fever  is 
observed  only  in  isolated  cases  when  the  tumor  enlarges  very  rapidly; 
sometimes  it  may  be  combined  with  chills,  it  may  be  remittent,  or  even 
continuous.  Total  duration:  A  month  to  a  year;  the  average  is  3  to  6 
months.  The  younger  the  individual,  the  more  rapid,  as  a  rule,  the  course. 
Death  may  take  place  in  coma;  more  frequently  it  occurs  with  the  symp- 
toms of  sheer  exhaustion.  Besides  the  ordinary  form  just  depicted,  Hanot 
and  Gilbert  describe  quite  a  number  of  special  "  varieties."  I  concur  with 
them  only  so  far  as  their  observations  accord  with  my  own  experience 
and  that  of  other  authors,  and  must  reiterate  that  the  clinical  symptoms 
of  nodular  cancer  are,  in  fact,  but  little  less  characteristic  and  uniform 
than  those  of  other  types  of  carcinoma  hepatis.  Fever  is  occasionally 
prominent  in  the  clinical  picture,  or  the  cancer  may  betray  itself  by  the 
predominance  of  a  cachexia,  while,  in  other  cases,  the  body  retains  its 
fulness  for  some  time.  Carcinoma  may,  during  long  periods  of  its  course, 
produce  no  other  functional  symptoms  than  paroxysms  of  intense  pain; 
in  other  cases,  continuous  vomiting  is  a  prominent  feature.  In  conclusion, 
permanent  jaundice  may  play  a  leading  role. 

3.  Cirrhosis  Carcinomatosa. — Symptoms  at  the  onset:  Dyspeptic  dis- 
turbances (loss  of  appetite,  sense  of  weight  in  the  stomach,  flatulence, 
eructations,  vomiting).  Indefinite  pain,  loss  of  strength,  emaciation,  ane- 
mia. Frequent  epistaxis.  Early  enlargement  of  the  abdomen.  At  the 
height  of  the  disease:  Cachexia,  ascites,  often  increasing  so  rapidly  that 


NEOPLASMS  OF  THE  LIVER  449 

aspiration  becomes  necessary.  Dilated  veins  of  the  abdominal  skin.  The 
liver  may  be  enlarged,  and  increase  under  the  eyes  of  the  observer;  or,  it 
cannot  be  palpated,  and  decreases  in  size.  If  still  palpable,  the  surface 
appears  coarse,  nodular,  and  occasionally  granular.  The  spleen  is  often 
enlarged  (but  only  moderately),  even  palpable;  sometimes,  however,  it  is 
normal.  Jaundice  is  found  in  all  the  well-marked  cases;  it  occurs  early 
or  sometimes  even  late.  There  may  be  constipation,  or,  on  the  other 
hand,  diarrhea;  toward  the  end  the  feces  become  acholic.  Hematemesis 
and  melena  appear.  Fever  plays  no  role;  toward  the  end  there  is  edema. 
The  total  duration  of  the  disease  is  1  to  16,  upon  an  average,  4  to  5, 
months.  After  anasarca  has  appeared  death  occurs  in  coma  and  from 
extreme  exhaustion. 

As  will  be  noted,  in  the  development  of  the  three  anatomical  types 
of  primary  cancer  of  the  liver,  the  same  constitutional  disturbance,  dis- 
orders of  digestion,  as  well  as  very  similar,  but  only  slightly  characteristic, 
pain,  and  the  wretched  appearance  of  the  patient  are  common.  Absence 
of  jaundice  is  the  rule.  Massive  cancer,  and  cirrhosis  carcinomatosa  with 
a  relatively  small  liver,  often  exist  for  some  time  without  causing  local 
signs.  Symptoms  such  as  those  of  Bogdan  (flaky,  wine-red  discoloration 
of  the  cheeks,  and  varicosities  of  the  superficial  capillaries  of  the  same 
region  occurring  in  gastric  and  uterine  carcinomata),  or  that  of  Metten- 
heimer  (marked  emaciation  of  the  epigastric  region  with  an  especial  dis- 
tortion of  the  navel,  "  navel- fold,"  in  cancer  of  the  abdomen)  is  scarcely 
of  decisive  import.  The  tenacity  and,  still  more,  the  visibly  rapid  pro- 
gression of  the  previously  mentioned  symptoms  would  incline  us  to  the 
first  suspicion  rather  than  to  the  view  of  a  mild  gastric  or  intestinal  affec- 
tion. But  a  careful  study  of  the  clinical  reports  of  other  authors  and 
my  own  experience  teach  me  to  beware  of  the  danger  that  lurks  in  the 
latency  of  the  disease  and  the  absence  of  objective  symptoms  referable  to 
the  diseased  organ,  which,  as  a  rule,  continue  until  it  is  too  late  for  the 
physician  to  accomplish  anything  effectual.  Of  the  value  in  such  cases 
of  a  possible  diagnostic  exploratory  laparotomy  we  shall  speak  later.  In 
the  transitional  period,  the  main  stress  is  to  be  laid  upon  the  parallelism 
of  an  increasingly  rapid  loss  in  weight,  and  a  rapid  enlargement  of  the 
entire  liver.  Quickly  as  a  carcinomatous  liver  grows,  as  a  rule  only  certain 
forms  of  congestion  develop,  and  these  are  usually  not  difficult  to  exclude. 
There  is  scarcely  a  doubt  of  the  fact  that  when  a  palpable  tumor  of  the 
liver  can  be  determined,  it  is  too  late  for  effectual  operative  interference. 
Two  initial  symptoms  upon  which  much  stress  is  often  laid  are  hyper- 
leukocytosis  and  the  decreased  amount  of  urea  in  the  urine;  the  first  is 
of  minor  importance,  and  the  second  of  scarcely  any  differentio-diagnostic 
value.  In  my  experience,  leukocytosis  (and  especially  certain  forms  of 
digestive  leukocytosis)  favors  cancer;  I  have  reason,  however,  to  doubt 
that  this  actually  occurs  early.     The  symptom,  too,  is  variable.     In  my 


450  NEOPLASMS  OF  THE  LIVER  AND  BILIARY  PASSAGES 

cases,  the  number  of  leukocytes  to  the  cubic  millimeter  varies  between 
6,500-18,000;  but  my  experience  compels  me  to  differ  from  the  view  that 
urea  and  chlorin  are  invariably  decreased  in  the  urine  in  the  early  stages 
of  cancer  of  the  liver.  The  amount  of  urine  and  nitrogen  in  carcinoma 
hepatis  depends,  in  the  main,  upon  the  degree  of  inanition  existing,  and 
a  rapidly  increasing  ascites  may  influence  the  excretion  of  water.  In  the 
earlier  stages,  and  even  at  the  height  of  the  disease,  I  found  medium 
amounts  of  urea,  and  it  was  possible  even  to  bring  some  patients  tem- 
porarily into  N-equilibrium !  Alimentary  glycosuria  plays  no  diagnostic 
role,  and  acholia  is  not  an  actual  early  symptom. 


DIAGNOSIS 

At  the  height  of  the  disease  we  may  adhere,  in  a  diagnostic  respect, 
to  the  previously  described  types.  In  practice,  as  soon  as  a  well-developed 
cachexia  is  observed,  or  a  palpable  tumor  of  the  liver  appears  combined 
with  symptoms  of  compression  in  the  region  of  the  portal  vein  and  in  the 
biliary  passages,  a  special  differentiation  is  only  of  importance  as  an  indi- 
cation that  operation  is  unnecessary.  All  patients  succumb  soon  or  late, 
and,  therefore,  suffer  to  about  the  same  extent.  Ascites  is  a  frequent 
liindranee  to  the  recognition  of  the  affection  in  its  advanced  stages.  Special 
diagnostic  consideration  of  compression  (simultaneous)  of  the  biliary  pas- 
sages and  the  portal  veins  has  already  been  referred  to;  all  carcinomatous 
tumors  of  the  liver  are  characterized  by  the  great  increase  in  volume  which 
is  not  significant  in  any  other  affection  of  the  liver.  The  cases  of  soft 
cancer  of  the  liver,  in  which  the  sensation  through  the  abdominal  wall 
simulates  fluctuation,  are  rare  exceptions.  In  a  differentio-diagnostic  re- 
spect, besides  massive  cancer,  we  must  consider  the  following:  Melanomata 
(which  usually  also  cause  enlargement  of  the  liver  with  a  smooth  surface, 
but  in  most  cases  are  secondary  to  neoplasms  of  the  eye  or  skin,  and 
give  rise  to  melanuria),  Hanot's  hypertrophic  cirrhosis  (having  a  slower 
course  without  pain,  cachexia  and  marked  anemia,  hypercholia,  that  is, 
so-called  poussees,  jaundice,  hard  splenic  tumor),  Hutinel-Sabourin's  cir- 
rhosis adiposa  hypertrophica,  certain  forms  of  congestion  and  enlargement 
of  the  liver  in  diabetes,  malaria,  syphilis,  leukemia,  pseudo-leukemia,  amy- 
loidosis and  cholelithiasis.  Many  forms  of  nodular  cancer  so  completely 
fill  the  abdominal  cavity  that  it  becomes  difficult  to  determine  the  point 
of  origin.  Perplexity  in  diagnosis  may  also  arise  when  the  cancerous 
nodules  coalesce  and  form  a  few  larger  structures  or  a  tumor.  Confusion 
with  secondary  hepatic  cancer  is  a  frequent  occurrence.  When  a  tumor 
of  the  liver  is  present  we  should  never  fail  carefully  to  examine  the  entire 
l)ody  for  a  primary  neoplasm  (by  palpation  of  the  stomach,  digital  exam- 
ination of  the  rectum,  of  the  vagina,  etc.).  In  opposition  to  Leube's 
view,  I  must  state  that  the  determination  of  the  acidity  of  the  digesting 


NEOPLASMS   OF  THE  LIVER  .  '  451 

stomach  permits  no  decisive  conclusion;  even  in  unquestioned  primary  can- 
cer of  the  liver,  free  hydrochloric  acid  may  be  absent.  Pulmonary  and 
pleural  cancers,  as  previously  indicated,  occur  secondarily  somewhat  more 
frequently  in  the  course  of  cancer  of  the  liver;  similarly  mediastinal  and 
peritoneal  tumors,  but  rarely  growths  in  the  abdominal  wall  (umbilicus) 
and  small  tumors.  The  nodules  of  primary  carcinoma  are  generally  harder 
than  those  of  secondary  cancer.  The  umbilication  is  frequently  unrecog- 
nizable. In  secondary  cancer  of  the  liver  there  may  be  no  enlargement 
of  the  organ,  and  the  tumor  of  primary  cancer  of  the  gall-bladder  may, 
in  most  cases,  be  diagnosticated  with  certainty  according  to  criteria  which 
have  been  enumerated.  Exceptionally,  carcinoma  ventriculi  causes  dis- 
tributed tumor  formation  which  resembles  liver  nodules,  and  certain  neo- 
plasms of  the  omentum  may  simulate  the  form  of  the  liver.  Cancer  of  the 
right  kidney  has  been  repeatedly  confounded  with  carcinoma  of  the  liver. 
The  nodular  surface  of  nodular  cancer  is  common  also  to  syphilitic  liver, 
to  multilocular  echinococcus,  and  to  liver  cysts  of  non-parasitic  oiigin. 
We  differentiate  by  the  slighter  resistance  of  the  protuberances,  the  slow 
development  and  the  late  cachexia,  besides  the  history  and  other  symp- 
toms (for  example,  the  condition  of  the  spleen).  Syphilomata  may  occa- 
sionally appear  as  isolated  tumors  of  the  size  of  a  fist  (more  or  less  painful) 
below  the  right  arch  of  the  ribs  in  the  diffusely  enlarged  liver,  which  is 
of  normal  consistency.  Such  gummata  have  been  mistaken  for  cancer  and 
extirpated.  But,  inversely,  syphilomata  have  been  assumed,  and  mercury 
has  been  administered  until,  on  exploratory  laparotomy  being  later  per- 
formed, an  inoperable  soft  cancer  has  been  revealed.  Even  confusion  with 
chronic  abscess  of  the  liver  has  occurred.  In  cirrhosis  carcinomatosa  the 
symptoms  vary  according  to  the  degree  of  cirrhosis  present,  this  depending 
upon  the  situation,  the  number  and  the  size  of  the  cancer  nodules,  that  is, 
the  infiltrated  carcinoma  mass.  Correspondingly  the  liver  is  sometimes 
large,  or  very  large,  and  confusion  with  nodulated  cancer  or  secondary 
hepatic  carcinoma  is  possible;  under  these  circumstances  marked  ascites 
is  a  diagnostic  warning.  In  another  series  of  cases  with  but  slightly  en- 
larged liver  which  slowly  decreases  under  observation,  especially  if  alcohol 
may  be  regarded  as  the  cause,  we  are  inclined  to  make  a  diagnosis  of 
cirrhosis.  As  is  well  known,  there  are  also  forms  of  the  latter  disease 
which  run  a  subacute  course,  in  which  marked  parenchymatous  degenera- 
tion of  the  cellular  elements  of  the  liver  plays  an  important  role.  Gener- 
ally, however,  it  is  cirrhosis  carcinomatosa  in  which  the  rapid  develop- 
ment and  severe  nutritive  disturbances  are  peculiarj  and  which  soon 
terminates  in  death.  Finally,  there  are  cases  in  which  the  right-sided 
pleural  exudate  early  forms  and  appears  to  explain  the  entire  clinical 
picture. 

In  extremely  rare  cases  only  does  the  enlargement  of  superficial  lymph- 
glands  assist  us  in  the  diagnosis  of  cancer  of  the  liver.    The  jugular  gland, 

>_l  U  IN  -    \    *        ^ 


452  NEOPLASMS  OF  THE  LIVER  AND  BILIARY  PASSAGES 

especially,  plays  no  role.    Enlargement  of  the  inguinal  glands  is  sQmewhat 
more  frequent. 

Except  from  the  stroma,  secondary  cancer  of  the  liver  originates  exclu- 
sively from  cellular  elements  which  have  been  detached  from  an  extra- 
liopatic  carcinomatous  neoplasm,  and  by  the  lymphatic,  arterial,  and  venous 
cliannels  have  reached  the  liver  to  which  they  adhere,  then  pjoliferate 
in  the  capillaries.  There  is  scarcely  an  epithelial  tissue  from  which  the  liver 
may  not  thus  be  secondarily  affected.  Obviously  a  special  tendency  to 
infection  of  the  liver  is  found  in  carcinomata  of  those  abdominal  organs 
which  are  closely  related  to  the  portal  vein  (stomach,  rectum,  intestine, 
pancreas,  biliary  passages).  I  am  in  possession  of  accurate  histories  and 
autopsy  reports  of  27  cases  of  secondary  cancer  of  the  liver.  The  primary 
neoplasm  was  15  times  seated  in  the  stomach  (in  2  of  these  cases  only 
the  left  lobe  showed  circumscribed  implication),  4  times  in  the  gall-bladder, 
in  4  cases  in  the  rectum,  in  2  in  the  kidney,  and  in  2  in  the  esophagus. 
Hepatic  metastases  are,  however,  also  found  in  primary  cancer  of  the  tes- 
ticles, of  the  seminal  vesicles,  of  the  prostate  gland,  of  the  uterus,  of  the 
ovary,  of  the  breasts;  in  the  lungs  they  are  exceedingly  rare.  The  neo- 
plasms may  occur  secondarily  outside  of  the  actual  portal  vein  area  (due 
to  other  metastases),  having  reached  the  portal  vein  system  prior  to  their 
deposition  in  the  liver.  The  secondary  cancer  of  the  liver  possesses  an 
extraordinary  tendency  to  form  multiple  nodules,  which,  in  regard  to  their 
number,  volume,  consistence  and  shape,  do  not  differ  from  cancer  nodularis. 
As  a  rule,  the  liver  shows  very  diffuse  enlargement,  attaining  a  weight  of 
from  5  to  10  kilograms)  ;  its  surface  becomes  nodular.  Exceptionally  the 
secondary  growth  is  limited  to  the  left  lobe  of  the  organ;  more  rarely 
does  diffuse  infiltration  occur  (Litten).  The  conspicuous  tendency  to 
retrogressive  metamorphosis,  in  contrast  to  primary  carcinoma,  is  usually 
looked  upon  as  the  cause  of  the  marked  umbilication.  Breaking  down  of 
the  cancer  may  also  lead  to  the  formation  of  cysts,  to  hemorrhage,  even  to 
rupture  and  bleeding  into  the  peritoneal  cavity. 


TREATMENT 

The  limits  of  operabilitas  hepatis  quoad  resectionem,  as  it  is  called 
by  Langenbuch,  as  well  as  the  results  of  experimental  investigations  and 
of  operations  already  performed  in  man  (and  even  excluding  from  con- 
sideration the  great  danger  of  hemorrhage),  are  such  that  the  justification 
for,  and  the  technical  possibility  of,  the  removal  of  malignant  tumors  of 
the  liver  is  out  of  the  question.  The  animal  experiments  of  Ponfick, 
wliich  have  become  celebrated,  and  later  those  of  Meister,  Kusnezow,  Pen- 
ski  and  others,  are  decisive  indications  for  this  proceeding  in  surgery  of 
tlic  liver,  in  that  they  have  absolutely  proven  that  the  removal  of  even  a 
lolatively  large  portion  of  the  liver  may  be  borne  without  serious  damage. 


NEOPLASMS  OF  THE  LIVER  453 

Any  one  who  has  carefully  examined  a  number  of  carcinomata  and  sar- 
comata of  the  liver  must  admit  that  the  reason  why  tumors  of  the  liver 
are  rarely  removed  is  not  the  impossibility  of  the  operation,  but  the  diffi- 
culty of  early  recognizing  the  indication  for  the  operation,  and  its  con- 
sequent poor  results  explain  why  surgery,  which  is  constantly  advancing 
into  wider  domains,  unfortunately  cannot  completely  master  this  organ. 
Occasionally  it  may  occur  that  a  gastric,  intestinal  or  gall-bladder  cancer 
may  be  removed,  also  simultaneously  a  portion  of  the  liver,  which  is  ex- 
clusively the  seat  of  a  beginning  secondary  carcinomatous  development. 
In  all  other  cases,  metastatic  carcinoma  or  sarcoma  will  only  be  an  abso- 
lute contraindication  to  operative  procedure.  At  most  in  a  very  small 
fraction  of  the  rare  primary  malignant  neoplasms  of  the  liver  is  there 
any  indication  for  surgical  treatment.  Certain  types  of  carcinoma,  for 
example  cirrhosis  carcinomatosa,  which  is  observed  with  comparative  fre- 
quency, and  also  most  cases  of  nodular  cancer,  are  not  suitable  for  this  kind 
of  treatment.  The  peculiar  structure  of  the  liver  which  greatly  favors 
the  rapid  distribution  of  an  originally  circumscribed  affection  to  wide  areas 
of  the  organs,  the  multiplicity  of  the  malignant  neoplasms  which  soon 
become  obvious,  the  difficulties  of  an  early  diagnosis  which  have  been 
previously  described,  the  history  which  for  the  most  part  only  points  to 
a  disease  of  the  intestinal  system,  are  all  observed  too  late  to  be  absolute 
indications  for  operative  treatment  directed  to  the  liver.  Many  surgeons, 
therefore,  hold  that  these  early  symptoms  above  described,  which  with 
more  or  less  positiveness  point  to  a  serious  abdominal  disease,  indicate 
an  exploratory  laparotomy.  In  this  manner  a  tumor  of  moderate  size, 
from  that  of  a  hen's  egg  to  an  apple,  and  favorably  situated,  might  be 
removed;  personally  I  know  of  nothing  that  contraindicates  an  exploratory 
laparotomy.  If  we  consider,  however,  how  often  on  such  vague  signs  this 
operation  would  be  resorted  to  in  practice,  and  how  frequently,  from  obvi- 
ous diagnostic  errors,  it  would  be  practised  unnecessarily,  it  is  easy  to 
understand  that  the  carrying  out  of  such  a  proposition  would  meet  with 
objections  on  the  part  of  the  patient  and  his  relatives  and  would  even  be 
objected  to  by  those  physicians  who  themselves  have  committed  a  few  errors. 
Therefore,  many  favorable  circumstances  must  be  combined  to  enable  us 
to  perform  resection  of  the  liver  to  the  benefit  of  the  affected  patients. 
To  Hochenegg  belongs  the  honor  of  being  the  first  successfully  to  remove 
a  cancer  of  the  liver  from  its  point  of  origin  in  the  gall-bladder.  A  case 
of  Liicke's  is  very  instructive  as  a  guide  to  the  decision  for  the  operation. 
This  case  was  published  in  1891,  and.  on  account  of  the  successful  removal 
of  the  left  lobe  of  the  liver,  it  was  generally  looked  upon  as  an  example 
of  a  pure  primary  cancer  of  the  liver  until  a  more  recent  publication  of 
Madelung  (1898)  showed  that  it  was  only  a  syphiloma. 


ECHINOCOCCUS    OF  THE    LIVER* 

By  E.  STADELMANN,  Berlin 

Clinically  and  anatomically  we  may  differentiate  two  varieties  of 
echinococcus  in  man:  1.  Cystic  echinococcus ;  2.  Multilocular  or  alveolar 
echinococcus.  We  know  that  the  echinococcus  cysticus  may  develop  (Sie- 
bold,  Kiichenmeister,  Leuckart)  whenever  the  ova  of  the  tenia  echinococcus 
which  lives  in  the  intestinal  canal  of  the  dog,  the  wolf,  the  jackal,  etc., 
are  found  in  the  gastrointestinal  canal  of  man.  The  embryo,  which  is  set 
free  by  the  digestion  of  its  chitin  covering,  burrows  through  the  intestinal 
wall,  reaches  a  branch  of  the  portal  vein,  and  enters  the  liver  with  the 
circulation;  here  it  lodges  and  is  transformed  into  an  echinococcus  cyst. 
Naturally,  the  echinococcus  develops  not  only  in  the  liver  but  also  in 
many  other  organs  (lungs,  spleen,  brain,  kidneys,  etc.),  provided  it  can 
find  ingress  by  means  of  the  circulation  or  the  lymph  channels.  In  its  early 
existence  the  echinococcus  cyst  develops  but  slowly,  first  to  the  size  of  a 
tubercle,  later  to  that  of  a  pea,  but  it  is  a  firm  nodule  with  a  thick  wall 
which  is  composed  internally  of  muscle  and  vessels  (parenchymatous  layer), 
and  externally  of  a  tough,  lamellar  layer  of  tissue  (cuticula).  In  the 
affected  organ,  and  around  the  cyst  which  is  filled  with  a  clear,  non- 
albuminous  fluid,  a  tough  connective  tissue  capsule  forms  which  may  be 
easily  peeled  from  the  nodule,  and  in  which  are  many  vessels  by  means 
of  which  the  echinococcus  is  nourished.  After  four  to  six  months  the 
growing  vessel  attains  the  size  of  a  walnut,  and  in  its  interior  (endogenous), 
very  rarely  externally  (exogenous),  daughter-cysts  now  begin  to  develop 
(secondary  hydatid  cysts),  even  granddaughter-cysts  (tertiary  hydatid 
cysts)  which  are  partly  sterile,  and  partly  contain  the  heads  (scolices)  of 
the  echinococci.  These  heads  have  the  characteristic  shape,  and  are  sup- 
plied with  suctorial  discs  and  a  crown  of  booklets.  Usually  the  daughter- 
cysts  become  detached  from  the  inner  parenchymatous  wall,  and  float  free 
in  the  fluid,  so  that  in  such  a  mother-cyst  hundreds  of  daughter-cysts  may 
be  found. 

The  development  of  the  multilocular  echinococcus  is  different.  Virchow 
first  recognized  this  as  a  parasite;  it  forms  a  coarse  tumor  composed  of 

1  See  also  the  article  "  Echinococcus  Disease  "  by  Prof.  E.  Peiper  in  the  volume  on 
"Diseases  of  Metabolism  and  of  the  Blood;  Animal  Parasites;  Toxicology,"  page  526. 
454 


ECHINOCOCCUS  CYSTICUS  455 

vesicles  the  size  of  a  pea.  In  contrast  with  the  cystic  echinococcus,  its 
growth,  therefore,  takes  place  by  exogenous  proliferation  in  that  one  echi- 
nococcus  vesicle  attaches  itself  to  another.  It  betrays  the  same  nature  as 
malignant  neoplasms,  and  not  only  attacks  the  parenchyma  but  also  the 
blood-vessels,  such  as  the  portal  vein,  the  hepatic  veins,  the  hepatic  arteries 
and  the  lymph-vessels.  Constriction  may  take  place,  and,  as  in  malignant 
neoplasms,  give  rise  to  metastases.  It  is  a  mooted  question  whether  mul- 
tilocular  echinococcus  is  identical  with  cystic  echinococcus,  or  whether  we 
are  dealing  with  two  different  varieties  of  teniae.  A  number  of  factors 
favor  the  latter  view;  for  instance,  the  circumstance  that  echinococcus 
multilocularis  occurs  in  definite  localities  (South  Germany,  Austria,  and 
parts  of  Russia)  while  in  other  regions  (Iceland,  Mecklenburg,  and  Pom- 
erania)  the  echinococcus  cysticus  preponderates,  and  also  that  some  authors 
by  feeding  experiments  with  the  echinococcus  multilocularis  succeeded  in 
producing  this  parasite  experimentally;  this  statement,  however,  is  denied 
by  other  authorities.  Finally,  the  scolices  of  these  forms  are  said  to  differ 
from  each  other,  particularly  in  the  shape  of  their  booklets,  No  matter 
how  this  may  be,  the  question  whether  we  are  dealing  with  two  different 
varieties  of  echinococci  or  whether  the  same  echinococcus  produces  two 
different  forms  of  the  disease,  must  be  looked  upon  as  stiU  in  dispute. 


A.  ECHINOCOCCUS   CYSTICUS 

PATHOLOGICAL  ANATOMY 

The  origin  and  development  of  the  vesicles,  as  well  as  the  configuration 
of  the  walls  of  the  cyst,  have  already  been  described.  Besides  daughter- 
cysts,  the  vesicles  contain  a  clear,  almost  invariably  non-albuminous  fluid 
with  a  specific  gravity  of  from  1.009  to  1.015,  and  varieties  of  sugar 
(grape-sugar,  inosite),  succinic  acid  and  salts  (principally  sodium  chlorid). 
According  to  the  investigations  of  different  authors  (Mourson  and  Schlag- 
denhauffen,  Brieger),  toxic  substances  are  also  present  which  may  be  as- 
sumed to  be  ptomains,  since,  when  the  contents  of  the  cyst  are  injected 
into  animals,  they  produce  collapse  and  death.  Echinococci  are  usually 
found  in  the  right  lobe  of  the  liver.  The  vesicles  may  develop  in  any 
region  of  the  liver,  upon  the  upper  surface  (the  convex),  upon  the  lower 
surface  (the  concave),  centrally  as  well  as  subphrenically.  The  s3rmptoms 
of  .ijiisplacement  of  other  organs,  as  well  as  the  extent  of  the  growth, 
frequently  also  depend  upon  the  seat  of  the  echinococcus,  and  this  again 
produces  the  clinical  symptoms  as  well  as  the  diagnostic  determination  of 
the  pathologic  process.  We  would  digress  too  far  if  we  entered  upon  the 
individual  points  which  are  self-evident.  It  need  only  be  stated  that  the 
tumor  may  extend  to  the  crest  of  the  ilium,  may  force  the  diaphragm 
up  toward  the  pleural  cavity,  may  sometimes  be  found  deep  in  the  peri- 


456  ECHINOCOCCUS   OF  THE   LIVER 

toncal  cavity,  often  causing  the  abdominal  walls  to  assume  a  globular 
shape,  at  other  times  it  is  prominent  upon  the  surface  of  the  liver.  The 
death  of  tlie  echinococcus  may  result  from  various  causes  (entrance  of  bile 
into  tlie  ccliinococcus  sac,  nutritive  disturbances  in  consequence  of  pressure 
from  oiher  organs,  etc.),  then  the  contents  of  the  sac  become  turbid,  milky, 
and  resemble  pus,  but  are  without  pus  cells;  the  fluid  becomes  more  and 
more  inspissated,  the  friable  mass  consists  of  cholesterin,  calcium  carbon- 
ate, phosphate,  and  the  remains  of  scolices,  but  particularly  of  the  very 
resistant  booklets. 

Tiue  suppuration  of  the  echinococcus  cyst  is  not  rare.  This  develops 
in  consequence  of  trauma  or  from  the  entrance  of  pathogenic  agents  (bac- 
teria) into  the  interior  of  the  echinococcus  sac.  It  is  facilitated  when  an 
avenue  of  communication  forms  between  the  cyst  and  the  bile  channels 
so  tliat  bile  and  also  bacteria  penetrate  to  the  cyst.  This  not  only  causes 
the  death  of  the  echinococcus  but  suppuration  of  the  contents  of  the  cyst, 
after  which  all  the  symptoms  of  hepatic  abscess  appear. 


SYMPTOMATOLOGY 

The  echinococcus  produces  no  symptoms  in  the  initial  stages.  Quite 
large  cysts  may  remain  latent,  and  be  discovered  only  accidentally  at  the 
autopsy.  This  is  due  to  the  slow  growth  of  the  cyst,  as  well  as  to  the  slight 
oifect  it  produces  upon  the  surrounding  tissue.  Examination  will  reveal 
■jialpal^le  changes  only  when  the  tumor  is  quite  large  and  situated  upon 
the  surface.  Even  such  a  tumor  may  readily  be  confounded  with  others 
since  it  is  rarely  characteristic.  A  cyst  can  be  diagnosticated  only  when 
it  is  soft  and  shows  fluctuation,  and  thus  arouses  a  suspicion  of  echino- 
coccus. A  peculiar  vibration  in  the  cyst  upon  percussion  and  also  upon 
palpation  has  been  much  spoken  of,  and  to  this  the  name  "  hydatid  thrill " 
lias  l)een  attached.  This  is  said  to  be  produced  by  the  collision  of  the 
daughter-cysts  in  the  sac,  but  it  may  be  doubted  whether  this  explanation 
is  correct.  The  hydatid  thrill  has  also  been  detected  in  sterile  cysts.  The 
recognition  of  tension  of  the  membrane  is  also  important,  for  with  decided 
tension  this  thrill  does  not  appear.  The  hydatid  thrill  is  best  developed 
w  hen  several  fingers  of  one  hand  are  placed  upon  the  cyst  and  the  fingers 
of  the  other  hand  tap  successively,  as  if  performing  ballottement.  The 
Iiepatic  area  in  which  the  cyst  is  located  influences  greatly  the  production 
<if  the  different  symptoms.  Cysts  which  form  upon  the  lower  surface  of 
the  liver  extend  downward  into  the  abdomen;  they  may  produce  compres- 
sion of  the  porta  hepatis,  of  the  common  bile  duct,  of  the  portal  vein, 
of  the  veins  of  the  intestines,  etc.,  with  their  corresponding  sequelae. 
Xaturally,  the  entire  right  lobe  of  the  liver  is  enlarged,  while  the  greater 
])ortion  of  the  cyst  is  insusceptible  to  examination.  Echinococci  which 
develop  upon  the  upper  portions  of  the  liver  frequently  force  the  diaphragm 


ECHINOCOCCUS  CYSTICUS  457 

upward  and  decrease  the  thoracic  space  (subphrenic  seat),  so  that  the 
differential  diagnosis  from  pleural  exudate  becomes  necessary;  the  thorax 
is  distended  upon  the  right  side,  the  lung  more  or  less  compressed;  this 
gives  rise  to  cough,  dyspnea,  and,  by  inhibiting  cardiac  activity,  also  circu- 
latory disturbances  and  displacement  of  the  heart  to  the  left.  An  echino- 
coccus  of  the  left  lobe  of  the  liver,  which  is  rare,  causes  symptoms  of 
displacement  of  the  heart,  of  the  stomach,  and  finally  also  of  the  left  lung, 
and  produces  not  only  marked  enlargement  of  the  left  lobe  of  the  liver 
but  even  an  entire  change  in  the  organ's  position.  Central  echinococci 
give  rise  to  general  hepatic  enlargement  less  often  than  to  change  in  the 
form  of  the  liver. 

A  large  echinococcus  cyst  of  course  produces  numerous  symptoms  due 
to  enlargement  of  the  liver,  and  combined  with  this  also  symptoms  of 
displacement  which  are,  however,  not  typical.  Fulness,  signs  of  pressure 
in  the  abdomen,  dyspnea,  oppression  after  the  ingestion  of  food  are  the 
usual  complaints,  as  in  any  other  tumor  of  the  liver. 

Suppuration  of  the  echinococcus  cyst  produces  new  symptoms,  such  as 
remittent  or  intermittent  fever,  chills,  pain,  especially  in  the  hepatic  region, 
which  radiates  to  the  right  shoulder,  great  constitutional  disturbance,  signs 
of  local  peritonitis,  of  perihepatitis,  finally  also  of  general  pyemia.  None 
of  these  manifestations  can  be  differentiated  from  those  of  abscess  of 
the  liver. 

Rupture  of  the  echinococcus  cysts  and  the  penetration  of  the  parasite 
into  other  organs  call  for  a  special  description.  Aside  from  tumors  this 
is  mainly  due  to  a  too  voluminous  growth  of  the  cyst,  and  especially  to 
suppuration  in  the  same.  When  an  echinococcus  ruptures  into  the  biliary 
system  the  parasite  is  killed,  and,  in  consequence  of  secondary  infection 
on  the  part  of  the  bile  which  enters,  the  contents  of  the  cyst  frequently 
suppurate.  The  fluid  contents  of  the  cyst  may  be  discharged  into  the 
intestine  through  the  small,  communicating  biliary  channels  while  the  cysts 
themselves  remain.  If  rupture  occurs  into  the  hepatic  or  common  ducts 
it  is  possible  that  the  hydatid  may  be  discharged,  and  it  may  enter  the 
intestine,  perhaps  with  accompanying  symptoms  of  an  attack  of  cholelithia- 
sis; synchronous  with  this  the  cyst  rapidly  collapses. 

If  the  hydatids  remain  in  the  common  bile  duct,  stasis  jaundice  may 
be  the  consequence,  also  the  symptoms  of  acholia,  etc.  By  admixture  with 
bile,  the  contents  of  the  cyst  show  marked  icteroid  discoloration. 

Perforation  into  the  stomach  occurs  when  the  cyst  is  situated  in  the 
left  lobe  of  the  liver  or  upon  its  lower  surface.  Adhesions  to  the  wall 
of  the  stomach  must  have  preceded.  When  the  rupture  occurs,  the  patient 
vomits  profuse  watery  masses  containing  hydatids,  and  the  cyst  collapses. 
A  portion  of  the  contents  naturally  finds  its  way  into  the  intestine. 

Perforation  into  the  intestine  is  brought  about  in  the  same  way  by 
local  peritoneal  inflammation  and  adhesions  which  run  their  course  ac- 


458  ECHINOCOCCUS   OF  THE  LIVER 

companied  by  pain.  After  rupture,  the  cyst  rapidly  collapses,  the  feces 
become  watery,  and  sometimes  contain  blood,  hydatids,  or  their  remains. 
The  lesion  of  communication  may  close  or  it  may  persist.  In  the  latter 
case  fecal  contents  find  their  way  into  the  liver,  and  there  develop  a 
fecal  abscess. 

Perforation  into  the  peritoneal  cavity  results  Vhen  there  have  been  no 
adhesions  to  neighboring  organs,  as  is  so  frequently  the  case,  but  con- 
tusions, trauma,  sudden  violent  exertion,  force  or  pressure,  etc.,  may  be 
the  cause.  The  results  of  rupture  are  severe  shock,  syncope,  great  abdom- 
inal pain,  mental  disquietude,  the  sense  of  impending  death,  or  even  sudden 
dissolution.  The  patients  feel  as  though  a  part  of  the  abdomen  had  been 
torn;  they  are  pale,  anxious,  and  distressed.  Urticaria  frequently  appears 
in  consequence  of  the  toxins  which  have  developed  in  the  fluid.  If  the 
patients  do  not  succumb  to  the  rupture  the  hydatids  may  still  further 
develop  in  the  abdominal  cavity,  and  if  the  generators  of  infection  con- 
tained in  the  fluid  of  the  cyst  are  expelled  into  the  belly,  peritonitis  follows. 
This  process  is  much  more  favorable  if  adhesions  to  the  peritoneum  have 
previously  formed,  and  if  the  cyst  ruptures  into  an  encapsulated  portion 
of  the  abdominal  cavity,  so  that  diffuse  peritonitis  does  not  result. 

Rupture  into  the  urinary  passages  is  very  rare,  but  may  lead  to  renal 
colic  and  hydronephrosis  when  the  hydatids  are  caught  in  the  ureter. 
When  they  are  voided  by  the  urinary  channels,  we  find  in  the  urine  cysti- 
cerci  vesicles  which  are  occasionally  bile-stained. 

Rupture  into  the  pleural  cavity  results  in  cysts  in  the  subphrenic  space. 
According  to  the  composition  of  the  exudate,  we  then  have  the  signs  of 
serous  or  purulent  pleurisy.  By  exploratory  puncture  we  obtain  some  of 
this  fluid,  and,  microscopically,  we  are  sometimes  able  to  make  a  correct 
diagnosis  by  demonstrating  booklets  or  portions  of  the  membrane.  The 
slight  amount  of  albumin,  the  clearness  of  the  serous  fluid,  or  its  bile- 
stained  appearance,  may  awaken  our  suspicions  that  it  comes  from  an 
echinococcus  cyst.  The  rupture  of  the  sac  gives  the  patient  a  sensation 
as  though  something  within  the  chest  had  been  torn,  then  follow  a  feeling 
of  anxiety,  dyspnea,  or  even  collapse.  The  pulse  becomes  small  and 
frccjuent,  and  with  these  symptoms  death  may  soon  occur.  If  the  contents 
of  tlio  cyst  are  purulent,  the  well-known  symptoms  of  empyema  with  pain 
and  fever  are  produced.  The  empyema,  if  not  recognized  in  time  and 
treated  by  operation,  may  rupture  externally  or  into  the  lung.  In  the 
latter  case,  occasionally  with  severe  paroxysms  of  coughing,  great  numbers 
of  hydatid  vesicles  are  coughed  up,  and  complete  discharge  of  the  con- 
tents of  the  cyst  as  well  as  cure  results.  In  other  cases  a  pulmonary 
abscess  forms;  pneumothorax  from  the  rupture  of  an  exudate  into  a  bron- 
chus, and  even  direct  rupture  of  the  contents  of  the  cyst  into  the  lung, 
without  the  development  of  an  empyema  such  as  has  been  described  or  of 
pleurisy,  have  been  reported.     If  rupture  into  the  bronchi  or  the  trachea 


ECHINOCOCCUS  CYSTlCUS  459 

occurs  too  rapidly  in  consequence  of  the  great  mass  of  fluid  and  hydatid 
cysts  expelled,  the  patient  may  be  suffocated.  Large  cavities  may  develop 
and  produce  corresponding  phenomena.  Upon  rupture  of  an  echinococcus 
cyst  into  the  lung  the  sputum  is  frequently  bile-stained. 

Rupture  into  the  pericardium  is  most  infrequent,  and  probably  in  all 
cases  soon  causes  death  by  paralysis  of  the  heart. 

Rupture  into  the  portal  vein  produces  multiple  abscesses  in  its  various 
branches. 

Rupture  into  the  vena  cava  permits  the  entrance  of  hydatids  into  the 
circulation,  thence  to  find  their  way  into  the  right  heart,  and  later  into 
the  pulmonary  veins,  producing  pulmonary  emboli  with  all  the  symptoms 
of  a  hemorrhagic  infarct  or  even  a  pulmonary  abscess. 

Suppurating  cysts  may  also  rupture  externally  through  the  abdominal 
wall,  the  same  as  hepatic  abscesses,  unless  they  are  early  recognized. 


DIAGNOSIS  AITD  TREATMENT 

Small  echinococcus  cysts  cannot  be  recognized.  They  are,  however, 
occasional  autopsy  findings.  The  recognition  of  large  cysts  is  mainly  due 
to  their  position,  but  even  then  they  are  frequently  overlooked,  especially 
if  they  produce  no  symptoms  and  their  position  is  concealed.  If  we  dis- 
cover a  tumor  which  we  suspect  to  be  an  echinococcus,  this  diagnosis 
rather  than  that  of  other  tumors,  particularly  malignant  ones,  is  favored 
by  the  slighter  pain,  the  round,  smooth  surface,  the  mild  disturbance  of 
the  general  condition,  the  slow  growth,  the  tense,  elastic  consistence,  per- 
haps also  by  a  positive  hydatid  thrill.  If  remittent  or  intermittent  fever 
coexist,  the  differential  diagnosis  between  abscess  of  the  liver  and  a  sup- 
purating echinococcus  cyst  may  be  impossible  without  surgical  intervention. 

In  the  diagnosis  of  a  subphrenic  cyst  the  X-rays,  as  well  as  the  ob- 
servation of  Litten's  diaphragm  phenomenon,  will  be  of  value.  In  a 
pleural  exudate  the  diaphragm  is  forced  down,  in  a  subphrenic  echinococcus, 
on  the  other  hand,  it  is  forced  upward,  while  the  remaining  clinical  signs 
in  these  pathologic  conditions  differ  but  little  from  each  other. 

Cysts  of  the  spleen,  situated  near  the  left  lobe  of  the  liver,  may  be 
mistaken  for  echinococci,  also  those  of  the  pancreas  and  even  of  the  ovary, 
as  well  as  dropsy  of  the  gall-bladder  and  a  right-sided  hydronephrosis. 

In  many  cases  exploratory  puncture  with  the  subsequent  chemical  and 
microscopical  investigation  of  the  cyst  contents  which  have  been  obtained 
may  clear  up  and  decide  this  question.  This  is.  therefore,  an  important 
diagnostic  aid  which  may  be  employed  without  danger  in  case  of  a  punc- 
ture of  the  pleural  cavity,  provided  antiseptic  precautions  are  taken.  On 
the  other  hand,  puncture  of  the  abdomen  is  decidedly  hazardous.  Even 
thin  cannula  will  produce  holes  in  the  tense  cyst  wall  from  which  other 
contents  may  readily  ooze,  and,  particularly  if  they  are  infectious,  lead  to 


460  ECHINOCOCCUS  OF  THE  LIVER 

general  peritonitis.  Therefore  I  earnestly  advise  that  puncture  be  performed 
only  upon  tlie  operating  table,  and  when  operation  is  to  follow  immediately ; 
in  the  interests  of  the  patient  it  is  well  to  leave  a  definite  diagnosis  to 
the  sm-'j-eon.  It  is  certainly  fortunate  for 'the  patient  if  the  physician 
decline  the  triumph  of  making  the  decision,  and  work  hand  in  hand  with 
the  surgeon.  He  may  do  this  all  the  more  conscientiously  since,  if  echino- 
coccus  be  present,  the  only  possible  treatment  is  by  operation.  The  cyst 
must  be  opened,  and,  if  it  prove  to  be  an  echinococcus  cyst,  the  contents 
must  be  evacuated.  How  this  is  to  be  done,  and  which  method  of  pro- 
cedure is  the  best,  is  difficult  to  decide,  as  the  situation  of  the  cyst  in  the 
individual  cases  may  necessitate  different  methods.  Neither  can  it  here 
be  positively  stated  whether  the  single  or  the  double  method  will  give  better 
results.  At  all  events,  it  should  be  the  earnest  endeavor  of  every  surgeon 
to  avoid  in  every  possible  way  the  infection  of  the  neighboring  organs  by 
the  fluid  evacuated  from  the  cyst.  After  the  parasite  has  died  some  cysts 
heal  by  calcification. 

Drug  treatment  is  wholly  ineffectual,  and  it  is  advisable  not  to  at- 
tempt it. 

B.  ECHINOCOCCUS  MULTILOCULARIS  SEU  ALVEOLARISi 

The  question  as  to.  the  manner  in  which  multilocular  echinococcus 
differs  from  cystic  echinococcus  has  been  discussed,  as  well  as  the  nature 
of  its  development.  The  typical  difference  is  that  multilocular  echino- 
coccus forms  in  the  cavities  of  the  liver  (bile  ducts,  blood-vessels,  lymph- 
channels)  and  extends  by  gemmation,  destruction  going  on  in  the  interior 
of  the  colony,  and  thus  cavities  differing  in  size  are  formed,  also  that  its 
action  in  the  liver  resembles  that  of  malignant  neoplasms  since  it  destroys 
the  actual  hepatic  tissue  and  at  the  same  time  causes  an  extensive  connective 
tissue  proliferation.  Tn  consequence  of  this  mode  of  development,  the 
appearance  of  the  liver  in  echinococcus  multilocularis  may  vary  greatly. 

If  the  tumor  is  situated  in  the  interior  of  the  organ,  the  form  of  the 
liver  is  not  necessarily  altered  and  the  disease  process  is  revealed  only 
by  section.  In  other  cases,  nodular  protuberances  of  varying  size  are  found 
upon  the  surface,  and  between  these  are  connective  tissue  retractions; 
occasionally  distinct  echinococcus  cysts  are  recognizable  in  the  nodules. 
The  consistence  of  the  liver  is  sometimes  very  dense  owing  to  a  large 
deposit  of  chalk  frequently  found  in  the  connective  tissue.  In  old  echino- 
coccus cavities  in  the  interior  this  condition  is  found  as  the  consequence 

1  For  the  literature  compare  the  followinj?  works:  IJoppe-Sfeyler  in  "Die  Krank- 
hoiten  der  Leber  von  Quincke  und  Hoppe-Seyler  " ;  YothnageVn  specieJlc  Pnthologie 
mid  Thcrapie.  XVIII,  Theil  1;  Vierordt,  Berliner  Klinik,  Heft  28,  and  the  mono- 
graph upon  "Multilocular  Echinococcus"  published  in  Freiburg  in  1886;  Posselt, 
D(Ut.sc]ics  Archiv  fiir  klin.  Medicin,  LIX. 


ECHINOCOCCUS   MULTILOCULARIS   SEU   ALVEOLARIS         461 

of  decomposition  which  has  taken  place.  The  liver  is  usually,  and  some- 
times greatly,  enlarged,  cases  of  echinococcus  multilocularis  having  been 
described  in  which  two  liters  of  fluid  were  evacuated  from  the  cavities. 
Vicarious  hypertrophy  of  the  liver  substance,  chiefly  of  the  left  lobe  (the 
echinococcus  usually  develops  in  the  right  lobe),  has  been  reported. 

The  small  tumors  are  white  to  yellowish  green  in  color,  with  a  distinct 
Kne  of  demarcation  from  the  surrounding,  dark,  hepatic  tissue. 

Section  of  the  tissue  produces  a  grating  sound,  the  cut  surfaces  reveal 
numerous  apertures  (alveoli),  hence  the  tissue  resembles  a  honeycomb,  and 
the  echinococcus  has  been  designated  "  alveolar."  These  alveoli  are  of 
different  sizes,  ranging  from  that  of  a  pin's  head  to  that  of  a  pea,  a 
walnut,  an  apple,  a  child's  head,  etc.,  and  between  them  the  connective 
tissue  is  increased.  As  these  cavities  coalesce  a  peculiar  picture  may  de- 
velop; the  consistence  of  the  contents  varies  from  that  of  a  gelatinous 
material  to  a  tough,  dry,  friable,  even  calcareous  mass  which  is  usually 
a  bile-stained  yellow.  In  consequence  of  the  great  destruction  going  on, 
enormous  cavities  may  occasionally  form ;  these  are  partly  filled  with  fluid, 
partly  with  compact  masses  permeated  by  connective  tissue  striae  which 
represent  the  remains  of  large  blood-vessels  and  bile  channels.  The  con- 
tents of  the  cavities  often  have  a  thready,  cream-like,  gelatinous,  more  or 
less  bilious  or  even  brownish  appearance,  and,  according  to  microscopical 
and  chemical  investigation,  they  are  composed  of  mucus,  calcium,  choles- 
terin,  remains  of  blood,  bilirubin,  hematoidin,  remains  of  echinococei, 
hepatic  tissue,  albumin,  biliary  coloring  matter,  bile  acids  and  fat. 

Macroscopically  and  microscopically  the  hepatic  tissue  is  greatly  altered. 
The  bile  ducts  are  sometimes  dilated  by  the  tumors  growing  within  them, 
at  other  times  are  compressed  by  these  growths.  The  common  bile  duct 
may  be  occluded  from  compression;  the  same  is  true  of  the  cystic  and 
hepatic  ducts.  This  produces  various  other  anomalies  such  as  absolute 
occlusion  of  bile  with  severe  jaundice,  dropsy  of  the  gall-bladder,  etc. 

In  consequence  of  compression  of  the  portal  vein,  stasis  arises  with  en- 
largement of  the  spleen,  ascites,  etc.  The  lymph  tracts  are  also  frequently 
implicated  by  tumors,  and  consequently  have  a  peculiar  appearance;  they 
are  filled  with  echinococei  and  resemble  a  pearl  necklace  or  a  rosary.  This 
latter  condition  is  even  observed  in  the  lymph-glands  at  the  porta  hepatis. 
Metastases  of  echinococei  are  also  found  in  the  lungs,  the  spleen,  the  medi- 
astinal glands,  the  pericardium,  the  peritoneum,  the  pleura,  and  even  in 
the  endocardium.  Besides  the  already  described  contents  of  the  individual 
cavities  the  microscope  reveals  that,  surrounding  these  tissues,  a  structure- 
less membrane  is  first  formed  which  belongs  to  the  echinococcus  itself  and 
is  usually  distinctly  layered,  and  subsequently  an  extensive  connective  tissue 
proliferation  which  may  be  regarded  as  a  reaction  of  the  liver  to  the 
foreign  hody  that  has  encroached  upon  its  substance.  Upon  the  inner 
surface  of  the  cavity  there  is  also  a  parenchymatous  layer.     Booklets  and 


462  ECHINOCCKXIUS  OF  THE   LIVER 

scolices  are  frequently  absent  from  the  primary  tumor,  and  this  coincides 
with  the  existing  tendency  to  death  and  destruction  of  the  parasite;  they 
are,  however,  present  in  recent  growths  and  in  metastases.  The  mem- 
brane of  the  parasite  itself,  which  corresponds  to  the  cuticula  of  the  cystic 
echinococcus,  naturally  consists  largely  of  chitin. 

SYMPTOMS  AND   DIAGNOSIS 

Alveolar  echinococcus  runs  its  course  for  a  long  time  without  symp- 
toms, then  pressure  signs,  a  sensation  of  tension,  pains  in  the  epigastrium, 
loss  of  appetite,  nausea,  etc.,  appear — symptoms  which  are  by  no  means 
typical.  Fever  and  even  jaundice  (pressure  symptom)  may  be  present. 
The  patient's  sufferings  increase,  and  he  begins  to  emaciate.  Objectively 
we  find  a  more  or  less  enlarged  liver  of  increased  consistence,  and  if  the 
echinococcus  tumor  be  susceptible  to  palpation  hard,  nodular  masses  are 
felt.  Occasionally  we  obtain  distinct  fluctuation  even  with  a  very  large, 
superficially  situated,  decomposing  echinococcus  cyst.  In  other  cases  in 
which  there  is  a  hard,  tough  tumor  of  the  liver,  hypertrophic  hepatic 
cirrhosis  is  simulated. 

Sometimes  the  symptoms  of  jaundice  due  to  compression  of  the  com- 
mon bile  duct  may  be  particularly  prominent  and  combined  with  all  the 
familiar  manifestations  of  icterus  gravis.  In  other  cases,  the  signs  are 
those  of  portal  vein  stasis  with  ascites,  splenic  tumor,  etc.,  in  consequence 
of  the  compression  and  constriction  of  this  vessel  which  dominates  the 
clinical  picture,  as  well  as  the  familiar  gastrointestinal  symptoms  which 
are  so  frequent  in  portal  vein  stasis,  such  as  constipation,  diarrhea,  loss 
of  appetite,  etc.  Death  results  from  increasing  emaciation  and  exhaustion, 
edema,  and  cachexia,  usually  after  a  very  long  duration  of  the  disease. 

The  diagnosis  can  rarely  be  made  with  anything  approaching  positive- 
ness.  In  the  differential  diagnosis  hypertrophic  hepatic  cirrhosis  and  can- 
cer of  the  liver  will  usually  come  into  question,  according  to  the  symptoms 
of  the  individual  case.  Age,  the  environment  of  the  patient,  the  exam- 
ination of  the  gastric  juice,  fever,  and  enlargement  of  the  spleen  will 
usually  protect  us  from  error  in  the  differentiation  from  carcinoma.  When 
we  suspect  the  existence  of  a  cavity  in  the  liver,  exploratory  puncture  and 
the  subsequent  examination  of  the  contents  of  the  cyst  thus  obtained  will 
lead  us  to  a  definite  opinion.  Of  course,  in  echinococcus  alveolaris  the 
nature  of  the  contents  of  the  cavity  varies  according  to  its  seat.  Sometimes 
its  constituents  are  biliary,  such  as  biliary  coloring  matter,  bile  acids  and 
cholesterin;  at  other  times  fatty,  if  communication  of  the  tumor  with  the 
lymph  tracts  has  occurred;  and  in  still  others,  upon  communication  with 
the  blood-vessels,  blood  may  be  present. 

In  contrast  with  the  fluid  contained  in  the  cavities  of  cystic  echino- 
coccus, the  echinococcus  alveolaris  contains  extremely  lar^e  quantities  of 
albumin. 


ECHINOCOCCUS   MULTILOCULARIS   SEU   ALVEOLARIS         463 

When  we  suspect  echinococcus  alveolaris,  exploratory  laparotomy  and 
the  examination  of  an  excised  portion  of  the  tumor  is  clearly  indicated. 

Amyloid  liver  and  hepatic  abscess,  as  well  as  cystic  echinococcus,  may 
all  be  considered  in  the  differential  diagnosis.  The  first  two  are  easily 
excluded.  In  the  last,  the  result  of  the  examination  of  the  fluid  obtained 
by  exploratory  puncture  is  decisive. 


PROGNOSIS  AND  TREATMENT 

The  disease  is  nearly  always  fatal.  We  may,  however,  hop9  that  with 
increasing  knowledge  of  the  malady  and  a  timely  diagnosis,  proper  treat- 
ment, particularly  early  operative  measures,  may  be  instituted.  These 
should  consist  of  extirpation  of  the  tumor  and  resection  of  the  affected 
portion  of  the  liver,  but  they  can  only  lead  to  favorable  results  when  the 
operation  is  performed  in  the  initial  stages  of  the  affection.  The  possi- 
bility of  this  is  demonstrated  by  facts,  since  a  cure  of  the  disease  in  this 
way  has  certainly  been  effected   (Bruns^). 

^  Bruns'  Beitrdge  zur  klin.  Chirurgie,  XVII. 


31 


GALL-STONES 

Bv  E.  NEUSSER,  Vienna 

Cholelithiasis  is  a  border-land  for  the  physician  and  surgeon.  Both 
are  familiar  with  its  symptom-complex,  and  must  work  hand  in  hand 
to  discover  the  etiology,  to  make  the  diagnosis  and  prognosis  certain,  and 
to  formulate  its  therapeutic  indications. 

Many  results  in  this  realm  we  owe  to  the  physician,  many  to  the  sur- 
geon, who  actually  makes  autopsies  in  vivo.  But,  in  spite  of  numerous 
researches  and  statistics  from  both  sides,  they  have  not  completely  eluci- 
dated even  the  most  vital  questions  in  cholelithiasis,  such  as  the  question 
of  jaundice,  nor  even  that  of  the  mechanism  of  gall-stone  colic. 

SYMPTOMATOLOGY 

The  etiology  of  gall-stone  formation,  the  important  factor  which  to 
botli  would  be  explanatory,  and  would  also  decide  the  treatment,  is  still 
obscure:  here  aseptic  inflammation,  there  bacterial  infection;  upon  the  one 
side  confidence  in  sterile  bile,  upon  the  other  the  specter  of  the  bacterium 
coli,  the  exaggerated  fear  of  all  possible  anatomical  complications,  and 
the  old  belief  in  the  efficacy  of  a  mineral  spring  cure. 

It  cannot  be  denied  that,  at  the  present  time,  the  surgeon's  word 
carries  the  weight  of  authority,  and  already  almost  identifies  an  early 
operation  with  a  radical  cure.  Yet  he  may,  any  day,  be  surprised  by  the 
discovery  of  an  anti-bacterial  serum  which  will  render  gall-stones  inert, 
and  the  operation  for  radical  extirpation  will  meet  the  same  fate  as  did 
traclieotomy  in  true  diphtheria. 

Until  this  fortunate  epoch  arrive,  the  clinician,  in  justice  to  both  par- 
ties, must  limit  himself  in  the  given  case  to  protecting  the  patient  from 
tlie  two  extremes,  eagerness  to  operate  and  failure  to  recognize  the  right 
time  for  operation. 

'I'lie  usual  symptoms  of  cholelithiasis  are  pain  in  the  right  hypochon- 
driuin  which  radiates  to  the  back  and  the  region  of  the  shoulder,  which 
either  sets  in  suddenly  or  rapidly  increases  in  severity,  also  eructations 
and  vomiting,  chilliness  or  well-developed  chills,  sensitiveness  to  pressure 
in  tlic  region  of  the  gall-bladder  and  succeeding  jaundice.  In  the  over- 
whelming majority  of  cases  these  symptoms  will  justify  a  diagnosis  of 
cholelithiasis;  nevertheless,  there  are  also  cases  in  which  the  same  symp- 
4G4 


SYMPTOMATOLOGY  465 

tom-complex,  in  the  same  sequence,  is  present,  and  to  our  surprise,  in- 
stead of  finding  the  expected  gall-stones  in  the  feces,  the  passage  of  echino- 
coccus  cysts  completely  changes  our  diagnosis.  Even  from  this  one  example 
it  is  obvious  that  typical  cholelithiasis  may  cause  diagnostic  difficulty.  The 
situation  becomes  more  complex  when  we  deal  with  an  atypical  form  of 
this  polymorphic  disease  setting  in  with  strange  symptoms,  which  may 
appear  under  the  mask  at  a  meningitis,  an  endocarditis,  a  pulmonary 
abscess,  cancer  of  the  stomach  or  intestinal  obstruction. 

The  statistics  of  errors  in  the  diagnosis  of  this  affection  disclose  so 
many  that  it  is  evident  we  can  only  avoid  confusion  by  the  most  careful 
investigation  of  individual  symptoms.  This  necessitates  the  examination 
of  the  patient  from  head  to  foot,  with  the  aid  of  all  our  modern  methods ; 
for  there  is  obvious  danger  that  a  symptom  which  we  have  carelessly  over- 
looked upon  superficial  investigation  might  have  been  decisive  in  diagnosis. 

The  most  conspicuous  symptom  which,  from  the  first  moment  of  a  cur- 
sory inspection,  forces  itself  upon  the  attention  of  the  investigator  is 
jaundice. 

Its  diagnostic  importance  clears  up  the  cases  which,  for  a  time,  have 
been  regarded  as  ulcer  of  the  stomach,  as  cardialgia,  intestinal  colic,  or 
wandering  kidney;  in  these  the  appearance  of  jaundice  alone  reveals  the 
true  nature  of  the  malady. 

Jaundice  in  cholelithiasis  is  either  the  direct  consequence  of  gall-stone; 
or  enlargement  of  the  lymph-glands  at  the  porta  hepatis,  or  it  arises  inde- 
pendently of  these  by  an  accompanying  substantive  catarrh  of  the  mucous 
membrane,  by  neoplasms  of  the  stomach  or  of  the  duodenum,  by  tumors 
of  the  pancreas,  or  by  other  tumors  adjacent  to  the  liver,  for  example, 
hydronephrosis. 

Jaundice  is  usually  and  most  readily  explained  by  biliary  stasis  due 
to  obstruction  of  the  choledochus  or  hepatic  duct  by  stone,  therefore,  as 
Riedel  calls  it,  pure  Uthogenous  icterus.  The  intensity  of  this  jaundice 
depends  chiefly  upon  the  size  of  the  stones,  partly  also  upon  the  de- 
gree of  distention  of  the  biliary  passages  from  a  preceding  passage  of 
stone,  and  partly  also  to  the  position  of  the  stone  in  a  possible  diverticulum 
of  the  canal.  If  the  biliary  passages  are  dilated  at  the  point  where  the 
stone  is  impacted,  or  if  there  is  a  groove  in  the  stone  which  permits  the  bile 
to  flow  off  unhindered,  then,  even  with  very  large  stones  in  the  co"mmon 
bile  duct,  the  jaundice  may  be  slight  or  entirely  absent;  cases  such  as 
this  were  familiar  to  Morgagni. 

With  an  obstruction  by  stone  in  the  common  duct,  icterus  may  also  be 
absent  if  an  accessory  ductus  choledochus  exists  by  which  the  bile  may  flow 
into  the  intestine,  a  structural  anomaly  which  was  observed  by  Fallopius 
and  Vater.  Frank  describes  a  case  in  which  the  common  duct  bifurcated 
into  two  branches,  one  of  which  emptied  into  the  jejunum  and  the  other 
into  the  colon. 


466  GALL-STONES 

Furthermore,  jaundice  may  be  absent  in  spite  of  occlusion  of  the  com- 
mon duet  by  stone,  if  a  simultaneously  present  gall-bladder-colon  fistula 
permits  the  bile  to  flow  freely  into  the  intestine;  in  such  cases  bile  is 
never  found  in  the  vomitus,  while  the  feces,  particularly  if  peristalsis  is 
rapid,  show  greenish,  undecomposed  bile  which  contains  bilirubin  or  bili- 
verdin. 

,^Dn  the  other  hand,  intense  jaundice  may  exist,  even  with  small  im- 
pacted stones  in  the  common  duct,  provided  secondary  catarrh  of  the  biliary 
passages  develops. 

Obstructive  jaundice  and  cholelithiasis  may  also  occur  from  compres- 
sion of  the  common  duct;  either  by  the  gall-bladder  filled  with  stones,  or 
by  a  dropsical  gall-bladder,  or  by  a  volvulus  and  displacement  of  the  same 
with  adhesions  to  neighboring  organs,  or  by  abscesses  which  have  arisen 
s])outant'ously  in  the  region  of  the  gall-bladder  in  consequence  of  peri- 
cholecystitis or  after  operative  procedure. 

Diverticula  of  the  gall-bladder  and  cystic  duct  containing  stone  may  lead 
to  compression  of  the  common  duct,  and  cause  either  a  permanently  deep 
jaundice  or  one  varying  in  its  intensity. 

Besides  these  forms  of  lithogenous  occlusion,  or  compression  of  the 
common  duct  causing  jaundice,  Riedel  has  familiarized  us  with  another 
form  of  icterus,  which,  in  contrast  to  the  purely  mechanical  form,  he  has 
designated  infJammatory  jaundice.  This  arises  by  propagation  from  the 
inflammatory  mucous  membrane  swelling  of  the  gall-bladder,  extending 
through  the  cystic  duct  to  the  biliary  passages.  It  is  at  the  sam§  time  a 
catarrhal  jaundice,  but  with  the  difference  that  in  ordinary  catarrhal  jaun- 
dice the  process  proceeds  from  the  intestine  to  the  common  duct,  while 
here  the  starting  point  of  the  inflammatory  swelling  is  the  gall-bladder. 
Eiedel  bases  his  justification  for  the  assumption  of  such  a  jaundice  on 
the  findings  at  the  operation  in  those  cases  of  irregular  and  "non-success- 
ful "  cholelithiasis  which  have  been  preceded  by  typical  attacks  of  gall- 
stone colic,  in  which  the  operation  showed  only  large,  round,  non-faceted 
stones  in  the  gall-bladder  that  could  not  possibly  have  passed  through  the 
common  duct;  while,  on  the  other  hand,  the  examination  of  the  feces, 
which  was  repeatedly  undertaken  during  the  attacks,  never  revealed  the 
passage  of  stones. 

Unquestionably,  provided  no  stones  are  found  in  the  common  duct  at 
the  operation,  and  compression  of  the  choledochus  by  stone-containing 
diverticuli  of  the  cystic  duct  may  be  excluded,  to  this  form  of  inflamma- 
tory jaundice  belongs  the  transitory  jaundice  following  operations  upon 
the  gall-bladder  with  complete  discharge  of  the  stones,  which  probably 
originates  in  the  surgical  manipulation  of  the  gall-bladder  and  the  cystic 
duct,  apparently  by  a  propagation  of  the  inflammatory  swelling  of  the 
nuicous  membrane  of  the  cystic  duct  to  the  common  duct.  Hemorrhage 
from   the  damaged   wall   of   the  gall-bladder   into   the  biliary   passages. 


SYMPTOMATOLOGY  467 

and  coagulation  of  blood  in  the  same,  may  also  cause  obstructive  jaun- 
dice. It  must,  however,  be  remembered  that  the  inflammatory  changes 
in  the  wall  of  the  gall-bladder  lead  to  secondary  infection  and  intoxi- 
cation by  way  of  the  blood  current,  and  these  processes  may  give  rise 
to  jaundice  which,  in  patients  with  gall-stones,  may  also  be  looked  upon 
as  toxic,  and  as  the  origin  of  the  infection  in  some  other  point.  This  is 
also  true  of  post-operative  chloroform  jaundice,  which  differs  from  ob- 
structive jaundice  just  as  does  the  previously  mentioned  septico-toxic  jaun- 
dice by  insufficient  intestinal  acholia. 

Jaundice  may  vary  from  the  slightest  discoloration  of  the  sclera  to  the 
most  intense  icterus.  Intense  jaundice  is  always  the  sign  of  lithogenous 
closure  of  the  hepatic  or  common  duct,  a  cicatricial  stricture  in  conse- 
quence of  ulceration  at  the  point  at  which  the  stone  has  been  arrested. 
Jaundice  in  gall-stone  colic  may  develop  even  in  6  to  12  hours  after  the 
attack.  This  rapid  appearance  of  jaundice  after  the  attach  of  pain  differ- 
entiates gall-stone  colic  from  those  cardialgias  which  accompany  indiges- 
tion, and  sometimes  precede  by  several  days  the  appearance  of  catarrhal 
jaundice. 

But  in  cholelithiasis  the  development  of  jaundice  may  exceptionally 
be  also  slow  and  progressive,  giving  rise  to  new  diagnostic  errors  by 
confounding  this  with  neoplasms  of  the  biliary  passages  which  com- 
press the  duct  slowly  and  progressively.  A  chronic,  long-existing  jaun- 
dice, such  as  is  observed  after  the  passage  of  stone  by  perforated 
openings  into  the  intestine  and  a  cessation  of  the  biliary  stasis,  may  clear 
up  quickly. 

The  rapid  disappearance  of  jaundice,  however,  does  not  always  indicate 
a  perforation.  It  may  be  due  to  the  fact  that  the  impacted  stone  has 
become  loosened  and  moves  retrogressively  in  the  dilated  common  duct. 

After  the  passage  of  the  stone  into  and  through  the  duodenum,  a  per- 
manent constriction  or  closure  of  the  ductus  choledochus  may  be  produced 
by  cicatricial  retraction  at  the  point  of  perforation,  and  in  this  manner 
jaundice  which  had  cleared  up  may  reappear.  In  the  differential  diagnosis 
between  chronic  obstructive  jaundice  due  to  stones  arrested  in  the  common 
duct  and  compression  of  the  common  duct  by  stones  in  the  cystic  duct 
or  in  a  diverticulum,  the  circumstance  may  be  pointed  out  that,  in  lithog- 
enous closure  of  the  choledochus,  all  factors  which  stimulate  the  secretion 
of  bile  also  increase  the  jaundice,  while  the  same  factors,  as,  for  example, 
when  compression  of  the  choledochus  is  due  to  a  diverticulum,  the  plentiful 
ingestion  of  fluid  by  surmounting  the  obstruction,  renders  the  flow  of 
bile  into  the  intestine  possible,  and,  by  relieving  the  biliary  passages  from 
the  accumulated  bile,  may  cause  a  decrease  in  jaundice. 

As  a  well  marked  example  I  should  like  to  report  a  case  which  I  showed 
in  the  Clinic  upon  February  13,  1900,  that  of  a  railroad  conductor,  aged 
32,  who  for  four  years  suffered  from  gall-stone  colic  with  the  characteristic 


468  GALL-STONES 

radiation  of  pains  to  the  shoulder  and  chills.  In  the  last  attack  the 
patient  was  permanently  jaundiced. 

After  the  appearance  of  the  jaundice  the  colic  did  not  recur.  The 
icterus,  however,  remained,  and  showed  the  peculiarity  that  in  the  winter, 
especially  when  the  weather  was  very  cold,  it  was  particularly  intense, 
while  in  the  summer  it  was  less  noticeable.  A])petite  and  regularity  of 
the  bowels  were  undisturbed.  The  patient  had  no  symptoms  except  con- 
tinuous lassitude.  An  operation  was  performed  in  Albert's  Clinic,  and 
sliowed  a  stone  situated  in  the  diverticulum  of  the  cystic  duct  compressing 
the  common  duct.  As  with  chronic  although  varying  jaundice  we  usually 
diagnosticate  a  lithogenous  obstruction  of  the  common  duct,  the  history 
in  this  case  is  notable,  particularly  the  increase  of  the  jaundice  in  winter 
and  its  decrease  in  summer.  This  can  only  be  explained  by  the  hypothesis 
that  the  patient  took  more  fluid  in  summer,  and,  by  increasing  the  biliary 
secretion,  the  immobility  of  the  choledochus  was  overcome.  This  observa- 
tion is  all  the  more  interesting  since,  according  to  Hermann,  jaundice 
due  to  occlusion  of  the  ductus  choledochus  increases  during  a  mineral 
spring  treatment  at  Carlsbad, 

In  cholelithiasis  intrahepatica  the  jaundice  may  also  depend  upon  the 
concentration  of  bile.  It  may  be  entirely  absent  if  the  bile  is  a  thin  fluid, 
and,  on  the  other  hand,  may  be  intense  with  an  inspissated,  thick,  sandy, 
pappy  state  of  the  bile  (Leichtenstern), 

In  regard  to  the  development  of  jaundice  in  cholelithiasis  and,  in  fact, 
jaundice  in  general,  those  cases  are  of  special  significance  in  which  the 
flow  of  bile  is  from  the  biliary  fistula  which  has  been  produced  by  operation, 
and,  in  spite  of  which,  jaundice  continues  when  no  mechanical  obstruction 
can  be  demonstrated  in  the  biliary  passages. 

Inflammatory  swelling  of  the  cystic  duct  was  therefore  not  present, 
consequently  there  was  no  inflammatory  jaundice.  It  can  hardly  be  ex- 
plained in  any  other  manner  than  by  the  view  of  a  direct  lesion  of  the 
liver  cells;  whether,  in  Liebermeister's  sense,  as  a  diffusive  jaundice,  or, 
as  Minkowski  and  E.  Pick  believe,  due  to  a  perverted  secretion  of  the 
liver  cells,  cannot  be  decided  at  present. 

These  attempts  at  explanation  coincide  with  the  results  of  the  investi- 
gations of  Browicz,  who  refers  all  forms  of  jaundice  to  an  increased 
function  of  the  liver  cells,  which,  stimulated  by  various  influences,  take 
up  excessive  quantities  of  nutritive  and  functionating  material,  even  hemo- 
globin, and  transform  them  into  bile. 

The  circumstance  that  jaundice  sometimes  develops  to  its  fullest  in- 
tensity even  a  few  hours  after  the  onset  of  the  gall-stone  colic,  while 
experimental  jaundice  after  tying  the  common  duct  requires  at  least  24 
hours,  and  usually  2  to  3  days  or  even  longer,  led  Pick,  in  the  year  1895, 
contrary  to  current  opinion,  to  declare  that  jaundice  in  gall-stone  colic 
was  not  obstructive  jaundice,  but  was  reflex,  due  to  the  nerves  of  secretion 


SYMPTOMATOLOGY  469 

of  the  liver  (nervous  paracholia),  a  reflex  conveyed  from  the  sensory  nerves 
of  the  gall-bladder  to  the  nerves  of  secretion. 

The  rapidity  with  which  jaundice  develops  after  the  beginning  of  the 
attack  may  also  be  explained  by  a  mechanical  theory,  as,  in  fact,  is  done 
by  Gerhardt  in  his  lecture  upon  icterus  duodenalis  in  which  he  says: 
"  In  gall-stone  colic  the  bile  in  the  biliary  passages  is  not  only  under 
the  pressure  of  secretion,  but  under  that  of  the  pathologically  contracted 
gall-bladder;  therefore,  it  passes  very  rapidly  into  the  hepatic  veins;  6 
hours  after  the  beginning  of  the  attack,  traces  may  be  found,  and,  after 
12  hours,  there  is  a  well-developed  form  of  jaundice."  These  contractions 
of  the  gall-bladder,  however,  can  only  be  decisive  for  the  development  of 
jaundice  when  the  cystic  duct  is  permeable,  therefore  in  ordinary  chole- 
lithiasis with  the  passage  of  the  stone  through  the  cystic  duct;  while  in 
the  irregular  forms  of  cholelithiasis  with  occlusion  of  the  cystic  duct, 
jaundice  cannot  be  thus  explained  unless  we  attribute  to  the  substantive 
reflex  contractions  of  the  common  bile  duct  and  especially  of  the  circular 
terminal  muscle  (sphincter  cJioledochi)  at  the  duodenal  end  the  same 
role  which  we  ascribe  to  the  gall-bladder  itself.  Thereby  the  pressure 
of  the  biliary  system  exerts  a  degree  of  contraction  sufRcient  for  the 
propulsion  of  the  bile  into  the  circulation. 

We  see,  therefore,  that  a  satisfactory  explanation  of  jaundice  in  all 
cases  of  gall-stone  colic  has  not  yet  been  given,  and  that  m  its  production 
several  factors  are  probably  cooperative. 

A  symptom  which  is  intimately  connected  with  jaundice  is  pruritus 
cutaneus,  which  sometimes  precedes  the  attack  or  follows  it.  With  an 
existing  jaundice,  an  increase  of  pruritus  may  announce  an  approaching 
attack.  This  symptom,  markedly  disagreeable,  by  causing  scratching  of 
the  skin,  may  be  the  immediate  forerunner  of  serious  complications,  such 
as  furunculosis  and  secondary  staphylococcus  infection  of  the  biliary  pas- 
sages, a  condition  which  I  saw  in  a  patient  from  Salonica. 

Local  cutaneous  jaundice  in  the  form  of  a  greenish-hlacJc  discoloration 
of  the  skin  in  the  right  hypochondrium  was  observed  some  time  prior  to 
rupture  of  an  abscess  which  had  been  formed  by  a  perforation  of  a  gall- 
bladder containing  stones. 

Xanthoma  are  not  rare  in  jaundice;  nevertheless  I  have  frequently 
seen  xanthoma  in  the  canthus  of  the  eye  or  the  lids  of  gall-stone  patients 
who  had  no  jaundice,  a  finding  to  which  I  desire  to  attach  a  certain  im- 
portance, particularly  in  the  diagnosis  of  irregular  cholelithiasis. 

Symptoms  on  the  part  of  the  nervous  system  play  an  important  role 
in  cholelithiasis,  and  may  appear  during  the  paroxysm  as  well  as  in  the 
separate  phases  of  the  disease,  and  may  become  prominent.  It  is  self- 
evident  that  the  nervous  symptoms  may  vary  according  to  whether  we  are 
dealing  with  a  neurasthenic  or  hysterical  individual,  with  a  child  or  with 
an  aged  person. 


470  GALL-STONES 

Marked  psychical  disturbances,  attacks  of  mania,  general  convulsions, 
confusions  and  hallucinations,  clonic  spasms  which  begin  in  the  muscles 
of  the  right  side  of  the  abdomen  and  extend  to  those  of  the  extremity 
or  affect  the  muscles  at  the  back  of  the  neck,  and  symptoms  of  hemiplegia 
may  occur  during  the  attack  and  so  completely  dominate  the  picture  that, 
in  exceptional  cases,  they  may  be  the  cause  of  death. 

The  position  of  the  patient  during  the  paroxysm  may  vary;  some  lie 
upon  the  back,  others  upon  the  side  or  the  abdomen,  others  are  bent  over 
or  kneel,  propping  the  head  upon  the  floor,  and  others  again  resort  to  a 
cradle  motion  resembling  a  mother  nursing  her  child. 

The  patient  that  I  saw  showed  during  the  attack  the  characteristic 
"  arc  de  cercle  "  with  hyperesthesia  of  the  skin  in  the  hepatic  region  and 
hysterical  contractions. 

Reflex  paralyses,  such  as  occur  after  affections  of  the  bladder  and 
uterus,  were  noted  by  Trousseau  as  sequels  of  gall-stones. 

Headache  is  frequently  mentioned  in  the  literature  of  gall-stone  disease. 
Frerichs  observed  cases  in  which  marked  headache,  cardiac  palpitation, 
active  pulsation  of  the  abdominal  aorta,  and  epistaxis  became  prominent 
accompaniments  of  the  attacks.  Kehr  saw  cases  in  which  migraine  dis- 
appeared after  the  removal  of  gall-stones.  Kraus  found  migraine  a  feature 
in  the  history  of  many  gall-stone  patients,  and  remarks  that  in  some  of 
these,  on  the  first  appearance  of  gall-stone  colic  the  attacks  of  migraine 
became  rarer  or  ceased  entirely.  I,  too,  have  seen  cases  of  the  latter  kind, 
but  I  believe  that  in  most  of  them  the  finding  of  the  two  frequent  path- 
ologic conditions  is  a  mere  coincidence. 

Headache  in  chronic  jaundice  is  sometimes  a  phenomenon  of  cholemia; 
in  other  cases  it  is  due  to  anatomical  disease  of  the  meninges,  as,  for 
example,  pachymeningitis  hemorrhagica  or  meningitis,  which  latter  affec- 
tion is  not  infrequently  combined  with  infectious  cholangitis,  and  forms 
the  terminal  phase  of  gall-stone  disease.  Therefore,  in  the  course  of  a 
cholelithiasis,  we  may  meet  with  severe  cerebral  symptoms,  with  delirium, 
with  sopor  and  stupor.  On  this  account,  cholelithiasis  is  intimately  re- 
lated in  a  differentio-diagnostic  respect  to  acute  atrophy  of  the  liver,  in 
which  the  early  appearance  of  psychical  disturbances  out  of  proportion  to 
the  other  symptoms  forms  a  striking  diagnostic  factor.  Years  ago,  when 
an  assistant  in  Bamberger's  Clinic,  I  was  called  to  Braun's  Obstetrical 
Clinic  to  see  a  pregnant  woman  who  was  suddenly  attacked  by  severe  pain 
in  the  hepatic  region  accompanied  by  jaundice,  so  that  at  first  she  was 
thought  to  be  suffering  from  gall-stones.  Soon  afterward  delirium  set  in 
and  the  liver  dulness  progressively  decreased.  The  autopsy  showed  acute 
yellow  atrophy  of  the  liver.  Decrease  of  liver  dulness  in  pregnancy  is 
by  no  means  easy  to  determine.  Delirium  and  psychical  disturbance  may 
be  oljsorvod  in  l)oth  diseases,  and,  besides,  a  chemical  analysis  of  the  urine 
for  leuein  and  tyrosin  cannot  be  immediately  made  at  the  bedside,  nor  is 


SYMPTOMATOLOGY  471 

such  test  absolutely  decisive,  for  cases  of  cholelithiasis  have  been  observed 
in  which  leucin  and  tyrosin  were  present  in  the  urine  and  were  apparently 
due  to  focal  necrosis  of  the  liver  cells. 

Among  the  nervous  symptoms,  the  pains  which  accompany  the  paroxysm 
of  gall-stone  colic  form  the  most  prominent  symptom  in  the  clinical  pic- 
ture. They  begin  usually  3  to  4  hours  after  a  meal,  therefore  when  the 
chief  bulk  of  the  acid  food  mass  is  passing  into  the  duodenum,  in  contrast 
to  the  cardialgias  of  gastric  ulcer  and  acute  catarrh  which  appear  soon 
after  the  intake  of  food.  Owing  to  the  active  peristalsis  of  the  biliary 
passages,  the  stone  is  caught  in  the  neck  of  the  gall-bladder,  and  is  thus 
forced  further  into  the  cystic  duct.  When  the  spasm  of  the  musculature 
of  the  gall-bladder  ceases,  the  stone  may  regurgitate  into  the  bladder,  but, 
as  a  rule,  it  is  carried  onward  until  it  finally  reaches  the  duodenal  mouth 
of  the  choledochus,  and,  eventually,  the  intestine.  This  transit  of  the 
stone  from  the  gall-bladder  to  the  duodenum  in  typical  cholelithiasis 
usually  runs  its  course  under  the  well-known  picture  of  gall-stone  colic. 
The  pains  are  here  due  to  an  acute  dilatation  of  the  biliary  passages  and 
irritation  of  their  sensory  nerve  fibers,  either  by  the  stone  or  by  the  inspis- 
sation  of  bile  caused  by  the  stone,  or  also  to  an  erosion  of  the  mucous 
membrane  by  a  stone  with  sharp  edges. 

Exacerbations  of  pain  in  an  acute  irritation  of  the  biliary  passages  are 
caused  by  contractions  of  the  musculature  of  the  gall-bladder  and  of  the 
biliary  passages,  analogous  to  uterine  contractions  in  the  period  of  expul- 
sion. The  greatest  obstruction  to  the  passage  of  stones  is  formed  by  the 
narrow  cystic  duct  and  the  portio  intestinalis  of  the  choledochus. 

The  two  phases  of  pain  which  theoretically  are  said  to  occur  in  the 
passage  of  the  cystic  duct  and  of  the  duodenal  papilla  in  typical  chole- 
lithiasis, and  which  are  not  to  be  undervalued  as  diagnostic  factors  as  two 
entirely  distinct  exacerbations  of  pain  in  the  clinical  picture  of  chole- 
lithiasis as  it  has  been  described  by  some  authors,  may  occur,  but  I  have 
not  as  yet  observed  them  in  my  cases.  The  cessation  and  the  exacerba- 
tions of  pain  are  due  to  contractions,  and  I  believe  that,  analogous  to 
rapidly  succeeding  uterine  contractions,  it  is  subsequently  impossible  to 
determine  whether  the  first,  the  middle,  or  the  last  of  the  paroxysm  was 
the  most  painful.  I  also  believe  that,  in  cholelithiasis,  the  line  of  demar- 
cation between  these  two  periods  of  pain,  which  is  said  to  mark  the 
passage  of  the  stone  from  a  narrow  into  a  wider  canal,  is  more  theoretic 
than  real. 

According  to  Riedel,  the  paroxysms  of  pain  in  cholelithiasis,  also  the 
less  marked  pain  at  the  onset  of  the  attack,  are  not  to  be  attributed  to 
the  impaction  of  stone  in  the  cystic  duct  but  to  cholecystitis.  The  vis  a 
tergo,  which  forces  the  stone  into  the  cystic  duct,  is  the  pressure  of  the 
rapidly  oncoming  inflammatory  exudate  in  the  gall-bladder  (inflammatory 
dropsy  of  the  gall-bladder). 


472  GALL-STONES 

Riedel  even  attributes  the  colics  which  recur  after  the  impaction  of 
the  stone  to  renewed  inflammation  of  the  gall-bladder. 

The  attacks  of  colic  which  accompany  lithogenous  closure  of  the  cystic 
duct  are  designated  by  Riedel  as  ineffective  if  the  stone  does  not  pass  the 
cystic  duct,  and  are  in  contrast  to  effectual  colic  in  which  the  stone,  after 
having  passed  the  cystic  duct,  enters  the  common  duct,  and  finally  reaches 
the  duodenum. 

Similarly,  Eiedel  considers  the  attacks  of  colic  including  the  jaundice 
which  appears  after  the  stone  has  reached  the  supraduodenal  portions  of 
the  choledochus  without  occluding  them  and  without  producing  stasis  of 
bile,  to  be  caused  by  a  sudden  inflammatory  reaction  of  the  mucous  mem- 
brane to  the  foreign  body. 

We  see,  therefore,  that  even  the  mechanism  of  gall-stone  colic  is  sus- 
ceptible of  different  explanations. 

In  cases  of  cholelithiasis  in  which  the  colic  manifests  itself  only  by 
gastric  spasm,  vomiting  and  sensitiveness  to  pressure  in  the  region  of  the 
gall-bladder,  the  exacerbations  of  pain  upon  movement  in  opposition  to 
pain  of  other  origin  may  have  diagnostic  importance. 

A  patient  in  the  Clinic  with  cholelithiasis  complained  of  exacerbations 
of  pain  when  riding  in  poorly  paved  streets,  and  when  jolting  during  the 
drive  to  the  hospital,  this  being  analogous  to  the  onset  of  the  pain  in 
patients  with  stone  in  the  bladder;  another  patient,  who  besides  sensitive- 
ness of  the  gall-bladder  upon  pressure  also  had  friction  sounds  in  the  same 
region,  remarked  that  upon  using  the  right  foot  in  jumping  the  pain  in 
the  gall-bladder  region  and  above  the  right  Poupart's  ligament  was  par- 
ticularly severe.  Upon  jumping  on  the  left  foot  painful  sensations  were 
felt  only  in  the  gall-bladder  region,  and  this  was  the  case  in  rapid  running 
or  when  lying  upon  the  right  side.  In  ascending  a  staircase  the  pains 
were  more  severe  than  in  descending,  but  they  were  especially  severe  in 
jumping  upon  the  right  foot.  The  vertebral  column,  from  the  second 
to  the  sixth  thoracic  vertebra  inclusive,  was  painful  upon  pressure,  and 
within  this  zone  of  pain  cutaneous  hyperesthesia  was  present  and  more 
marked  upon  the  right  than  upon  the  left  side. 

The  radiation  of  the  pain  in  cholelithiasis  demands  special  notice.  In 
classical  cases,  the  pains  begin  in  the  region  of  the  gall-bladder  and 
radiate  to  the  right  shoulder.  At  the  onset  of  the  attack,  some  patients 
experience  a  peculiar  chilliness  and  a  drawing  sensation  along  the  back. 
Combined  with  this  the  region  of  the  gall-bladder  is  sensitive  to  pressure. 
In  contrast,  there  is  quite  an  array  of  cases  in  which  the  localization  of 
pain  is  an  irregular  one,  and  the  pain  radiates  toward  various  regions  of 
the  body.  The  pains  may  be  localized  immediately  below  the  xiphoid 
process  witliout  radiating  toward  the  hypochondriac  region,  and  without 
increasing  upon  pressure.  Confusion  with  pretuberculous  gastralgias,  dys- 
])('psia.  \ilcer  and  cancer  of  the  stomach,  and  gastric  crises  is  therefore 
possible. 


SYMPTOMATOLOGY  473 

Sometimes  the  pains  are  localized  in  the  breast,  in  the  thorax,  in  the 
esophagus,  sometimes  in  the  region  of  the  mamma,  so  that  the  patients 
believe  they  are  suffering  from  cancer  of  the  breast.  When  the  pain 
radiates  to  the  abdomen,  particularly  around  the  navel,  intestinal  colic 
and  enteralgia  are  simulated.  The  diagnosis  between  saturnine  colic  and 
gall-stone  colic  may,  under  some  circumstances,  cause  difficulty,  as  in  a 
case  which  came  under  my  notice,  occurring  in  a  worker  in  artificial 
flowers;  the  patient  simultaneously  showed  a  lead  line  and  mild  jaundice. 
In  women,  affections  of  the  genitalia,  metritis,  parametritis  and  the  like 
are  suggested  to  us,  all  the  more  so  as  gall-stone  colic  sometimes  appears 
during  menstruation.  Frequently  appendicitis  comes  into  consideration, 
particularly  if  the  vermiform  process  is  bent  upward  or  is  even  adherent 
to  the  gall-bladder. 

The  pains  are  stabbing  or  tearing ;  sometimes  there  is  a  girdle  sensation. 
They  may  also  wander  with  a  change  of  position.  The  colicky  pains  in 
the  right  hvpochondrium  may  be  quite  transitory  or  may  last  for  several 
days.  Radiation  to  the  back  or  to  the  lumbar  region,  as  occurs  in  carci- 
nomata  of  the  pancreas,  in  ulcer  of  the  posterior  wall  of  the  stomach,  in 
carcinoma  of  the  stomach  with  metastases  of  the  retroperitoneal  glands, 
and  in  ulcer  and  carcinoma  of  the  duodenum,  is  also  observed  in  rare 
cases  of  cholelithiasis.  In  this  affection  the  sensitiveness  of  the  lumbar 
and  dorsal  vertebrae  to  pressure  and  to  percussion  is  similar  to  that  ob- 
served in  ulcer  of  the  stomach.  But  pain  upon  tapping  the  vertebra  with 
the  fingers  appears  to  be  more  readily  induced  in  gall-stone  disease.  In 
a -patient,  aged  68,  added  to  the  typical  hepatic  colic  were  burning  pains 
radiating  into  the  lumbar  region  and  the  region  of  the  urinary  bladder, 
with  strangury  and  the  discharge  of  dark  urine  depositing  a  profuse,  red 
sediment.  The  patient  suffered  formerly  from  rheumatism  of  the  joints 
of  the  hand  and  of  the  ankle-joints. 

[Tenderness  on  palpation  in  the  region  of  the  gall-bladder,  due  to 
cholelithiasis  or  to  cholecystitis,  is  characterized  by  a  radiation  of  pain 
to  the  epigastrium.  This  fact  I  have  observed  in  my  own  ease  and  in 
many  patients.  Tenderness  upon  palpation  in  the  right  hypochondrium 
due  to  other  causes  may  radiate  or  may  not,  but  is  not  felt  in  the  epi- 
gastrium.— Ed.] 

In  such  cases,  particularly  if  jaundice  is  absent,  gall-stone  colic  is  apt 
to  be  confounded  with  renal  colic. 

Irradiation  of  pain  to  the  breast  may  be  confounded  with  pleurodynia, 
rheumatism  and  intercostal  neuralgia. 

In  the  differential  diagnosis  of  gall-stone  colic  and  nervous  hepatic 
colic,  Th.  Fuchs  remarks  tersely  that  nervous  hepatic  colic  is  invariably 
aggravated  by  a  Carlsbad  treatment.  I  have  not  as  yet  seen  such  an 
instance.  The  majority  of  cases  which,  upon  superficial  investigation,  were 
supposed  to  be  hepatic  colic,  proved  later  to  be  intercostal  neuralgia.    Some 


474  GALIr-STONES 

cases,  too,  of  hysterical  pseudo-appendicitis  were  found  upon  minute  in- 
vestigation to  be  nothing  more  than  neuralgia  of  the  12th  intercostal  nerve 
and  its  ramus  perforans  anterior.  In  such  cases  the  painfulness  of  the 
vertebral  and  lateral  pressure  points,  as  well  as  the  presence  of  other 
nervous  symptoms,  and  the  hysterical  stigmata  are  decisive. 

In  those  cases  in  which  the  pain  radiates  toward  the  cardiac  region  and 
toward  the  left  arm,  the  diagnosis  may  become  very  perplexing  and  even 
impossible.  I  observed  a  case  of  this  radiation  of  the  pain  in  a  patient 
about  50  years  of  age,  who,  for  some  years,  suffered  from  slight  paroxysmal 
glycosuria,  uraturia  and  oxaluria.  Suddenly  the  pain  appeared  in  the 
gall-bladder  and  thence  radiated,  the  amount  of  sugar  in  the  urine  was 
increased  to  4.5  per  cent.,  the  pulse  rate  declined  to  45.  Cardiac  exam- 
ination was  negative  except  for  a  moderate  accentuation  of  the  second 
aortic  sound.  The  diagnosis  of  competent  physicians  varied  between  angina 
pectoris,  as  a  consequence  of  sclerosis  of  the  coronary  arteries,  and  chole- 
lithiasis. The  patient  consulted  me  several  months  after  the  attack,  and 
I  made  a  diagnosis  of  gall-stones,  chiefly  for  the  reason  that  the  gall- 
bladder was  sensitive  upon  pressure,  that  the  patient  showed  xanthomata 
bilaterally  upon  the  eyelids,  and  because  the  glycosuria  which  had  been 
observed  after  the  attack  but  had  now  improved  so  that  only  traces  of 
sugar  were  present  could  be  best  reconciled  with  the  diagnosis  of  chole- 
lithiasis. A  marked  increase  in  the  excretion  of  sugar  in  angina  pectoris 
of  the  diabetic  is  unknown  to  me. 

In  contrast  to  this  I  remember  a  case  in  Bamberger's  Clinic,  occurring 
in  a  woman,  aged  35,  who  suffered  from  aortic  insufficiency  with  coronary 
angina  (angina  pectoris).  After  such  an  attack,  which  ran  its  course 
with  vomiting  and  slight  jaundice,  sensitiveness  upon  pressure  over  the 
liver  appeared.  The  diagnosis  was  insufficiency  of  the  aortic  valve,  sclerosis 
of  the  coronary  arteries,  cholelithiasis.  The  patient  died  soon  afterward 
during  an  attack;  the  autopsy  showed  insufficiency  of  the  aorta,  narrowing 
of  the  coronary  arteries,  but  no  gall-stones. 

These  two  cases  prove  that  we  may  meet  with  the  serious  dilemma  of 
being  doubtful  whether  angina  pectoris  or  cholelithiasis  is  present,  and  in 
this  case  every  objective  sign  which  may  be  of.  importance  in  the  differential 
diagnosis  between  these  affections  must  be  minutely  investigated. 

Colic-like  intestinal  pains  in  the  hypochondrium  and  right  hypogas- 
trium,  with  meteorism  and  constipation,  may  occur  in  cholelithiasis  and 
be  due  to  adhesion  of  the  gall-bladder  to  the  transverse  and  ascending 
colon.  The  development  of  adhesions  of  this  kind  is  especially  favored 
by  a  pendulous  belly  and  hepatoptosis.  Tearing  and  drawing  pains  in 
the  hepatic  region  before  each  movement  of  the  bowel,  and  pain  radiating 
to  the  ri2:ht  shoulder,  were  observed  by  Kelling  in  a  case  of  cholelithiasis 
in  which  the  transverse  colon  formed  adhesions  with  the  border  of  the 
liver.     After  breaking  up  the  adhesions,  the  pains  disappeared. 


SYMPTOMATOLOGY  475 

Typical  attacks  of  colic  with  chronic  jaundice  may  be  due  to  simple 
adhesions  without  gall-stones.  In  such  a  case,  reported  by  Leichtenstern, 
the  entire  gall-bladder  was  atrophic,  and  firmly  adherent  to  the  surround- 
ing tissues ;  no  stones  were  present,  neither  in  the  cystic  nor  in  the  common 
duct.  The  adhesions  were  broken  up,  the  jaundice  disappeared  soon  after 
the  operation,  and  the  patient  was  completely  cured. 

Unlike  many  forms  of  pain  arising  in  saturnine  colic,  the  pain  is  usually 
unrelieved  by  pressure.  Sometimes  there  is  amelioration  after  the  eructa- 
tion of  gas  or  after  the  passage  of  flatus  and  feces.  Such  cases  may  be 
confounded  with  hepatic  colic  and  flatulent  colic. 

In  the  majority  of  cases  the  ingestion  of  food  and  fluid  does  not  specially 
influenci'  the  pain.  Though  it  sometimes  happens  in  gaU-stones  that  the 
attack  of  pain  develops  immediately  after  the  intake  of  food,  and  errone- 
ously leads  to  the  diagnosis  of  ulcer  of  the  stomach,  and  although,  on 
the  other  hand,  in  the  case  of  an  ulcer  with  decided  secretion  of  gastric 
juice  and  hyperchloria,  not  rarely  the  pain  ceases  after  the  ingestion  of 
food,  whereby  the  HCl  is  combined,  yet  the  influence  of  the  character 
of  the  food  and  the  fluid  ingested  must  not  be  undervalued.  Patients 
who  formerly  experienced  no  difficulty  in  taking  food  which  was  highly 
spiced  and  seasoned  now  find  themselves  unable  to  partake  of  this  with- 
out severe  gastric  pain;  this  circumstance,  in  a  given  case  in  which  the 
diagnosis  hinges  between  ulcer  and  cholelithiasis,  decides  us  in  favor  of 
ulcer,  as  in  a  case  I  observed,  which,  by  the  later  occurrence  of  hematemesis, 
proved  to  be  ulcer.  The  pain  is  sometimes  augmented  after  drinking 
sour  wine,  and  this  may,  under  some  circumstances,  favor  ulcer,  while 
a  patient  with  gall-stone,  who  was  known  to  me,  after  taking  quite  a 
quantity  of  wine,  noted  amelioration  of  her  pains. 

Gall-stone  patients  can  sometimes  digest  heavy  and  irritating  foods  very 
well,  but  there  may  be  idiosyncrasies  for  certain  foods.  A  patient  whom 
I  knew,  according  to  his  account,  invariably  had  an  attack  of  gall-stone 
colic  after  eating  fish  with  mayonnaise;  some  drugs,  pepsin  and  hydro- 
chloric acid,  administered  for  gastric  difficulty  of  doubtful  origin,  may  be 
a  guide  in  the  diagnosis  of  these  cases  which  are  so  frequent  in  practice. 
While  I  have  seen  no  noteworthy  influence  upon  the  symptoms  of  chole- 
lithiasis after  the  administration  of  pepsin  and  hydrochloric  acid,  I  saw  a 
case  in  which  this  remedy  was  given  for  cardialgia;  the  pains  increased 
and  a  few  days  after  the  use  of  the  remedy  hematemesis  occurred.  This 
observation  led  us  to  be  more  cautious  in  the  use  of  an  active  pepsin  in 
doubtful  cases;  and  it  may  be  noted  that  even  such  a  therapeutic  experi- 
ment, which  was  here  accidental,  may  be  of  value  in  those  which  are 
obscure. 

The  nocturnal  exacerbations  of  pain  which  occur  in  a  great  number 
of  cases  of  cholelithiasis  are  explained  by  Kehr  as  being  due  to  the  accu- 
mulation of  bile  in  the  gall-bladder.     In  biliary  fistula  we  observe  that 


476  GALL-STONES 

the  excretion  of  bile  during  the  day  is  very  slight,  but  it  is  profuse  during 
the  night.  "  During  the  night  when  a  person  sleeps  and  no  food  is  taken, 
bile  collects  in  the  gall-bladder."  Although  this  remark  and  explanation 
of  Kehr  are  quite  correct,  and  may  be  utilized  in  the  ditferential  diagnosis 
between  gastric  ulcer  and  cholelithiasis,  inasmuch  as  pain  from  ulcer  is 
rarely  present  in  an  empty  stomach  or  at  night,  while  gall-stone  colic 
frequently  occurs  at  night  with  an  empty  stomach,  no  absolute  proof  can 
be  attached  to  this  symptom,  the  less  so  as  pains,  particularly  at  night 
(Hesse)  have  been  observed  ip  ulcer,  as  well  as  amelioration  of  the  pain 
on  the  ingestion  of  food,  especially  when  there  is  simultaneously  existing 
hypersecretion.  The  nocturnal  appearance  of  pain  is  emphasized  in  the 
rare  syphilitic  form  of  gastric  ulcer.  • 

I  have  not  tried  the  effect  of  a  hunger  cure  carried  out  systematically 
for  several  days  in  suitable  cases  for  diagnostic  purposes,  although  it  is 
reasonable  to  assume  that  such  an  attempt  is  justified  in  complicated  cases, 
especially  when  the  question  of  operation  is  under  consideration.  A  priori, 
it  must  be  taken  for  granted  that,  for  example,  the  gastric  crises  of  the 
tabetic  .are  uninfluenced  by  such  a  hunger  cure ;  the  same  is  very  likely 
true  to  some  extent  of  pains  due  to  stone  in  the  biliary  passages,  while 
in  ulcer,  because  of  insufficient  gastric  secretion  in  the  overwhelming 
majority  of  cases,  the  pain  either  ameliorates  considerably  or  ceases 
entirely. 

The  variable  intensity  of  the  pains  in  cholelithiasis  is  not  always  in 
proportion  to  the  other  reflex  symptoms  on  the  part  of  the  stomach,  for 
example,  vomiting.  In  a  patient  observed  in  the  Clinic,  a  day  laborer, 
John  Sch.,  aged  57,  the  paroxysms  of  pain  in  the  right,  upper  abdominal 
region,  running  their  course  with  jaundice,  were  of  such  extraordinary 
severity  that  the  patient  writhed  in  bed,  moaning.  In  this  severe  paroxysm 
of  pain  which,  according  to  the  accounts  of  the  patient,  was  much  more 
severe  than  the  earlier  ones  in  which  vomiting  occurred,  symptoms  on  the 
part  of  the  stomach  were  entirely  absent. 

The  pains  which  are  due  to  pericholecystitis,  perihepatitis,  circum- 
scribed abscesses  or  rupture  into  the  peritoneum,  belong  to  the  realm 
of  peritonitis. 

It  must  not  be  forgotten  that  abdominal  pain  and  pain  in  the  right 
hypochondrium  during  menstruation  may  also  be  due  to  gall-stone  colic. 
The  same  is  also  true  in  pregnancy. 

Cases  have  been  reported  in  which,  at  the  normal  termination  of  preg- 
nancy, gall-stone  or  renal  colics  have  been  mistaken  for  labor  pains;  also 
in  childbed,  when  pains  arise  in  the  abdomen  with  vomiting,  fever,  and 
chills,  cholelithiasis  may  be  simulated.  Here  only  an  exact  history,  the 
appearance  of  pain  a  few  hours  after  meals,  the  pulse,  and  a  most  thorough 
examination  of  the  gall-bladder  region  and  the  right  hypochondrium  will 
lead  to  the  diagnosis  of  a  complicating  cholelithiasis. 


SYMPTOMATOLOGY  477 

The  differential  diagnosis  between  gall-stones  and  pancreatic  stones, 
especially  as  jaundice  may  occur  also  in  the  latter  affection,  causes  great 
perplexity. 

Simultaneous  diabetes,  or  that  occurring  in  combination  with  colic, 
fatty  stools,  azoturia,  and,  finally,  the  passage  of  stones  of  calcium  car- 
bonate and  phosphate,  are  important  diagnostic  points  of  support. 

When  tabetic  gastric  crises  and  jaundice  occur  simultaneously,  the 
diagnosis  is  sometimes  only  possible  by  the  careful  discrimination  of  the 
individual  symptoms. 

I  saw  a  patient  who  for  four  years  suffered  from  attacks  of  painVhich 
occurred  irregularly  at  intervals  of  from  three  weeks  to  three  months; 
the  patella  tendon  reflex  was  absent;  there  was  immobilitj'^  of  the  pupil. 
During  an  attack  a  year  ago  jaundice  lasted  for  two  weeks.  A  person 
suffering  from  tabes  may,  therefore,  simultaneously  have  cholelithiasis,  or, 
by  a  temporary  indigestion,  catarrhal  jaundice  may  be  superadded. 

Prior  to  this  we  have  considered  two  of  the  most  frequent  and  marked 
symptoms  of  cholelithiasis,  jaundice  and  pain.  Just  as  there  are  cases  of 
cholelithiasis  without  jaundice,  there  are  others,  with  or  without  jaundice, 
which  run  their  course  with  freedom  from  pain.  Cholelithiasis  without 
pain  is  certainly  a  very  rare  form.  Complete  but  painless  occlusion  of 
the  choledochus  by  stone  may  appear  under  the  guise  of  catarrhal  jaundice 
or  of  a  neoplasm  at  the  porta  hepatis.  In  chronic  empyema  of  the 
gall-bladder,  local  pain  may  be  very  slight  or  entirely  absent. 

In  these  indolent  forms  of  cholelithiasis,  another  element  becomes 
prominent  and  almost  substitutes  for  the  attacks  of  colic,  namely,  fever, 
which,  therefore,  may  substantively  be  of  great  diagnostic  significance. 

In  the  aged,  in  whom  attacks  of  gall-stone  colic  need  not  necessarily 
cause  serious  disturbance,  a  mere  chill  may  be  the  only  manifestation 
of  the  disease. 

In  other  cases,  chills  may  alternate  with  pain  in  the  right  hypochon- 
drium.  The  chill  may  run  its  course  with  collapse,  cyanosis  of  the  lips 
and  cold  extremities,  followed  by  fever  with  or  without  sweating.  The 
paroxysms  of  fever  in  cholelithiasis  begin,  as  a  rule,  a  few  hours  after 
eating,  therefore  in  the  evening  or  during  the  night,  in  contrast  with 
those  of  malarial  attacks. 

Even  when  the  stones  are  large  and  completely  obstruct  the  common 
duct,  this  intermittent  fever  may  dominate  the  clinical  picture.  As  an 
assistant  in  Bamberger's  Clinic,  I  once  saw  a  patient  with  obstructive 
jaundice  and  intermittent  fever,  who,  according  to  her  report,  had  never 
suffered  from  colic,  and  who,  upon  objective  examination,  showed  no  local 
sensitiveness  in  the  hepatic  region;  at  the  autopsy,  a  stone  the  size  of  a 
walnut  obstructing  the  common  duct  was  found,  while  no  signs  of  a  pre- 
ceding lithiasis  were  present  in  the  gall-bladder.  Bamberger  regarded  this 
case  as  a  secondary  gall-stone  formation  in  the  common  duct,  developed 


478  GALL-STONES     ' 

l)y  the  apposition  of  the  cholesterin  tp  a  stone  which  had  wandered  into 
the  common  duct  without  giving  rise  to  symptoms,  and  the  painlessness 
of  its  course  as  due  to  the  mucous  membrane  becoming  accustomed  to  the 
foreign  body  slowly  growing  in  situ. 

The  onset  of  the  pain  with  chills  is  important  in  the  diagnosis  between 
pjall-stone  colic  and  cardialgia  in  ulcer  of  the  stomach.  Kises  in  tempera- 
ture in  ulcer  of  the  stomach  may  be  caused  by  circumscribed  peritonitis. 
The  preceding  gastric  disturbances,  the  dependence  of  pain  upon  a  co- 
existing peritonitis,  the  absence  of  chills  will  also,  aid  in  the  diagnosis 
of  such  complicated  cases. 

Doubt  may  arise  in  the  differentiation  of  duodenal  ulcers  which  de- 
velop upon  the  basis  of  a  paroxysmal  hemoglobinuria.  An  interesting  case 
of  this  kind  was  admitted  to  the  Clinic  in  May,  1895^  with  a  diagnosis  of 
ulcer  of  the  stomach.  The  patient  was  always  well  until  July,  1892, 
when  he  was  taken  ill  after  having  been  for  two  days  previously  exceed- 
ingly pale,  and,  according  to  the  statement  of  his  wife,  the  sclera  having 
become  yellow.  During  a  journey  he  was  attacked  by  nausea,  severe 
gastric  pains,  vomiting  of  greenish  masses,  and  collapse  without  loss  of 
consciousness.  The  vomiting  was  repeated  once,  but  did  not  recur.  On 
the  other  hand  there  was  gastric  spasm,  loss  of  appetite,  acid  eructations 
and  a  feeling  of  heat;  the  bowels  were  constipated.  Helena  and  hematem- 
esis  never  occurred;  the  urine  was  blood  red  in  color.  A  few  days  after 
the  patient  had  left  his  bed,  he  completely  recovered. 

Up  to  January,  1895,  the  patient  had  three  such  attacks.  In  the  last, 
which  caused  him  to  come  to  the  Hospital,  there  was  pallor  and  loss  of 
appetite,  the  gastric  pains  recurred  and  radiated  toward  the  lumbar  region 
to  the  right  of  the  navel.  He  vomited  greenish  masses  of  an  acid  odor; 
there  was  pyrosis  and  eructation.  Acid  food  increased  the  gastric  dis- 
tress, while  the  pains  were  lessened  by  sodium  bicarbonate.  The  objective 
examination  showed  high-grade  anemia  and  a  moderate  degree  of  gastric 
dilatation.  The  majority  of  the  symptoms,  therefore,  indicated  ulcer  of 
the  stomach,  and  two  only  were  calculated  to  obscure  the  diagnosis :  On  the 
one  hand,  the  chill  which  actually  introduced  the  first  attack,  and,  on 
the  other  hand,  his  wife's  report  of  the  yellow  discoloration  of  the  sclera 
in  the  first  attack.  These  two  symptoms  favored  cholelithiasis.  Never- 
theless, our  tentative  diagnosis  was:  Ulcer  of  the  stomach. 

The  patient  left  the  Hospital.  Four  months  later  he  returned  to  the 
Clinic  with  the  same  symptoms,  and,  in  addition,  a  nephritis  and  hemo- 
globinuria. The  attack  was  introduced  by  a  chill.  Several  months  later 
the  patient  died.  The  autopsy  showed  ulcer  of  the  duodenum.  We  see, 
therefore,  that  with  the  symptom-complex  obtained  by  the  history — car- 
dialgia, chills  and  jaundice — ^instead  of  the  looked-for  gall-stones,  an  un- 
expected combination  of  two  rare  affections  prevented  a  correct  diagnosis. 
In  the  majority  of  cases,  however,  the  occurrence  of  rare  cases  of  this 


SYMPTOMATOLOGY  479 

kind  is  not  calculated  to  lessen  the  clinical  value  of  the  previously  men- 
tioned triad  of  symptoms  in  the  diagnosis  of  cholelithiasis. 

The  chills  which  accompany  fever  and  gall-stone  colic  were  formerly 
believed  to  be  reflex  and  due  to  the  influence  of  the  heat-regulating  center. 
On  this  conception  of  fever  as  a  pain  reflex,  Bamberger  chiefly  based  his 
opinion  of  the  favorable  action  of  morphin,  which,  in  some  cases,  by 
relieving  the  pain,  simultaneously  had  an  antipyretic  effect.  In  many 
other  cases,  however,  we  are  compelled  to  assume  a  pre-existing,  or  subse- 
quent, infection  of  the  biliary  passages.  This  is  true,  in  particular,  of 
those  cases  in  which  the  febrile  paroxysm  is  not  combined  with  an  attack 
of  pain,  and  even  more  so  in  those  instances  in  which  the  febrile  attack  is 
the  only  manifestation  of  cholelithiasis.  Infection  of  the  biliary  passages 
may  occur  in  various  ways,  one  of  which  is  that  the  bacteria  find  a 
passage  directly  from  the  intestine  into  the  common  duct.  If,  by  disease 
of  the  biliary  passages,  a  locus  minoris  resistentice  is  formed  for  the  en- 
trance of  bacteria,  the  latter,  on  the  other  hand,  is  favored  by  dilatation 
of  the  biliary  passages  and  the  opening  of  the  duodenal  mouth,  and  thus 
infection  with  intestinal  bacteria  takes  place.  There  is  also  the  possibility 
of  infection  with  virulent  bacteria  from  the  oral  and  pharyngeal  cavities, 
for  example,  from  tonsillar  abscesses  the  discharges  of  which  are  swallowed 
with  the  saliva.  Infection  of  the  biliary  passages  may  also  occur  via  the 
circulation  from  distant  foci  in  the  organism,  as  from  otitis  media  and 
angina  tonsillaris,  etc.,  as  is  also  assumed  to  be  the  case  in  appendicitis. 
These  manifold  sources  of  infection  also  explain  the  bacterial  polymorphic 
nature  of  infectious  cholecystitis  and  cholangitis  (bacterium  coli,  diplo- 
oocci,  streptococci,  staphylococci  and  typhoid  bacilli). 

The  attacks  of  fever  which  accompany  paroxysms  of  pain  in  chole- 
lithiasis are,  at  present,  almost  universally  referred  to  infection  of  the 
biliary  passages,  and  are  not  considered  as  reflex  fever,  as  was  formerly 
the  case.  Although  we  must  admit  the  possibility  that  a  typical  colic 
fever  in  which  chills,  fever  and  paroxysms  of  pain  go  hand  in  hand 
may  be  a  nervous  reflex  fever,  analogous  to  the  febrile  attacks  in  paroxysmal 
hemoglobinuria,  or  a  purely  toxic  fever  due  to  pyrogenous  derivatives, 
perhaps  of  hemoglobin,  nevertheless,  it  cannot  be  denied  that,  in  the  over- 
whelming majority  of  cases  of  intermittent  hepatic  fever  infectious  proc- 
esses in  the  biliary  passages  and  in  the  liver  are  the  causative  factors. 
This  is  particularly  true  of  the  cases  in  which  fever  appears  in  a  substantive 
form  and  independent  of  the  colicky  pain,  and  further,  of  those  cases  in 
which  there  are  objective  signs  of  a  pericholecystitis  or  perihepatitis,  and, 
finally,  when  we  have,  as  accompanying  symptoms  of  the  fever,  signs  of 
a  local  inflammation  or  infection  in  other  organs  removed  from  the  liver, 
or  in  the  blood,  as,  for  example,  enlargement  of  the  spleen,  nephritis, 
endocarditis,  pericarditis,  bacteriemia  and  septic  leukocytosis. 

There  are  many  transitional  stages  between  the  periodic  intermittent 


480  GALL-STONES 

hepatic  fever  and  the  severest  intrahepatic  infectious  processes,  hence  it  is 
clear  that  the  differential  diagnosis,  whether  intermittent  hepatic  fever, 
or  pyemic  fever  in  consequence  of  an  ulceration,  or  cholangitis  which  has 
caused  abscess,  or  pylephlebitis,  can  only  be  arrived  at,  in  the  given  case, 
bv  the  most  minute  investigation  of  the  patient's  entire  condition.  Inter- 
mittent fever  in  consequence  of  cholangitis  is  not  rare  in  obstructive  jaun- 
dice. ]t  is  true  it  is  more  frequent  in  occlusion  of  the  common  duct  due 
to  stone  than,  for  example,  in  carcinoma  at  the  porta  hepatis.  It  may 
occur  in  cholelithiasis  without  jaundice  by  the  propagation  of  the  infec- 
tion from  the  gall-bladder  to  the  biliary  passages,  or,  with  an  existing 
gall-stone  formation,  in  the  branches  of  the  hepatic  duct.  Intermittent 
fever,  with  or  without  jaundice  (the  latter  of  which  so  frequently  occurs 
in  cholelithiasis  intrahepatica),  may  occasionally  cause  great  diagnostic 
perplexity  if,  after  the  gall-bladder  has  been  extirpated,  we  must  decide 
the  important  question  of  the  treatment  which  is  to  follow  (whether  a  cure 
at  Carlsbad  or  another  operation),  whether  the  stone  has  formed  in  the 
operated  stump  of  the  cystic  duct  or  in  the  branches  of  the  hepatic  duct. 
This  secondary  cholelithiasis  intrahepatica  may,  therefore,  make  the  result 
of  a  successful  extirpation  of  the  gall-bladder  illusionary,  may  prove  that 
the  intermittent  fever  existing  before  the  operation  was  the  initial  sign 
of  an  intrahepatic  gall-stone  formation,  and  will  necessitate  caution  on 
the  part  of  the  surgeon  in  the  choice  of  his  operation  (cholecystostomy, 
drainage  of  the  hepatic  duct).  In  contrast  to  diffuse  cholangitis,  which 
sometimes  runs  its  course  with  high  temperature  but  without  profound 
changes  in  the  walls  of  the  biliary  passages,  a  localized  choledochitis  from 
impaction  of  stone  with  ulceration  of  the  duodenal  portion  of  the  chole- 
dochus  may  also  be  the  cause  of  the  fever,  in  that,  from  the  point  of  the 
stone  up  to  the  diverticulum  of  Vater,  a  portion  remains  like  a  blind  sac 
communicating  with  the  duodenum  which  is  not  touched  by  bile.  In  this 
dead  angle,  similarly  as  in  the  appendix,  bacteria  may  collect  and  produce 
ulceration  with  general  sepsis.  By  a  propagation  of  the  ulcerative  process 
to  the  portal  vein,  pylephlebitis  and  pylethrombosis  may  develop.  The 
diagnosis  of  purulent  cholangitis  or  suppurative  pylephlebitis  with  ab- 
scesses of  the  liver  may  be  extremely  puzzling.  But,  in  cholangitis,  the 
individual  attacks  are  frequently  separated  by  afebrile  intervals,  and  during 
tliese  the  pulse  is  more  quiet,  and  there  is  relative  euphoria.  In  pylephle- 
bitis, on  the  other  hand,  chills  frequently  recur  several  times  a  day,  the 
thermometer  shows  steep  curves  of  abnormally  high  rise  and  subnormal 
fall.     High  pulse  rate  and  marked  collapse  point  to  pyemia. 

Furthermore,  in  pylephlebitis  diarrhea  becomes  prominent,  there  is 
marked  enlargement  of  the  spleen,  metastases  form  in  the  lungs  and  other 
portions  of  the  body,  and,  finally,  there  is,  besides,  occlusion  of  the 
portal  vein. 

Abscesses  of  the  liver  may  also  be  produced  by  actinomycosis.     We 


SYMPTOMATOLOGY  481 

observed  in  our  Clinic  a  classic  example  of  such  actinomycotic  abscess 
of  the  liver  following  appendicitis  actinomycotica  and  metastatic  miliary 
actinomycosis  of  the  lungs;  there  was  sensitiveness  of  the  liver  upon 
pressure,  chills  and  pyemic  fever. 

Intermittent  fever  is  not  always  produced  by  infections  or  purulent 
processes,  especially  in  the  biliary  passages,  the  liver,  and  the  branches 
of  the  portal  vein.  A  non-purulent  peripylephlebitis  intrahepatica  chiefly 
characterized  histologically  by  wandering  cell  infiltration  around  the  portal 
vein  branches  in  the  liver  may,  similarly,  run  its  course  with  intermittent 
fever,  as  was  proven  by  a  case  in  our  Clinic. 

The  same  is  true  of  tuberculosis  at  the  porta  hepatis,  which  may  appear 
under  the  mask  of  cholelithiasis.  In  a  servant,  aged  43,  in  whom  no 
hereditary  disease  was  evident,  and  who  was  treated  for  intermittent  fever 
and  severe  pain  in  the  hepatic  region,  sometimes  accompanied  by  chills 
and  severe  vomiting,  cholelithiasis  was  at  first  diagnosticated;  but  the 
later  course  of  the  affection,  with  increasing  emaciation,  night  sweats,  signs 
of  infiltration  at  the  apex  of  the  lung,  and  tubercle  bacilli  in  the  sputum, 
showed  the  true  nature  of  the  malady.  The  autopsy  revealed  tuberculosis 
of  the  glands  at  the  porta  hepatis,  tuberculosis  of  the  pulmonary  apices; 
no  gall-stones. 

Intermittent  fever  in  carcinoma  of  the  liver  is  not  rare.  In  the  year 
1894,  in  our  Clinic,  there  was  a  cachectic  patient  with  typical  tertian 
intermittent  fever,  in  whom,  about  midday,  rises  in  temperature  to  104° 
and  105.8°  F.,  but  without  chills  and  sweating,  recurred  regularly.  An 
examination  for  malarial  parasites  was  negative.  The  liver  was  enlarged, 
hard,  and  showed  coarse  nodules.  A  diagnosis  of  carcinoma  of  the  liver 
was  made,  and  was  confirmed  by  the  subsequent  course.  In  connection 
with  this  I  should  like  to  mention  another  case  which  soon  afterward 
presented  itself  in  the  Clinic.  This  occurred  in  a  patient  whose  liver  was 
hard  and  nodular,  the  spleen  enlarged,  and  in  whom,  besides,  there  was 
hard,  indolent,  glandular  enlargement  of  the  neck.  This  patient  also  had 
intermittent  fever.  Our  diagnosis  at  first  was  carcinoma  of  the  liver  with 
metastases  in  the  glands  of  the  neck.  As,  however,  the  affection  in  its 
progress  showed  no  conspicuously  malignant  character,  we  concluded  to 
administer  potassium  iodid,  and  to  employ  intravenous  injections  of  cor- 
rosive sublimate. 

During  this  treatment  the  enlargement  of  the  liver,  especially  its  iso- 
lated nodules,  as  well  as  the  swelling  of  the  glands  of  the  neck,  decreased 
in  size,  the  fever  disappeared,  and,  in  consequence,  we  changed  our  diag- 
nosis to  syphilis  of  the  liver  and  the  lymphatic  glands.  This  compelled 
us  to  bring  into  relation  with  each  other  the  intermittent  fever  which 
disappeared  under  antisyphilitic  treatment  and  the  underlying  process, 
syphilis. 

Moreover,  intermittent  fever  is  also  associated  with  adhesions  of  the 


482  GALL-STONES 

gall-bladder,  yet  no  stones  are  found  at  the  operation.  Gersuny  performed 
an  operation  on  the  wife  of  an  apothecary  who  had  irregularly  recurring 
colic,  chills  with  fever,  enlargement  of  the  liver,  pain  in  the  region  of  the 
gall-bladder,  splenic  tumor  and  gastric  dilatation.  He  found  the  gall- 
bladder contracted,  no  cholangitis,  no  stone;  but  the  gall-bladder  was 
adherent  to  the  duodenum,  and  there  was  gastric  dilatation.  After  break- 
ing up  the  adhesions  the  fever  disappeared  and  recovery  took  place.  The 
process  may,  perhaps,  have  been  due  to  retention  of  bile  in  the  adherent 
gall-bladder,  which  formed  a  favorable  culture  media  for  the  mi- 
crobes tliere  present.  By  the  succeeding  restoration  of  free  communica- 
tion between  the  gall-bladder  and  the  cystic  duct,  the  condition  was 
relieved. 

As  a  cause  of  the  development  of  intermittent  fever,  chronic  morphin- 
ism is  yet  to  be  discussed.  A  case  of  this  kind  is  known  to  me  in  a 
iiiorphin  habitue  in  whom  the  most  minute  investigation  of  the  various 
organs  revealed  no  cause  for  the  fever.  Examination  of  the  urine  showed 
acetone  and  a  conspicuous  increase  of  uric  acid  excretion  to  40  grams  per 
day.  In  gall-stone  patients  who,  in  consequence  of  preceding  colic,  have 
])oconie  morphin  habitues,  this  possibility  must  be  borne  in  mind,  and  an 
examination  be  made  of  the  urine,  which,  in  hepatic  fever,  shows  a  decrease 
in  the  excretion  of  nitrogen. 

The  foregoing  remarks  prove  conclusively  the  many-sided  nature  of 
intermittent  fever,  and  how  easily  errors  in  diagnosis  may  be  made  in 
cases  of  cholelithiasis  without  pain  or  jaundice. 

All  infections  of  the  biliary  passages  are  not  accompanied  by  fever. 
Even  severe  cholangitis  and  empyema  of  the  gall-bladder  with  threatening 
perforation  may  run  their  course  entirely  without  fever  and  pain,  particu- 
larly in  marantic  individuals  and  diabetics.  Hypothermia  is  observed  par- 
ticularly in  infections  by  the  bacterium  coli. 

If,  after  describing  the  cardinal  symptoms  of  gall-stone  disease,  either 
isolated  or  combined  with  other  affections,  we  proceed  to  the  examination 
of  the  different  organs  of  the  body,  we  will  in  some  cases  meet  with  a 
symptom  which  is  noteworthy  in  prognosis  as  well  as  in  regard  to  the 
proper  therapy  to  be  employed.  Epistaxis  may  be  the  first  signal  of  the 
hemorrhagic  diathesis  due  to  the  obstruction  of  bile  excretion,  but  it  may 
also  occur  in  cases  in  which  there  is  no  occlusion  of  the  choledochus  with 
complete  stasis  of  bile  and  jaundice  as  a  consequence  of  severe  damage  to 
the  hepatic  cells,  and  thus  complicate  the  clinical  picture.  Acute,  subacute 
and  chronic  infections  of  the  biliary  passages  and,  particularly,  secondary 
cirrhosis,  may  cause  a  peculiar  predisposition  to  hemorrhage  which  in- 
fluences the  clinical  picture  in  a  dangerous  manner,  and  may  be  especially 
troublesome  to  the  surgeon.  Even  after  jaundice  of  brief  duration  hemor- 
rhages ajipear  from  the  skin,  the  gums,  the  nose,  the  uterus,  the  urinary 
passages,  the  stomach  and  the  intestines,  which,  inasmuch  as  the  wound 


SYMPTOMATOLOGY  483 

produced  by  the  operation  shows  no  cause  for  the  condition,  necessitates 
the  utmost  caution  on  the  part  of  the  surgeon. 

A  dancer,  aged  22,  was  admitted  to  the  Hospital — special  stress  must 
be  laid  upon  her  occupation,  since,  in  the  etiology  of  cholelithiasis,  a 
sedentary  habit  is  considered  to  be  predisposing — after  an  undoubted  chole- 
lithiasis with  alternating  jaundice  which  had  existed  for  seven  weeks; 
there  were  cutaneous  hemorrhages  upon  the  hands  and  feet,  and  after 
scratching  off  a  wart  ad  nates,  a  hemorrhage  occurred  which  could  scarcely 
be  controlled. 

In  an  examination  of  the  neck,  the  jugular  glands  must  not  be  over- 
looked since  tAey  are  of  importance  in  the  differential  diagnosis  of  car- 
cinomata  of  the  biliary  passages  and  of  the  liver.  It  is  sometimes 
advantageous  to  have  the  patient  cough  during  the  examination.  Deeply 
situated,  isolated  glands  behind  the  clavicle  become  prominent  during 
coughing,  and  are  thus  made  susceptible  to  palpation. 

Examination  of  the  lungs  is  important  inasmuch  as,  according  to  some 
authors,  tuberculosis  predisposes  to  the  formation  of  gall-stones.  In  my 
experience,  however,  clinically  well-developed  cholelithiasis,  as  well  as  cho- 
langitis, is  an  extremely  rare  complication  of  tuberculosis,  and  this  is  all 
the  more  remarkable  as,  in  ulcerative  phthisis,  bacteriemia  (streptococcia 
and  staphylococcia),  which  is  so  very  frequent,  furnishes  a  fertile  soil  for 
infection  of  the  biliary  passages.  I  have  found,  on  the  contrary,  that  the 
tubercular  have  a  certain  immunity  from  gall-stone  formation,  and  patients 
with  cholelithiasis  from  tuberculosis. 

Attacks  of  cough  occurring  in  paroxysms  (the  tussis  hepatica  of  the 
older  authors)  followed  by  aphonia,  hoarseness  and  severe  pains  in  the 
back  of  the  neck,  have  been  observed  in  cholelithiasis  and  have  disappeared 
after  operative  removal  of  the  stones. 

Dyspnea,  sensations  of  fear,  even  attacks  of  suffocation,  also  occur  as 
symptoms  of  gall-stone  colic,  and  may  be  due  to  reflex  spasm  of  the 
muscles  of  respiration. 

Immotility  of  diaphragmatic  respiration,  therefore,  the  costal  respira- 
tion type,  in  adults,  particularly  in  men,  is  an  important  symptom  in 
peritonitis,  in  contrast  to  the  respiration  in  gall-stone  colic;  while  small 
children  who,  as  is  well  known,  normally  almost  exclusively  show  the 
abdominal  type  of  respiration,  present  the  costal  type  of  respiration,  and 
this  symptom  is  an  important  sign  in  the  differential  diagnosis  of  infantile 
gall-stone  colic,  in  opposition  to  intestinal  colic  of  other  origin.  Sensitive- 
ness to  pressure  over  the  gall-bladder,  especially  when  in  a  warm  bath, 
and  muscular  rigidity  on  the  right  side  of  the  abdomen,  combined  with 
the  preceding  symptoms,  form  additional  proof.  Cholelithiasis  under 
twelve  years  of  age,  and  even  under  fifteen  years,  belongs,  in  fact,  among 
the  greatest  rarities. 

In  children,  provided  Jaundice  does  not  point  to  the  possibility  of  gall- 


484  GALL-STONES 

stones,  epigastric  pain,  vomiting  and  convulsions  are  many-sided  symptoms, 
and  this  doubtless  will  sufficiently  explain  the  fact  that  the  disease  is 
usually  overlooked  in  early  childhood. 

In  the  aged,  as  the  result  of  gall-stone  colic,  which,  as  has  been  stated, 
sometimes  manifests  itself  only  by  chilliness  and  fever,  a  congestion  of 
the  lower  lobe  of  the  right  lung  is  observed,  which,  when  combined  with 
cough,  muco-viscid  expectoration  and  numerous  crepitant  and  fine  moist 
rales  at  the  base  of  the  right  lung,  also  with  fever  and  pain,  may  be 
mistaken  for  pneumonia.  This  hyperemia  of  the  lungs,  appearing  under 
the  guise  of  pneumonia,  may  clear  up  in  two  or  three  days  after  the 
rudimentary  attack  of  colic.  It  may,  however,  also  form  the  starting 
point  of  a  secondary  pneumonia.  In  cases  in  which  cholelithiasis,  by  in- 
fection of  the  biliary  passages,  has  led  to  suppurative  cholangitis,  biliary 
abscesses  of  the  liver,  or  subphrenic  suppuration,  important  diagnostic 
processes  may  take  place  at  the  base  of  the  right  lung:  unilateral,  high 
position  of  the  diaphragm  with  retraction  of  the  lung,  pleurisy,  symptoms 
of  perforation,  fetor  of  the  respired  air  and,  a  few  days  prior  to  rupture, 
distressing  cough  with  purulent,  bile-stained  expectoration  and  rales  at 
the  base  of  the  right  lung.  Nevertheless,  rupture  of  the  diaphragm  and 
pleura,  as  well  as  subphrenic  abscess,  with  the  formation  of  a  pyopneumo- 
thorax, supraphrenicus  and  subphrenicus,  are  very  rare  episodes  in  the 
course  of  infectious  cholelithiasis,  in  contrast  to  echinococcus  of  the  liver, 
which,  as  is  well  known,  frequently  forces  a  passage  into  the  lungs  by 
perforation  of  the  biliary  channels  and  of  the  diaphragm. 

In  the  course  of  cholelithiasis  symptoms  on  the  part  of  the  heart  and 
circulation  may  dominate  the  situation  to  such  an  extent  that,  in  some 
cases,  a  gall-stone  patient  resembles  one  aifected  by  cardiac  disease.  Col- 
lapse, cyanosis  of  the  lips,  and  cold  extremities  during  the  paroxysms  of 
pain  are  observed  in  nervous,  hysterical  individuals,  particularly  in  women, 
and  may  appear  also  without  chill  and  fever  as  a  vasomotor  reflex,  or  in 
old  persons  as  signs  of  cardiac  asthenia.  Cardiac  arrhythmia,  dyspnea, 
gallop  rhythm,  with  accentuation  of  the  second  pulmonary  sound,  dilata- 
tion of  the  right  heart,  and  displacement  of  the  apex  beat,  relative  tri- 
cuspid insufficiency,  pulsation  of  the  jugular  vein  with  cyanosis,  and  a 
small,  easily  compressible  pulse  may  occur  in  consequence  of  an  attack 
of  colic  and  be  a  serious  symptom-complex  in  a  prognostic  sense;  with 
an  intact  myocardium  these  are  considered  as  reflex,  transmitted  by  irri- 
tation from  the  sensory  nerves  of  the  biliary  passages  to  the  pneumogastric 
nerves  and  to  the  sympathetic  plexus  of  the  cardiac  fibers. 

The  p^ilse  in  gall-stone  colic  is  of  moderate  intensity,  either  normal  or 
slow.  Bamberger  found  it  slow  and  small  in  the  majority  of  cases;  in 
others  again  it  is  small  and  frequent,  especially  when  there  is  a  simultaneous 
inflammation  of  the  gall-bladder  and  biliary  channels.  A  small,  frequent 
pulse,  naturally,  may  also  occur  in  general  peritonitis  and  in  gastric  and 


SYMPTOMATOLOGY  485 

intestinal  hemorrhages,  as  well  as  in  septic  and  pyemic  fever  in  gall-stone 
patients,  and  during  the  apyrexia,  especially  if  an  infection  from  the  biliary 
passages  and  the  liver  localizes  itself  in  the  heart  as  a  pericarditis,  endo- 
carditis or  myocarditis. 

The  tension  and  configuration  of  the  abdomen  may  furnish  objective 
signs  of  importance  in  the  diagnosis,  particularly  as  regards  the  compli- 
cations of  cholelithiasis.  Contraction  of  the  abdominal  muscles,  mainly 
upon  the  right  side,  which  the  French  designate  as  defense  musculaire, 
frequently  accompanies  the  attack  of  colic;  but  there  are  also  cases  in 
which  the  abdomen,  in  spite  of  severe  pain,  is  everywhere  soft,  sometimes 
even  showing  meteorism.  Meteorism  which  occurs  in  Jaundice  in  conse- 
quence of  intestinal  acholia,  or  with  a  co-existing  peritonitis  in  an  ob- 
struction of  the  intestine  by  stones,  or  in  intestinal  stenosis  in  consequence 
of  adhesions,  is  easy  to  explain.  Ascites  may  occur  in  cholelithiasis  by 
occlusion  of  the  portal  vein.  The  irritation  of  the  incarcerated  stone  in 
the  common  duct  produces  consecutive  induration  in  the  hepato-duodenal 
ligament,  and,  as  a  further  result,  thrombosis  of  the  portal  vein  and  an 
ulcerative  perforation  of  the  walls  by  which  stones  enter  its  lumen. 

In  this  group  belongs  the  case  that  is  everywhere  quoted  of  Ignatius 
de  Loyola,  in  whose  portal  vein  Realdus  Columbus  found  three  gall-stones. 
In  general,  however,  ascites  in  cholelithiasis  is  rare  in  comparison  with 
carcinoma  at  the  porta  hepatis,  which,  by  frequent  compression  of  the 
portal  vein,  as  well  as  by  secondary  carcinosis  of  the  peritoneum,  leads  to 
ascites.  This  is  particularly  true  of  the  cases  running  their  course  with 
obstructive  jaundice,  just  as  an  ascites  developing  simultaneously  with 
jaundice  almost  always  indicates  an  abdominal  neoplasm. 

In  gall-stone  patients  the  panniculus  adiposis  (subcutaneous  fat)  is 
often  markedly  developed,  particularly  in  the  abdomen,  which  naturally 
renders  the  physical  examination  difficult. 

Peter  observed,  during  the  attacks  of  colic,  a  local  rise  of  temperature 
in  the  right  hypochondrium.  The  temperature  in  this  region  may  be  as 
high  as  that  of  the  axilla,  or  exceed  it,  while,  under  normal  circumstances, 
it  is  two  to  five  degrees  lower  than  that  of  the  axillary  temperature.  In 
the  gastric  crises  of  tabes  such  a  local  hyperthermia  in  the  right  hypo- 
chondrium is  not  observed. 

In  cholelithiasis  the  liver  is  either  of  normal  size  or  enlarged,  and  this 
is  due  either  to  hyperemia,  biliary  stasis,  abscess  formation,  or  secondary 
carcinomatosis.  In  cases  in  which  cholelithiasis  occurs  in  cardiac  patients, 
according  to  my  experience  a  very  frequent  combination,  the  diagnosis  of 
acute  enlargement  of  the  liver  may  cause  perplexity,  and  the  disease  may 
either  be  attributed  to  gall-stone  affection  or  be  considered  as  acute  stasis 
hyperemia.  The  pain  may  be  due  to  the  gall-stone  or  to  tension  of  the 
capsule  of  the  liver.  I  remember  such  a  case  of  cholelithiasis  in  a  patient 
suffering  from  mitral  insufficiency  in  which  at  first  I  wavered  in  the 


486  GALL-STONES 

diagnosis  and  was  in  doubt  as  to  the  therapy  to  be  instituted.  Digitalis 
was  without  effect,  but  a  carefully  conducted  treatment  at  Carlsbad  caused 
the  swelling  and  painfulness  of  the  liver  to  disappear.  The  diagnosis  of 
cholelithiasis  w^as  confirmed  by  the  passage  of  small  stones. 

Enlargement  of  the  liver,  which  is  frequently  observed  in  patients  with 
gall-stones  without  jaundice,  may  be  due  to  parenchymatous  swelling  or 
simultaneously  active  hyperemia  of  the  organ,  and  this  is,  in  fact,  the  view 
of  French  clinicians  {congestion  hepatique). 

If  to  the  cholecystitis  calculosa  an  infectious  cholangitis  be  added,  the 
latter  sufficiently  explains  the  enlargement  of  the  liver.  There  are,  how- 
ever, cases  characterized  by  irregular  fever,  intermittent  enlargement  of 
the  liver  with  sensitiveness  upon  pressure,  yet  without  well-developed  colic 
or  jaundice.  This  rapid  increase  in  the  volume  of  the  liver  can  hardly 
be  explained  except  by  the  existence  of  acute  hyperemia.  This  is  illus- 
trated by  a  case  known  to  me  in  which,  at  the  onset,  a  diagnosis  was  made 
of  infiltrating  carcinoma  of  the  liver;  but  the  rapid  decrease  in  the  size  of 
the  organ  and  the  absence  of  pain  scarcely  permitted  a  different  interpreta- 
tion than  that  of  cholelithiasis  intrahepatica. 

Diffused  pain  in  the  enlarged  liver,  the  symptoms  otherwise  being 
]\vemic,  points  to  suppurative  cholangitis,  while  a  local  sensitiveness  to 
l)ressure  outside  the  gall-bladder  region,  particularly  when  the  pain  radi- 
ates to  the  right  shoulder,  is  found  in  abscess. 

An  enlargement  of  the  liver  with  an  induration  hard  as  wood,  chiefly 
in  the  region  of  the  incisura,  points  to  a  carcinoma  of  the  gall-bladder 
which  has  proliferated  into  the  liver;  particularly  when  cirrhosis  is  ex- 
cluded and  enlargement  of  the  spleen  is  absent. 

Elongation  of  the  suspensory  ligament  in  consequence  of  extreme  dila- 
tation of  the  gall-bladder,  especially  when  hepatoptosis  already  exists,  may 
jiroduce  a  wandering  liver  showing  extraordinary  power  of  motion.  Peri- 
Jirpatitis  in  cholelithiasis  demands  especial  attention.  In  a  case  observed 
in  the  Clinic,  a  shoemaker,  aged  53,  had  intermittent,  irregular  fever  with 
chills,  rises  in  temperature  above  102.2°  F.  combined  with  colic-like  pains 
in  the  liver,  a  conspicuously  rapid  pulse  even  in  the  afebrile  and  painless 
intervals,  varying  jaundice,  with  only  occasionally  bile-stained  stools;  dis- 
till )ut('d  perihepatitis,  manifesting  itself  over  the  whole  extent  of  the  liver 
by  friction  sounds,  was  the  dominant  feature  of  the  clinical  picture.  The 
fiutopsy  showed  obstruction  of  the  choledochus  due  to  stone,  dilatation  of 
tlic  up])er  portion  of  the  same,  of  the  hepatic  duct,  and  of  the  bile  ducts 
of  tho  liver,  ulceration  of  the  wall  of  the  common  bile  duct,  and  the  forma- 
tion of  multiple  abscesses  from  the  size  of  a  pea  to  the  size  of  a  bean, 
containing  pus,  mostly  grayish  yellow,  but  still  bile-stained,  and  the  walls 
of  which  consisted  of  discolored  hepatic  tissue.  In  regard  to  the  auscul- 
tatory findings  during  life,  such  a  general  perihepatitis,  if  accompanied 
1)}-  other  severe  symptoms,  must  awaken  suspicion  that  in  the  interior  of 


SYMPTOMATOLOGY  487 

the  liver  a  severe  infection  of  the  biliary  passages  has  taken  place  with 
the  formation  of  abscesses. 

Compression  of  the  hepatic  artery  may  produce  aneurysm.  Such  a  case 
was  observed  by  Schmidt.  Here  death  occurred  with  the  symptoms  of  fatal 
gastric  and  intestinal  hemorrhage ;  the  gall-bladder,  filled  with  stones,  com- 
municated with  the  aneurysm. 

The  circumstance  that  aneurysms  of  the  hepatic  region  sometimes  pro- 
duce murmurs  reminds  us  again  that  auscultation  of  this  region  should 
not  be  neglected. 

In  examination  of  the  liver  the  first  point  of  attack  is,  naturally,  the 
breeding  place  of  gall-stones — the  gall-bladder.  If  this  organ,  at  the  be- 
ginning of  the  attack,  contracts  about  its  fluid  or  solid  contents,  and 
provided  the  abdominal  muscles  are  not  too  tense,  it  is  found  as  a  globular, 
sometimes  fluctuating,  tumor  which  may  be  palpated  through  the  abdom- 
inal wall.  Some  patients  themselves  note  the  intermittent  contractions 
of  the  gall-bladder,  and  in  their  history  report  this  to  be  as  though  a 
tumor  were  being  inflated  in  the  right  hypochondrium,  but  after  cessation 
of  the  pain  this  disappears. 

These  sensations  of  the  patients  are  very  difficult  to  explain,  as  the 
intermittent  swelling  in  the  right  hypochondrium  may  also  be  due  to  an 
accompanying  acute  enlargement  of  the  liver.  The  contractions  of  the 
gall-bladder  may  be  extraordinarily  severe.  In  the  case  of  a  man  who 
succumbed  to  reflex  spasms  during  an  attack,  Gerhardt  found  impacted  at 
the  entrance  of  the  cystic  duct  a  large  stone,  splinters  of  which  had  broken 
off  from  the  anterior  end,  and  had  penetrated  the  mucous  membrane.  The 
gall-bladder  tumor  moves  upon  inspiration,  and  is  not  fixed  upon  expira- 
tion, which  is  explained  by  its  direct  connection  with  the  liver. 

The  lateral^  pendulum-lihe,  displaceability  of  the  tumor  is  important 
in  the  differential  diagnosis  of  tumors  of  the  gall-bladder  and  of  the  kidney. 
In  congenital  elongation  of  the  cystic  duct  the  tumor  may  be  very  movable. 
Such  a  gall-bladder,  displaced  and  filled  with  stones,  and  very  painful, 
may  be  mistaken  for  wandering  kidney. 

In  a  case  of  Fournier's  which  occurred  in  a  young  woman,  a  diagnosis 
was  made  of  myelitis,  neuralgia,  abscess  of  the  liver  and  floating  kidney, 
but,  over  the  right  kidney,  an  irregular  yellowish  tumor  the  size  of  an 
orange  was  found,  which  was  formed  by  the  gall-bladder  filled  with  stones. 
The  hypertrophic  ductus  choledochus  and  cystic  duct  had  a  length  of  from 
15-25  cm.,  which  explains  the  dislocation  of  the  gall-bladder.  But  the 
tumor  may  also  be  immobile,  and  adhere  to  the  convex  surface  of  the  liver, 
which,  in  certain  cases,  may  lead  to  the  assumption  of  hepatic  echinococcus 
and  abscess. 

A  tumor  of  the  gall-bladder,  which  is  distended  in  consequence  of 
closure  of  the  cystic  duct,  cannot,  naturally,  become  smaller  by  manual 
compression.     If,  however,  the  obstruction  in  the  cystic  duct  can  be  over- 


488  GALL-STONES 

come  by  this  manipulation,  a  decrease  in  the  size  of  the  tumor  may  be 
brought  about.  A  few  instances  of  a  gall-bladder  of  this  kind,  which  may 
be  expressed  by  paralysis  or  atrophy  of  the  musculature,  have  been  ob- 
served. Great  distention  of  the  gall-bladder  may,  in  rare  cases,  produce 
])ermancnt  jaundice  by  compression  of  the  hepatic  or  common  gall-ducts. 
In  lithogenous  or  cicatricial  closure  of  the  cystic  duct  the  behavior  of 
the  gall-bladder  depends,  in  the  main,  upon  the  texture  of  its  mucous 
membrane.  If  the  mucous  membrane  remains  intact,  secretion  continues, 
and  dropsy  of  the  gall-hladder  develops.  In  the  opposite  case,  with  marked 
damage  of  the  mucous  membrane  the  gall-bladder  is  obliterated,  and  be- 
comes adherent  to  its  surroundings.  Stones  may  thus  become  encapsulated 
in  the  gall-bladder  and  form  a  harmless  caput  mortuum,  as,  for  instance, 
an  encapsulated  bullet  after  a  gun-shot  wound.  A  gall-bladder  of  this 
kind  filled  with  stones  may  sometimes  be  felt  as  a  hard  body  in  the  in- 
cisura  hepatis.  Therefore,  a  lithogenous  closure  of  the  cystic  duct  is  an 
important  condition,  especially  for  the  surgeon,  who  most  frequently  deals 
with  such  adherent  gall-bladders,  less  so  for  the  internal  clinician,  who 
looks  upon  obliteration  of  the  gall-bladder  and  encapsulation  of  the  stones 
as  a  favorable  conclusion  of  irregular  cholelithiasis. 

In  lithogenous  occlusion  of  the  common  gall-duct  dilatation  of  the  gall- 
bladder is  very  rarely  found;  usually  it  follows  a  preceding  cholecystitis, 
while  in  carcinomatous  compression  or  obstruction  of  the  choledochus 
(excepting  lithogenous  choledochus  cancer)  distention  of  the  gall-bladder 
is  the  rule.  To  this  rule,  which  was  established  by  Courvoisier,  there  are, 
however,  many  exceptions  in  either  direction  if  we  bear  in  mind  that 
the  condition  of  the  gall-bladder  depends,  in  the  main,  upon  the  extent 
of  the  mucous  membrane  lesion. 

Impermeability  of  the  cystic  duct  may  be  due  to  a  lymph-gland  lying 
alongside  of  it,  which,  according  to  Kiedel,  may  be  palpated  at  the  operation 
as  a  small  tumor  and  may  be  confounded  with  stones  or  cicatrices. 

Acute  perforation  from  pressure  necrosis  of  the  wall  and  ulcerative 
perforations  of  the  gall-bladder  sometimes  leads  to  the  formation  of  ab- 
scesses in  the  surroundings  of  the  same,  producing  cavities,  which  are 
limited  by  the  peritoneal,  perihepatic,  and  pericystitic  tissue  formation. 
These  cavities  communicate  with  the  gall-bladder,  and  may  also  perforate 
the  abdominal  wall,  discharging  greenish  purulent  fluid,  and  frequently 
stones,  in  large  quantities.  With  an  elongated  gall-bladder,  abscesses  may 
thus  form  in  the  right  iliac  fossa.  Such  a  deeply-situated,  purulent  chole- 
cystitis may  readily  be  confounded  with  perityphlitis,  and,  inversely,  a 
vermiform  process  curving  upward,  or  even  adherent  to  the  gall-bladder 
in  the  gall-bladder  region,  may  resemble  perit3q)hlitis. 

The  tumors  of  the  gall-bladder  which  are  filled  with  stones  may  some- 
times, by  adhesion  and  displacement  of  the  omentum,  appear  to  be  hard, 
and  of  considerable  size. 


SYMPTOMATOLOGY  489 

A  hard  tumor  in  the  gall-bladder  region  may  be  formed  by  a  tongue- 
like process  of  the  liver,  if  a  corset  lobe  follows  the  direction  of  the  slowly 
enlarging  gall-bladder,  and  reaches  beyond  it.  This  so-called  Riedel's  lobe 
may  give  rise  to  difficulties  in  the  differential  diagnosis  between  chole- 
lithiasis and  syphilis  of  the  liver.  Echinococci  bordering  upon  the  portions 
of  the  liver  in  the  incisura  hepatis  (original  observation)  may  also  lead  to 
perplexity. 

An  excessive  hardness  of  the  distinctly  enlarged  and  usually  nodular 
gall-bladder,  which  is  generally  sensitive  to  pressure,  and  which  then  con- 
tinues to  the  liver  {infiltration  ligneuse  of  the  French),  points  to  carcinoma 
of  the  gall-bladder,  particularly  when  the  infiltration  of  the  gall-bladder 
is  continuous  to  the  liver.  Hard  nodules  in  the  latter  confirm  the  diagnosis. 
The  lancinating  character  of  the  pains,  meteorism,  periodic  vomiting,  pro- 
gressive jaundice  and  cachexia,  a  repugnance  to  meat  and  fatty  foods,  and 
monotonous  anorexia  Avhich  at  the  same  time  becomes  prominent,  which 
is  permanent  and  invariable,  enable  us  to  differentiate  typical  cases  of 
carcinoma  of  the  gall-bladder  from  the  lithiasis  of  old  persons  in  which 
the  appetite  may  be  capricious,  but  in  which,  in  the  majority  of  cases,  the 
painful  exacerbations  of  the  affection  leave  no  doubt  of  its  dependence 
upon  gastric  disturbance.  Yet,  even  here,  there  are  deviations  from  the 
ordinary  type,  as  in  a  case  observed  in  my  Clinic. 

Johanna  A.,  a  woman  aged  56,  was  taken  ill  with  burning  pain  in  the 
gastric  region  and  jaundice,  and  was  treated  by  her  family  physician  for 
gall-stones.  During  the  entire  course  of  the  disease  the  patient  had  a 
good  appetite,  although  it  was  somewhat  decreased.  Free  HCl  was  de- 
terminable in  the  vomitus,  pepsin  was  positive.  Fifty  per  cent,  of 
albumin  solution  was  digested.  Digestive  leukocytosis  present.  The 
steadily  growing  tumor  of  the  gall-bladder  with  increasing  jaundice 
was  shown  at  the  autopsy  to  be  due  to  an  endotheliosarcoma  of  the  gall- 
bladder. 

While  secondary  stone  formation  in  primary  lithiasis  of  the  gall-bladder 
is  very  frequent,  we  find  in  primary  cancer  of  the  gall-bladder,  provided 
necrotic  particles  form  the  basis  for  stone  formation  and  contraction  of 
the  gall-bladder  is  inhibited,  that  it  is  somewhat  rare — therefore,  in  spite  of 
biliary  stasis  and  the  presence  of  centers  of  crystallization,  no  gall-stones; 
in  the  rare  instances  of  primary  carcinoma  of  the  gall-bladder,  they  did 
not  consist  of  cholesterin  but  of  calcium  phosphate  and  carbonate. 

In  cases  that  are  difficult  of  solution,  in  which  the  diagnosis  between 
a  tumor  of  the  gall-bladder  and  one  of  the  transverse  colon  must  be  made, 
naturally,  all  of  the  manipulations  which  are  employed  in  the  differential 
diagnosis  of  abdominal  tumors,  for  example,  inflation  of  the  stomach  and 
intestines  with  air  and  with  water,  must  be  employed.  Upon  bimanual 
examination  in  the  left  lateral  position,  and  by  making  strong  pressure 
against  the  right  hypochondrium  with  the  right  hand,  we  sometimes  sue- 


490  GALL-STONES 

ceed  in  pressing  the  gall-bladder  to  the  right  wall,  and  thus  make  it 
possible  for  the  left  hand  to  palpate  the  organ. 

If  the  abdominal  walls  are  flaccid,  the  gall-bladder  is  sometimes  visible, 
which  is,  perhaps,  impossible  in  the  recumbent  posture. 

By  adhesion  of  the  stone-containing  gall-bladder  to  the  large  omentum, 
the  transverse  colon  may  be  lacerated,  constipation,  meteorism  and  the 
like  may  be  the  further  consequences,  and  an  atypical  cholelithiasis  may 
thus  present  itself  under  the  picture  of  intestinal  or  pyloric  stenosis. 

By  a  contracted  and  displaced  gall-bladder,  and  by  pericholecystitic 
adhesions,  the  stomach,  the  duodenum,  the  gall-bladder,  and  the  biliary 
passages  may  be  torn;  according  to  the  tension  of  these  organs,  vomiting 
may  be  produced,  and,  by  the  bending  of  the  cystic  duct,  intermittent 
colic. 

From  these  adhesions  between  the  stomach  and  biliary  passages  which 
resist  all  internal  treatment,  the  gastric  symptoms  become  prominent,  and 
among  the  digestive  disturbances  which  play  such  an  important  role  in 
the  picture  of  cholelithiasis  vomiting  is  of  special  diagnostic  import.  Vom- 
iting with  severe  i^etching,  as  a  rule,  accompanies  the  attack  of  colic,  and 
generally  produces  little,  if  any,  amelioration  of  the  pain;  while,  in  acute 
dyspepsia,  gastralgia  and  ulcer,  the  pain  usually  ceases  after  vomiting. 
This  vomiting  in  gall-stone  affection  usually  occurs  several  hours  after 
eating,  but  not  invariably.  In  stone  obstruction  of  the  duodenal  end  of 
the  common  bile  duct,  irritation  of  the  papilla  of  Vater  may  cause  pain 
in  the  gastric  region  as  well  as  vomiting  soon  after  the  ingestion  of  food, 
the  condition  simulating  ulcer  of  the  stomach  or  ulcer  of  the  duodenum. 

In  addition,  it  must  be  emphasized  that,  according  to  Fleiner,  in  con- 
sequence of  cholecystitis  calculosa,  actual  gastric  and  intestinal  ulcers  may 
develop,  as  well  as  those  of  the  large  intestine,  beginning  from  the  serosa, 
which  may  perforate.  Therefore,  an  accurate  history,  particularly  in  re- 
gard to  the  localization  and  radiation  of  the  pain,  should  be  obtained.  It 
may  be  easily  understood,  however,  and  has  already  been  observed,  that 
true  ulcer  of  the  stomach,  confirmed  by  operation,  and  particularly  ulcer 
of  the  duodenum  combined  with  jaundice  and  pains  radiating  toward  the 
liver,  has  been  mistaken  for  cholelithiasis. 

Vomiting  in  gall-stones  may  occur  in  the  early  morning  hours,  as 
vomitus  matutinus.  A  cook,  aged  34,  Rosalia  Sch.,  who  admitted  the 
excessive  iise  of  alcohol,  had  attacks  of  gall-stone  colic  due  to  a  tumor 
of  the  gall-bladder  of  the  size  of  a  walnut.  Colic  only  occurred  after 
midnight  or  toward  the  early  morning  hours,  and  ended  with  vomiting 
which  appeared  soon  after  arising  from  bed  while  the  stomach  was  still 
empty.  Frequently  the  origin  of  matutinal  vomiting  is  very  obscure.  Al- 
though in  the  history  of  women  suffering  from  gall-stones  the  abuse  of 
alcohol  is  sometimes  expressly  emphasized,  yet  it  is,  nevertheless,  a  con- 
spicuous fact  that  in  classic  atrophic  alcoholic  cirrhosis,  according  to  my 


SYMPTOMATOLOGY  491 

observation,  cholelithiasis  neither  shows  itself  as  a  complication  during 
life,  nor  is  it  found  at  the  autopsy  to  be  auxiliary. 

This  experience  all  the  more  furnishes  food  for  thought  inasmuch  as 
in  cirrhosis,  in  spite  of  the  profound  damage  of  the  liver-cells,  the  bile 
in  the  gall-bladder  shows  no  conspicuous  anomaly,  at  least,  none  in 
appearance. 

Vomiting  in  gall-stone  disease  may  be  alimentary,  bilious,  stercobilious, 
or  stercoral. 

The  gastric  contents  are  usually  normal  or  show  diminished  acidity; 
sometimes,  however,  there  is  even  hyperchlorhydria,  especially  if  the  gall- 
bladder is  adherent  to  the  pylorus,  secondary  gastric  dilatation,  and  irri- 
tation of  the  gastric  mucous  membrane  by  the  retention  of  the  ingesta. 

Whether  the  gastric  contents  are  vomited,  or  the  bilious  contents  of  the 
duodenum,  depends  mainly  upon  the  intensity  of  the  act  of  vomiting.  As 
a  rule,  vomiting  is  so  violent  in  gall-stone  colic  that  the  ejected  material 
is  bilious.  In  infrapapillary  duodenal  stenosis  due  to  laceration  and  com- 
pression of  the  duodenum,  the  appearance  of  bile  in  the  vomited  material 
may  be  readily  understood.  On  the  other  hand,  in  occlusion  of  the  chole- 
dochus,  the  vomited  material  will  contain  no  bile. 

Uncontrollable  vomiting  with  intense  pain,  great  anxiety,  constipation 
and  meteorism,  particularly  in  the  hepatic  region,  is  usual  in  perforation 
of  the  gall-bladder  and  in  biliary  abscesses.  Uncontrollable  vomiting  of 
ingested  food  after  the  intake  of  nourishment,  with  severe  pain  in  the 
hypochondrium  radiating  to  the  right  shoulder  and  back,  stubborn  con- 
stipation, unquenchable  thirst,  and  singultus  were  the  clinical  symptoms 
in  a  case  of  duodenal  stenosis  observed  by  Fauconneau-Dufresne  which 
was  due  to  compression  of  the  tumor  by  the  gall-bladder. 

Stercobilious  vomiting  is  almost  always  a  sign  of  disturbance  in  the 
lumen  of  the  intestine,  and  the  appearance  of  stercobilin  in  the  vomitus 
is  of  serious  import  in  the  course  of  cholelithiasis.  I  emphasize  this 
because  intestinal  occlusion  due  to  incarceration  of  stones  in  the  intestine 
may,  on  the  one  hand,  appear  under  the  picture  of  ileus  and  run  its  course 
as  the  first  manifestation  of  a  latent  cholelithiasis,  or,  on  the  other  hand, 
gall-stones  may  appear  under  the  mask  of  an  acute  intestinal  stenosis,  in 
which  laparotomy  reveals  no  obstruction  of  the  intestine,  neither  invagina- 
tion, torsion,  nor  stones,  no  peritonitis  and  no  perforation;  at  the  autopsy 
a  large  gall-stone  is  found  in  the  common  duct.  These  cases  resemble  those 
of  nephrolithiasis,  running  their  course  under  the  picture  of  intestinal 
occlusion,  of  which  I  have  seen  3  examples,  and  in  this  category  also 
belongs  the  case  of  a  fat  woman,  aged  58,  who  suffered  from  severe  pain 
in  the  upper  abdominal  region,  chills,  fever  and  bilious  vomiting.  An 
irreducible  umbilical  hernia  was  found,  painful  upon  pressure,  which  had, 
according  to  report,  existed  for  some  years.  A  diagnosis  was  accordingly 
made  of  incarcerated  umbilical  hernia.     Laparotomy  revealed  cholecystitis 


492  GALL-STONES 

calculosa  and  nothing  abnormal  in  the  umbilical  hernia.    Removal  of  the 
stone  was  followed  by  recovery. 

Large  stones,  which  by  perforation  of  the  common  duct  or  the  gall- 
bladder reach  the  intestine,  may  produce  symptoms  of  occlusion,  and  either 
soon  after  their  entrance  or  a  long  time  afterward,  even  weeks,  months 
or  years,  severe  symptoms  of  intestinal  stenosis  may  appear.  After  pro- 
longed retention  in  the  intestine  owing  to  peristaltic  and  antiperistaltic 
movements,  they  may  become  fixed  in  some  portion  by  spastic  contraction, 
either  in  the  duodenum,  jejunum  or  ileum,  usually  in  the  region  of  the 
ileo-cecal  valve.  Large  stones  may  also  reach  the  cecum  and  the  large 
intestine  after  dilatation  or  ulceration  of  Bauhin's  valve  (ileo-cecal).  In 
this  manner  even  stones  the  size  of  a  hen's  egg  may  be  discharged  with  the 
feces.  In  other  cases,  they  lead  to  ulceration  or  perforation  of  the  intes- 
tine with  all  their  consequences.  Eupture  may  occur  directly  into  the 
peritoneal  cavity  and  into  cavities  formed  by  preceding  inflammation,  and 
thus  circumscribed  abscesses  develop.  This  shows  how  valuable  for  correct 
diagnosis  are  many  obscure  cases  of  intestinal  occlusion  or  ulceration  in 
tlie  ileo-cecal  region,  and  how  important  is  an  accurate  history  which 
may  eventually  point  to  a  preceding  cholelithiasis.  This  is  all  the  more 
true  since  the  stones  which  have  reached  the  intestine  by  perforation  may 
have  been  present  for  months  and  even  for  years  in  the  intestinal  mucous 
membrane  without  having  caused  distinct  disturbance.  For  this  reason 
close  attention  should  be  given  to  pains  in  the  right  hjrpochondrium  and 
epigastrium,  and  to  fever  and  vomiting  occurring  one  or  two  hours  after 
the  principal  meal  and  disappearing  after  a  few  hours.  For  the  appear- 
ance of  these  symptoms  after  partaking  of  food  may  be  the  initial  symp- 
tom of  fistula  of  the  gall-bladder  and  intestine,  and,  therefore,  significant 
in  the  diagnosis  of  a  succeeding  stenosis  of  the  intestine  due  to  gall-stones. 
In  cases  in  which  the  stones  find  their  way  into  the  intestinal  canal,  the 
cause  of  intestinal  occlusion  is  not  the  mechanical  closure  of  the  intestine, 
for  the  stones  are  rarely  so  large  as  wholly  to  obstruct  its  lumen,  and 
because,  at  the  autopsy,  the  calculi  are  found  to  be  freely  movable  in  the 
intestine.  The  occlusion  is  often  due  to  a  contraction  of  the  organ  around 
the  stone,  which  is  directly  proven  by  those  cases  of  stenosis  of  the  in- 
testine due  to  gall-stone  in  which  laparotomy  is  performed.  In  the  case 
of  Eogner-Gusenthal,  upon  removal  of  the  stone  the  spasmodic  contraction 
of  the  intestine  around  it  was  seen.  Stones  which  are  impacted  in  the 
duodenum  simulate  pyloric  stenosis.  Frequent  vomiting,  dilatation  of  the 
stomach,  sensitiveness  of  the  right  hypochondrium  upon  pressure,  con- 
traction of  the  musculature  of  the  abdomen  upon  the  right  side,  or  friction 
sound  in  the  gall-bladder  region,  will  indicate  the  correct  diagnosis,  as 
well  as,  usually,  the  absence  of  melena  and  hematemesis,  and,  under  some 
circumstances,  the  results  of  chemical  and  bacteriological  examination  of 
the  gastric  contents.     If  the  stones  are  impacted  in  the  vicinity  of  the 


SYMPTOMATOLOGY  493 

ileo-cecal  valve,  appendicitis  must  be  considered  in  the  diagnosis.  The 
localization  of  the  pains  in  McBurney's  point,  rises  in  temperature,  the 
age  of  the  patient,  etc.,  may  lead  to  the  true  diagnosis.  Stones  in  the 
sigmoid  flexure  have  been  mistaken  for  carcinoma.  In  very  rare  cases 
they  may  also  lead  to  volvulus  of  the  sigmoid.  Diagnostically,  it  must 
be  emphasized  that  in  acute  obstruction  of  the  intestine  from  gall-stones 
the  meteorism  is  usually  slight;  in  volvulus  of  the  sigmoid  flexure,  mete- 
orism  occurs  early,  increases  rapidly,  and  reaches  a  high  degree.  In  ex- 
ceptional cases,  the  stones  wandering  in  the  intestine,  if  low  down,  and 
the  abdominal  walls  flaccid,  may  be  palpated  by  rectum  in  spite  of  meteor- 
ism and  sensitiveness  of  the  abdomen. 

When  the  stone  is  lodged  in  the  upper  portion  of  the  intestine,  neoplasm 
is  much  more  readily  thought  of  than  stone.  In  some  cases  of  obstruc- 
tion of  the  intestine  due  to  gall-stones,  the  patients  experience  a  sensation 
as  though  a  firm  body  were  moving  in  their  intestines.  Intestinal  ob- 
struction due  to  stone  may  be  favored,  that  is,  the  stones  may  increase 
in  size,  by  the  apposition  of  fecal  masses,  such  cases  having  been  observed 
by  Korte  and  Frerichs.  Preceding  colic,  perhaps  palpable  tumor  of  the 
gall-bladder,  the  disappearance  of  the  tumor  with  simultaneous  symptoms 
of  eifusion  of  bile  into  the  intestine,  bilious  vomiting,  severe  pains  in  the 
abdomen,  and  the  symptoms  of  intestinal  occlusion  must  all  be  considered 
in  a  diagnostic  sense.  The  fact  that  stones  have  been  previously  found, 
the  discharge  of  the  same  with  the  feces,  as  well  as  other  symptoms  of 
cholelithiasis,  render  the  diagnosis  positive.  The  occasional  discharge 
of  flatus,  as  well  as  the  severity  and  rapid  sequence  of  vomiting  in 
intestinal  obstruction  due  to  gall-stone,  in  contrast  to  the  longer  inter- 
vals of  vomiting  in  intestinal  occlusion  from  other  causes,  may,  in  some 
cases,  furnish  a  clue  to  the  disease.  The  symptoms  of  occlusion  may  dis- 
appear and  then  recur.  In  the  case  of  the  aged  a  relapsing  intestinal 
occlusion  must  suggest  to  us  the  possibility  of  a  rupture  of  the  stones 
into  the  intestine. 

We  see,  therefore,  that  in  the  course  of  cholelithiasis  the  composition 
of  the  vomited  material,  the  intensity  of  the  act  of  vomiting,  and  the 
changes  present  in  the  lumen  of  the  intestine  may  vary.  First,  as  a  rule, 
the  contents  of  the  stomach,  subsequently  those  of  the  duodenum,  and, 
finally,  those  of  the  jejunum  and  ileum  are  discharged.  In  the  cases  in 
which  fecal  vomiting  occurs,  the  diagnosis  of  intestinal  occlusion  will  not 
be  difficult.  If,  however,  the  vomited  material  does  not  show  fresh,  un- 
changed bile,  but  bile  which  has  already  been  acted  upon  by  intestinal 
bacteria,  which,  therefore,  originates  from  the  lower  portions  of  the  in- 
testine, its  diagnostic  significance  as  a  premonitory  sign  of  intestinal  occlu- 
sion is  obvious.  In  the  early  diagnosis  of  acute  intestinal  stenosis,  the 
vomiting  of  stercohilin  is,  under  some  circumstances,  an  important  finding, 
and  I  advise  that  an  examination  for  stercohilin  be  made,  particularly  in 


494  GALL-STONES 

tliose  cases  in  which,  after  laparotomy,  the  question  must  be  decided  whether 
the  acute  appearance  of  so-called  bilious  vomiting  is  the  consequence  of 
peritonitis  or  of  a  change  in  the  lumen  of  the  intestine. 

Ilematemesis  occurring  in  long-existing  jaundice  may  be  a  sign  of  the 
hemorrhagic  diathesis,  of  ulcerative  rupture  of  the  biliary  passages  into 
the  stomach,  of  secondary  gastric  ulceration,  or  the  consequence  of  throm- 
bosis of  the  portal  vein. 

That  lithogenous  carcinoma  of  the  choledochus  and  of  the  duodenum 
may  sometimes  run  its  course  with  hematemesis  and  melena  is  obvious. 
Tliis  is  the  more  apparent  since  cases  have  been  reported  in  which  large 
stones  situated  in  the  choledochus,  with  and  without  accompanying  jaim- 
dice,  the  stones  being  palpable  through  the  abdominal  walls,  have  been 
confounded  with  carcinomata  of  the  pylorus  and  of  the  duodenum.  The 
absence  of  hydrochloric  acid  in  the  vomited  material,  and  the  signs  of 
gastrectasis,  may  in  such  cases,  as  is  reported  in  literature,  assist  in  the 
diagnosis.  Stones  in  the  common  duct  may  change  their  position  upon 
respiration,  and  even  upon  palpation  may  show  slight  movability,  as  is 
the  case  in  carcinoma  of  the  pylorus,  in  which  circumstance,  however,  they 
differ  from  carcinoma  of  the  head  of  the  pancreas. 

With  an  existing  jaundice  the  condition  of  the  gall-bladder  may  be  of 
diagnostic  importance,  the  latter,  as  has  been  mentioned,  in  carcinoma 
of  the  head  of  the  pancreas  being  frequently  felt  as  a  tensely  filled  tumor 
and  also  sometimes  visible,  while  in  a  tumor  of  the  gall-bladder  stones 
in  the  common  duct  are  frequently  absent  in  consequence  of  a  preceding 
contraction  of  the  gall-bladder.  The  motility  of  stones  in  the  choledochus, 
in  contrast  to  carcinomatous  obstructions  therein,  may  also  aid  the  surgeon 
during  laparotomy. 

]\Ierkel  describes  a  case  of  cholelithiasis  which  was  very  difficult  to 
diagnosticate;  it  occurred  in  a  woman,  aged  51,  who  suffered  from  dis- 
tressing, uncontrollable  singultus,  intense  abdominal  pains  which  were  not 
localized,  with  exacerbations  after  meals,  and  who  had  a  pear-shaped,  pain- 
less tumor  in  the  epigastrium.  There  was  no  jaundice,  no  vomiting;  the 
stools  were  normal.  The  diagnosis  wavered  between  tumor  of  the  pylorus 
and  movable  kidney.  Operation  showed,  after  incision  of  the  tumor  which 
])roved  to  be  the  adherent  gall-bladder,  a  gall-stone  weighing  15  grams, 
wliich  was  an  exact  model  of  the  gall-bladder  that  had  contracted  com- 
pletely around  it.     Eecovery. 

The  differential  diagnosis  between  gastric  carcinoma  and  cholelithiasis 
may  also  give  rise  to  perplexity  in  cases  in  which  the  gastric  carcinoma 
is  ushered  in  with  the  signs  of  an  acute  attack  of  cholelithiasis,  yet  without 
producing  a  palpable  tumor. 

Such  a  case  I  presented  to  the  Clinic  on  Nov.  24,  1893;  it  occurred 
in  a  servant  girl,  aged  34,  who  reported  that  she  had  previously  always 
been  well,  but  was  suddenly  attacked  by  colic-like  pains  in  the  right  hypo- 


SYMPTOMATOLOGY  495 

chondrium.  These  attacks  steadily  increased  in  frequency,  and  were  fol- 
lowed by  vomiting  two  or  three  hours  after  the  ingestion  of  nourishment, 
loss  of  appetite,  and,  in  the  further  course,  jaundice.  Free  HCl  was  absent 
in  the  vomited  material  as  well  as  lab  ferment  and  lab  zymogen;  elon- 
gated lactic  acid  bacilli  could  not  be  demonstrated,  but  several  eosinophilic 
cells  were  repeatedly  found  in  the  vomitus.  Autopsy  showed  an  infiltrated 
scirrhus  of  the  pylorus  with  extreme  stenosis  of  the  latter,  metastases  of 
the  mesenteric,  retroperitoneal  and  periportal  lymph-glands,  compression 
of  the  common  duct,  and  general  jaundice. 

In  this  case,  which,  on  account  of  the  sudden  appearance  of  the  symp- 
toms, as  well  as  by  jaundice  which  was  soon  observed,  resembled  chole- 
lithiasis, the  finding  of  eosinophilic  cells  in  the  vomited  material  was  of 
diagnostic  importance,  for  the  reason  that  these  are  significant  of  small 
cell  infiltration  of  the  interglandular  tissue  which  consists  of  an  accumu- 
lation of  eosinophilic  cells,  as  Hammerschlag  demonstrated  in  gastric  car- 
cinoma. 

The  dilatation  caused  by  cicatricial  closure  of  the  choledochus  may 
reach  an  extreme  degree,  and  may  be  palpated  during  life  as  a  cyst-like 
tumor.  Large  stones  impacted  in  the  choledochus  may  compress  the  pan- 
creatic duct  and  thus  produce  secondary  infection  of  the  pancreas  and 
retention  cysts;  in  complete  closure  of  the  pancreatic  duct,  by  preventing 
the  pancreatic  juice  from  entering  the  intestine,  they  may  give  rise  to 
oxtreme  cachexia.  The  differential  diagnosis  of  this  latter  form  of  chole- 
lithiasis from  carcinoma  of  the  head  of  the  pancreas  may,  therefore,  be 
exceedingly  difficult. 

Morgagni  reports  a  case  in  which  the  common  duct  was  dilated  to  the 
size  of  a  stomach  and  filled  with  stones.  Such  enormous  dilatations  of 
tlie  common  duct  may  readily  be  mistaken  for  pancreatic  cysts,  all  the 
more  so  as,  on  account  of  the  topographico-anatomical  relations  of  the 
common  duct  to  the  pancreas  and  also  from  clinical  experience,  secondary 
affections  of  the  pancreas  (closure  of  the  pancreatic  duct,  indurative  pan- 
creatitis, retention  cysts)  have  been  proven  to  depend  upon  cholelithiasis. 
Tlie  diagnosis  of  these  conditions  becomes  even  more  puzzling  in  view  of 
the  fact  that  intense  pains  having  the  character  of  gall-stone  colic  occur 
also  in  pancreatic  cysts,  as  in  a  case  which  I  showed  in  the  Clinic  upon 
June  16,  1901,  and  in  which  I  believed  myself  justified  in  making  a 
diagnosis  of  pancreatic  cyst.  A  farmer,  aged  67,  from  Galicia,  reported 
that  for  twenty-seven  years  he  had  been  suffering  from  pains  in  the  right 
epigastrium  radiating  directly  to  the  lumbar  region,  usually  occurring  at 
night  and  lasting  from  one  to  two  hours.  These  pains  recurred  at  intervals 
of  from  one  to  two  months  up  to  the  year  1900.  There  was  never  any 
jaundice.  Preceding  the  attacks  the  urine  was  said  to  have  been  some- 
times remarkably  clear;  during  the  attacks  it  was  of  a  reddish  color, 
without  sediment  or  blood,  and  without  stone.  The  bowels  during  the 
33 


496  GALL-STONES 

entire  time  were  irregular  and  constipated,  so  that  the  patient  took  purga- 
tives for  many  years.  In  August,  1900,  the  patient  was  again  attacked 
by  very  severe  spasmodic  pains  in  the  liver,  this  time  accompanied  by 
fever  and  sweating.  There  was  vomiting  and  very  marked  meteorism; 
the  pains  were  so  intense  that  he  writhed  with  agony.  In  February,  1901, 
a  tumor  slowly  developed  in  the  epigastrium.  At  present  his  abdomen 
and  epigastric  region  are  prominent  on  account  of  a  globular  tumor,  the 
size  of  a  head,  which  extends  anteriorly  from  the  right  parasternal  line 
to  the  left  mammary  line  and  reaches  to  the  navel.  The  tumor  shows  a 
distinct  vertical  pulsation,  synchronous  with  the  heart's  action,  and  dis- 
tinct fluctuation.  It  is  evidently  displaced  by  respiration  and  pressure, 
and  may  also  be  moved  laterally.  Slight  lateral  displacement,  particu- 
larly to  the  left,  occurs  when  the  patient  lies  upon  the  side.  The  tumor 
is  almost  painless.  The  feces  are  not  excessive  in  amount,  and  are  of 
normal  appearance.  Microscopically  nothing  abnormal  is  found  in  the 
feces  or  the  urine.  According  to  this  history,  a  diagnosis  of  anything 
else  than  pancreatic  cyst  was  scarcely  possible. 

Enlargement  of  the  spleen  does  not  belong  to  the  picture  of  pure  chole- 
lithiasis, even  when  the  attack  runs  its  course  with  intense  jaundice.  Ex- 
ceptions to  this  rule  are  formed  by  those  cases  in  which  infectious  chole- 
cystitis and  cholangitis  exist  simultaneously;  here  the  splenic  tumor  is 
of  an  infectious  nature.  In  the  diagnosis  of  secondary  cirrhosis  which 
develops  in  the  course  of  cholelithiasis,  enlargement  of  the  spleen  is  sig- 
nificant, in  contrast  to  carcinoma  of  the  common  duct  and  of  the  head 
of  the  pancreas,  as  well  as  of  the  glands  at  the  porta  hepatis  which  cause 
enlargement  of  the  spleen  only  when  they  compress  the  portal  vein.  In 
metastatic  carcinomatosis  of  the  porta  hepatis,  which  originates  from 
cancer  of  the  gall-bladder,  enlargement  of  the  spleen  may  be  an  infec- 
tious residuum  of  the  precarcinomatous  lithiasis  of  the  gall-bladder. 

An  examination  of  the  feces  may  give  us  valuable  guidance  in  the  diag- 
nosis of  cholelithiasis.  In  obstruction  from  stone  in  the  common  duct  and 
in  the  hepatic  duct,  and  in  long-continued  inspissation  of  bile,  the  feces, 
as  is  well  known,  become  clay-coloi  3d,  or  ashy-gray.  In  lithogenous  occlu- 
sion of  the  common  duct,  as  has  already  been  stated,  the  bile  may  occasion- 
ally flow  into  the  intestine,  provided  stones  which  have  become  loosened 
move  in  a  retrograde  direction  in  the  dilated  common  duct.  This  is  in 
contrast  to  cicatricial  and  carcinomatous  occlusion  of  the  common  duct, 
especially  carcinomatous  compression  of  the  same,  which  is  explained  by 
the  aggressive  motion  of  the  proliferating  secondary  mass.  Tuberculosis 
of  the  glands  at  the  porta  hepatis  may  also  lead  to  permanent  occlusion  of 
the  common  duct,  but  not  invariably.  I  once  observed  a  case  in  which  the 
color  of  the  feces  varied,  and,  at  the  autopsy,  stenosis  of  the  choledochus 
was  found,  which  was  due  to  a  mass  of  tuberculous  glands.  By  an  inter- 
mittent increase  of  the  intrabiliary  pressure,  in  consequence  of  the  stasis 


/  SYMPTOMATOLOGY  497 

of  bile  above  tbe  stenosis,  tbe  variation  in  the  color  of  the  feces  is  ex- 
plained similarly  as  the  dribbling  of  urine  in  hypertrophy  of  the  prostate 
gland.  Analogous  conditions  may  also  occur  in  gall-stones  which  com- 
press the  common  duct  externally. 

The  patients  sometimes  first  notice  a  whitish-gray  color  of  the  stools 
during  the  attack  of  colic,  while  they  expressly  emphasize  that  the  urine 
a  few  days  later  resembles  dark  beer,  and  the  skin  becomes  yellow.  As 
regards  the  sequence  of  symptoms  there  are  cases  of  gall-stone  colic  in 
which  intestinal  acholia  precedes  the  jaundice  and  choluria. 

Frequently  this  intermittent,  ashy-gray  color  of  the  stools  is  combined 
with  an  acutely  developing  meteorism,  which  is  the  only  objective  mani- 
festation of  gall-stone  colic. 

A  singer,  aged  46,  who  was  attacked  by  chills,  pains  radiating  to  the 
right  shoulder,  vomiting  and  diarrhea,  reported  that  during  the  attack 
the  abdomen  became  as  tense  as  a  drumhead,  and  the  skin  of  the  abdomen 
was  glistening  in  appearance.  The  feces  resembled  those  of  an  infant. 
There  was  no  jaundice.  This  paradoxical  phenomenon  of  intestinal  acholia 
without  jaundice  requires  special  consideration,  as  it  occurs  particularly 
in  those  cases  in  which  palpation  of  the  gall-bladder  reveals  a  distinct 
tumor.  It  is  obvious  in  this  instance  that  the  gall-bladder  acts  as  a 
reservoir,  receiving  the  regurgitating  bile  from  the  over-filled  biliary  pas- 
sages, which  is  naturally  only  possible  when  the  cystic  duct  remains  open. 

The  gall-bladder  appears — at  least  in  man  and  in  many  animals — to 
be  a  regulator  of  the  intrabiliary  pressure.  This  view  is  favored  by  the 
opinions  of  some  authors  who  have  observed  a  vicarious  dilatation  of 
the  biliary  passages  after  the  closure  of  the  gall-bladder  and  the  cystic 
duct.  Acholia  of  the  feces  without  jaundice  occurs  also  in  fistula  of  the 
gall-bladder  and  abdominal  walls  after  cholecystotomy ;  the  explanation 
of  this,  according  to  Leichtenstern,  may  be  that  if  a  gall-bladder  fistula 
exists  biliary  pressure  cannot  reach  a  degree  necessary  to  overcome  the 
tonus  of  the  duodenal  sphincter.  Permanent  intestinal  acholia  does  not, 
therefore,  justify  the  conclusion  that  an  obstruction  due  to  stone  is  present 
in  the  common  duct,  neither  can  it  by  any  means  be  regarded  as  an 
indication  for  renewed  operative  interference. 

According  to  Doyon,  irritation  of  the  central  end  of  the  vagus  produces 
contraction  of  the  gall-bladder  and  relaxation  of  the  duodenal  sphincter. 
It  follows  from  this  that  a  condition  must  exist  in  the  living  organism 
which  necessitates  the  removal  of  this  obstruction  by  antagonistic  irrita- 
tion of  the  peripheral  branches  of  the  pneumogastric  nerve ;  therefore,  this 
closed  door  may  occasionally  open,  and  become  permeable  for  bile  as  well 
as  for  incarcerated  stones  in  the  common  duct. 

If,  with  the  passage  of  stones  into  the  intestine,  the  stasis  of  bile 
ceases,  the  retained  bile  pours  into  the  intestine,  and  the  acholic  stools, 
or,  at  least,  the  stools  deficient  in  bile,  suddenly  contain  profuse  amounts  of 


498  GALL-STONES 

bile;  the  color  of  the  feces  in  such  cases  depends  principally  upon  the 
intensity  of  the  intestinal  peristalsis.  If  this  is  very  intense,  unaltered 
biliary  coloring  matter  may  be  detected  in  the  fluid  stools.  The  feces  are 
then  yellow  or  green,  and  contain  bilirubin  and  biliverdin.  If  the  passage 
of  the  intestinal  contents  is  so  slow  that  the  biliary  coloring  matter  may 
be  reduced,  the  feces  become  dark  brown,  sometimes  tarry,  and  contain 
large  amoimts  of  stercobilin.  The  same  is  true  in  rupture  of  the  gall- 
bladder or  of  the  common  duct  into  the  duodenum.  If,  however,  rupture 
occurs  into  the  colon,  it  is  evident  that  with  the  shorter  road  which  the 
bile  must  traverse,  and  particularly  with  rapid  peristalsis,  the  stools  al- 
most always  contain  undecomposed  bile. 

In  the  majority  of  cases  the  intestine  is  overflooded  with  accumulated 
bile,  and  diarrhea  occurs.  Ulcerating  carcinomata  of  the  biliary  passages 
which  perforate  into  the  intestine  may  have  the  same  effect.  In  a  case 
in  which,  after  the  appearance  of  stools  markedly  stained  with  stercobilin 
without  admixture  of  blood,  and  in  which  jaundice  which  had  lasted  a 
long  time  suddenly  disappeared,  the  diagnosis  of  an  ulcerative  carcinoma 
of  the  common  duct  was  made  on  account  of  the  persisting  marasmus  of 
the  patient.  The  autopsy  showed  an  ulcerating  villous  cancer  of  the  com- 
mon duct.  Accordingly,  the  composition  of  the  stools  may  be  utilized 
in  the  diagnosis  of  high  or  low  perforation  of  the  intestine. 

Usually  stubborn  constipation  is  noted  during  the  attack  of  colic.  But 
tliere  are  also  cases  with  diarrhea  so  profuse  that,  during  the  prevalence 
of  a  cholera  epidemic,  they  may  be  mistaken  for  an  attack  of  cholera. 
The  diagnosis  may  also  become  difficult  if  poisoning,  for  example  with 
arsenic,  produce  biliary  colic;  such  cases  have  been  observed.  Stubborn 
diarrhea  usually  accompanies  the  forms  of  cholelithiasis  which  run  their 
course  in  combination  with  acute  septic  infections,  for  example,  endo- 
carditis. But  diarrhea,  sometimes  with  hemorrhagic  admixture,  combined 
with  anorexia,  anemia  and  cachexia,  may  also  be  the  principal  manifesta- 
tion of  an  insidious,  but  nevertheless  severe,  infection  of  the  biliary 
passages. 

Stones  which  have  reached  the  intestine  by  perforation  may,  as  is  well 
known,  be  lodged  in  the  intestinal  mucous  membrane  for  months,  but  they 
may  also,  as  is  shown  by  cases  reported  in  literature,  cause  stubborn  diar- 
]  hea.  Such  diarrhea  may  be  due  to  ulceration  of  the  intestine,  particularly 
in  the  region  of  the  ileo-cecal  valve.  In  cases  in  which  there  is  a  suspicion 
of  intestinal  ulceration,  it  is  advisable  to  examine  the  feces  for  pyogenic 
cocci,  which,  according  to  Gram,  are  positive  (staphylococci  and  strepto- 
cocci). 

This  aid  to  diagnosis,  communicated  to  me  by  Kretz,  has  been  suc- 
cessfully tested  in  our  Clinic.  As  is  well  known,  the  majority  of  the  normal 
intestinal  flora  of  an  adult  consist  of  bacterium  coli  varieties,  which  are 
negative  according  to  Gram,  while  cocci  are  present  in  the  minority.     In 


SYMPTOMATOLOGY  499 

ulcerative  processes  of  the  large  intestine  we  find  the  pus  flora  positive  to 
Gram,  in  contrast  to  intestinal  flora  negative  to  Gram,  to  be  most  promi- 
nent. The  feces,  dried  upon  a  cover-glass,  are  stained  according  to  Gram, 
and,  as  a  contrast  color  for  the  microbes  negative  to  Gram,  a  watery  rubin 
fuchsin  solution  is  utilized.  In  a  case  of  tuberculous  ulcers  I  found  this 
reaction  distinctly  developed  in  the  mucus  particles  of  the  stools,  not, 
however,  in  the  diarrheic  dejecta  of  enteric  fever,  in  which  bacilli  positive 
according  to  Gram  prevailed  in  the  microscopic  picture. 

Melena  in  cholelithiasis  is  produced  by  the  same  causes  that  give  rise 
to  hematemesis,  which  have  already  been  enumerated.  In  rare  cases  of 
wandering  stone  from  the  irritation  of  the  mucous  membrane,  the  feces 
may  show  hemorrhagic  admixture,  and  this  must  be  especially  borne  in 
mind  in  the  differential  diagnosis  of  neoplasms  or  intussusceptions  of  the 
intestine. 

Special  weight  must  be  attached  to  the  examination  of  the  stone  passed 
in  the  feces,  which  is  simultaneously  a  corpus  delicti  of  cholelithiasis. 
Negative  examination  of  the  stool,  however,  does  not  permit  the  conclusion 
that  no  stones  have  been  passed;  for,  according  to  Naunyn,  stones  of  soft 
consistence  may  be  disintegrated  in  the  intestine.  As  we  already  know, 
the  gall-bladder  is  the  point  of  formation  of  stones.  The  stones  which 
have  wandered  out  of  the  gall-bladder,  which  have  traversed  the  cystic 
duct,  may,  instead  of  taking  their  ordinary  course  into  the  wider  common 
duct  to  the  point  of  the  duodenal  papilla,  move  in  a  retrogressive  direc- 
tion, may  be  forced  upward  into  the  branches  of  the  hepatic  duct,  and 
thus  produce  a  cholelithiasis  intrahepatica  with  all  its  dangerous  tendency 
to  biliary  abscesses.  This  is  the  manner  in  which  cholelithiasis  intra- 
hepatica of  exogenous  origin  arises. 

The  development  of  stones  in  the  branches  of  the  hepatic  duct  may 
also  be  autochthonous  in  this  locality,  and  without  generating  particular 
disturbance,  they  may  find  their  way  into  the  wider  common  duct.  How- 
ever, it  is  quite  possible  that  the  stones  which  have  developed  in  the  hepatic 
duct,  instead  of  entering  the  common  duct  with  the  flow  of  bile,  find  their 
way  to  the  gall-bladder  where  they  then  enlarge.  We  see,  therefore,  that 
stones  in  the  choledochus  may  be  of  different  origin,  from  the  hepatic 
duct,  from  the  gall-bladder,  arising  autochthonously  by  crystallization 
around  cholesterin,  and,  finally,  by  the  perforation  of  the  gall-bladder  and 
its  diverticulum  into  the  common  duct. 

Kehr  has  observed  cases  in  which,  in  spite  of  large  stones  being  impacted 
in  the  neck  of  the  gall-bladder,  small  stones  were  found  in  the  common 
duct.  Stones  may  be  situated  in  the  cystic  duct,  and  also  simultaneously 
in  the  hepatic  duct.  After  the  extraction  of  stones  from  the  gall-bladder, 
stones  in  the  hepatic  duct  may  move  downward,  which  is  of  importance  in 
considering  the  question  of  cholecystotomy  or  cholecystectomy. 

The  seat  of  the  stone  in  some  cases  corresponds  to  a  local  area  of 


500  GALL-STONES 

pain,  which  persists  even  when  narcotics  are  administered  to  the  patient, 
as,  for  example,  injections  of  morphin. 

The  seat  of  the  stone  may  sometimes  be  revealed  by  the  sequence  of 
the  symptoms.  In  the  overwhelming  majority  of  cases  preceding  colic 
with  local  signs  in  the  gall-bladder,  a  tumor,  a  collection  of  fluid,  pain, 
then  the  disappearance  of  these  symptoms,  and  an  outbreak  of  permanent 
jaundice  indicate  that  the  seat  of  the  stone  is  the  common  duct. 

The  fate  of  the  gall-stones  in  the  intestine  varies.  They  may  break 
up  in  their  passage  through  the  intestine,  they  may  do  much  damage, 
small  stones  may  be  arrested  in  the  appendix,  and  large  ones  in  the  ileo- 
cecal valve.  Stones  which  have  formed  in  the  gall-bladder  may,  by  pro- 
ducing a  diverticulum,  directly  penetrate  the  substance  of  the  liver,  by 
perforation  of  the  posterior  wall  of  the  gall-bladder  they  may  produce  a 
paranephritic  abscess,  after  rupture  they  may  appear  in  the  lumbar  region ; 
in  perforating  downward  they  may  also  find  their  way  into  the  urinary 
l)ladder,  and,  after  long  wanderings,  we  may  be  surprised  to  find  them 
even  in  distant  parts  of  the  body;  for  instance,  as  in  a  case  of  Forges, 
who  extracted  a  quantity  of  gall-stones  from  a  fistula  in  the  thigh  of 
a  woman. 

In  examining  the  stones  passed  in  the  feces,  above  all  their  size  is  to 
be  noted.  The  question  whether  large  stones  can  pass  the  conical,  terminal 
portion  of  the  ostium  duodenale  is  variously  answered  by  pathological 
anatomists.  In  opposition  to  the  view  of  Eokitansky,  who  believes  it 
possible,  on  account  of  the  great  power  of  dilatation  of  the  common  duct, 
that  even  stones  the  size  of  a  hen's  egg  may  pass  the  ostium  duodenale 
choledochi,  Eoth  maintains  that  such  seeming  dilatations  are  really  typical 
perforations  of  the  common  duct,  these  being  usually  situated  from  5  to 
10  mm.  above  the  ostium  duodenale,  and  in  these  perforations  the  upper 
portion  of  the  portio  intestinalis  ductus  choledochi  communicates  with  the 
descending  part  of  the  duodenum.  The  greatest  dilatation  of  the  ostium 
duodenale  produced  by  gall-stones  had,  according  to  Roth,  the  diameter 
of  a  medium-sized  pea.  He  does  not  believe  it  likely,  therefore,  that 
stones  of  greater  dimensions  reach  the  intestine  naturally. 

At  the  bedside,  the  passage  of  large  stones  after  preceding  grave  symp- 
toms is  a  sign  of  perforation,  and  with  renewed  colic  forms,  as  Riedel 
says,  a  contra-indication  to  operation,  as  it  is  obviously  possible  that  more 
stones  may  pass  through  the  perforation.  If  at  first  small  stones,  and  then 
somewhat  larger  ones  pass,  we  are  justified  in  concluding  that  the  common 
gall-duct  is  dilated. 

After  a  single  passage  of  stones  the  biliary  passages  remain  dilated, 
and  this  facilitates  the  later  passage  of  succeeding  stones  so  that,  if  small, 
tliey  may  easily  be  discharged  in  the  feces. 

The  passage  of  equally  large  stones  which  are  faceted  may — cceteris 
paribus — form  a  contra-indication  to  operation,  inasmuch  as  we  assume 


SYMPTOMATOLOGY  501 

that  the  stones  remaming  in  the  gall-hladder  may  pass  in  the  same  way 
as  did  their  predecessors.  The  repetition  of  attacks  without  the  passage  of 
stones  awakens  the  suspicion  that  large  stones  are  also  present  in  the  gall- 
bladder. According  to  Eiedel,  the  small  stones  which  hide  themselves  in 
the  common  gall-duct,  and  occasionally  slip  into  the  hepatic  duct,  cause 
anxiety  to  the  surgeon.  A  stone  that  possesses  only  one  facet  permits 
the  conclusion  that  it  is  the  first  or  the  last  of  a  series. 

As  the  nucleus  of  stones,  intestinal  parasites,  portions  of  the  distoma 
hepaticum,  and  once  the  stone  of  a  plum  have  been  found. 

Gall-stones  are  composed  chiefly  of  cholesterin  with  a  slight  admixture 
of  bilirubin  calcium.  Carbonate  and  phosphate  stones  must  be  regarded  as 
pancreatic  stones,  but  are  not  invariably  so,  as  is  proven  by  the  two  cases 
published  by  Eichhorst,  who,  in  a  case  of  mucous  colic,  found  a  profusion 
of  small  granular  stones  of  from  ^  to  2  mm.  in  diameter  which  consisted 
of  calcium  carbonate.  The  seed  of  fruit  (pears),  the  vertebra  of  birds, 
and  chalk  introduced  for  medical  purposes  must  also  be  considered.  It 
follows  from  this  that  the  chemical,  microscopical  (for  distoma),  and 
perhaps  also  the  bacteriologic  (for  typhoid  bacilli)  investigation  of  stones 
that  have  been  passed  may  furnish  valuable  information  regarding  their 
origin,  their  past,  and,  eventually,  also  their  etiology. 

The  amount  of  urine  in  cholelithiasis  is  either  normal,  diminished,  or 
increased.  A  few  cases  have  been  observed  of  polyuria  with  bulimia  and 
thirst  but  without  glycosuria.  In  some  instances,  at  the  onset  of  the 
attack  the  excretion  of  a  transparent  urine  in  increased  amount  is  reported 
(urina  spastica).  Eetention  of  urine  also  occurs,  particularly  after  the 
internal  or  subcutaneous  administration  of  morphin.  Choluria  in  jaundice 
is  a  well-known  symptom.  Conspicuous  choluria  without  jaundice  must 
lead  us  to  suspect  a  perforation  of  the  gall-bladder  into  the  urinary 
bladder.  Transitory  albuminuria  from  hyperemia  of  the  kidneys  arises 
during  the  attack,  and  disappears  after  its  cessation.  Albuminuria  with 
blood  and  casts  occurs  in  cholangitis  in  consequence  of  infectious  nephritis. 
Similar  conditions  are  observed  in  occlusion  of  the  common  duct  and 
chronic  jaundice.  Glycosuria,  peptonuria,  and  acetonuria  during  the  attack 
have  been  reported  by  different  authors. 

The  excretion  of  sodium  urate  and  uric  acid  as  a  sedimentum  lateritium 
is  not  of  rare  occurrence. 

In  one  case  leucin  and  even  tyrosin  crystals  were  found  for  weeks. 
The  excretion  of  indican  is  usually  normal;  sometimes,  however,  it  has 
been  found  increased. 

A  woman,  aged  38,  the  widow  of  a  letter  carrier,  was  admitted  to 
the  clinic  with  a  diagnosis  of  cholelithiasis;  during  the  attack,  a  con- 
spicuous increase  in  indican  was  found.  Operation  revealed  a  contracted 
gall-bladder  largely  adherent  to  the  omentum,  which  was  tensely  filled  with 
stones.     It  may  be  that  the  adhesion  of  the  gall-bladder  to  the  omentum 


L_lIclE   Oi-    <r:Tl£0 


502  GALL-STONES 

and  the  consequent  hindrance  of  peristalsis  had  an  influence  upon  the  in- 
crease of  indican  in  the  urine. 

A  marked  increase  of  indican  in  the  urine  in  cholelithiasis  is  evidently 
exceptional,  in  contrast  to  what  is  invariably  found  in  perityphlitis,  a 
circumstance  which  has  been  emphasized  by  Naunyn. 

The  doubtful  value  of  the  indigo  reaction  in  the  differential  diagnosis 
is  best  illustrated  by  the  two  following  cases. 

In  a  robust  baker,  aged  55,  in  whom  obstructive  jaundice  appeared 
with  colic-like  pains,  constantly  increasing  anorexia,  as  well  as  diarrhea, 
the  constant  absence  of  the  indigo  reaction  during  his  stay  in  the  Clinic 
was  particularly  emphasized.  Examination  of  the  feces  failed  to  show 
disease  referable  to  the  pancreas,  nor  was  alimentary  glycosuria  present. 
With  a  probable  diagnosis  of  "  cholelithiasis  with  cicatricial  closure  of  the 
common  bile  duct"  the  patient  was  transferred  to  the  surgical  division. 
There  operation  showed  a  carcinoma  arising  from  the  head  of  the  pancreas. 

A  contrast  to  this  was  formed  by  the  case  of  a  book-keeper,  aged  42, 
Avho  was  also  transferred  to  the  surgical  division  with  a  probable  diagnosis 
of  carcinoma  of  the  head  of  the  pancreas  and  occlusion  of  the  pancreatic 
and  common  ducts;  the  daily  examination  of  the  massive  feces,  containing 
large  amounts  of  fat  and  starch,  revealed  the  constant  absence  of  the 
indigo  reaction,  and  justified  to  a  certain  extent  the  diagnosis  of  disease 
of  the  pancreas.  At  the  operation  (cholecystentero-anastomosis),  the  com- 
mon bile  duct  was  found  to  be  of  the  thickness  of  a  small  finger,  the 
duodenum  with  the  large  mesentery  and  the  entire  freely  movable  pancreas 
unchanged. 

From  many  observations  (Charcot,  Eegnard,  Pick  and  my  own)  it  is 
noted  that  the  rises  in  temperature  upon  the  day  of  attack  in  intermittent 
hepatic  fever,  contrasted  with  malarial  paroxysms,  correspond  to  a  de- 
crease in  the  amount  of  urea.  According  to  F.  Pick,  this  decrease  affects 
not  alone  the  urea,  but  also  the  entire  nitrogen  and  ammonia  excretion. 
An  exact,  quantitative  urinary  analysis,  employing  all  the  care  which  is 
necessary  in  metabolism,  may  also  furnish  valuable  aid  in  those  difficult 
cases  in  which  the  diagnosis  hinges  between  hysteria  and  cholelithiasis. 

In  a  patient  who  presented  distinct  symptoms  of  right-sided  hemi- 
anesthetic  hysteria  I  found,  in  contrast  to  the  ordinary  type  of  ovarian 
hyperesthesia,  a  marked  sensitiveness  in  the  gall-bladder  region.  Upon 
examination  of  the  urine,  it  was  evident  to  jue  that  the  precipitate  which 
formed  after  the  addition  of  barium  chlorid  and  HCl  was  very  voluminous, 
from  which  I  inferred  an  increased  excretion  of  sulphate  in  the  urine; 
tlie  patient  had  taken  no  preparations  containing  either  Glauber's  salt  or 
sulphur.  The  pains  in  the  region  of  the  gall-bladder  increased,  and  after 
three  days  a  typical  picture  of  hepatic  colic  with  jaundice  was  presented. 
Tlie  qualitative  analysis  of  a  twenty-four-hour  amount  of  urine  voided 
during  the  attack  revealed  the  following:   Quantity  of  urine  1,040  c.c. 


PROGNOSIS  503 

urea  24.5,  phosphoric  anhydrid  in  combination  with  earths  0.51,  combined 
with  alkalies  2.09,  urinary  indigo  but  slightly  increased;  biliary  coloring 
matter  in  small,  bile  acids  in  smaller,  amounts ;  total  sulphuric  acid  6.22 ; 
combined  sulphuric  acid  0.19 ;  relation  100  S :  N  =  47.83  instead  of  15.1 ! 

This  was,  therefore,  a  proof  that  the  sulphuric  acid  did  not  owe  its 
origin  to  the  organic  albumin  rich  in  sulphur.  Without  endeavoring  to 
explain  this  phenomenon,  I  should  like  to  call  attention  to  the  excretion 
of  sulphuric  acid  in  the  urine  in  cholelithiasis  before  the  attack  of  colic, 
particularly  in  febrile  cases;  here  the  excretion  of  nitrogen  has  been  con- 
sidered, but  the  relation  of  sulphuric  acid  to  the  nitrogen  curve  has  as 
yet  been  but  little  utilized  for  diagnostic  purposes. 

An  exact  quantitative  investigation  of  the  urine  is,  however,  advisable 
for  testing  the  function  of  the  liver  prior  to  operation.  If  points  of 
support  for  the  diagnosis  of  absence  of  function  of  the  liver  cells  may 
be  gained  from  the  urine  (marked  decrease  of  nitrogen  excretion,  espe- 
cially glycosuria  and  urobilinuria),  the  surgeon  must  observe  a  certain 
amount  of  reserve,  because,  in  such  cases,  severe  hemorrhage  from  the 
operative  wound  is  to  be  expected  just  as  in  long-continued  jaundice. 

In  examining  the  Mood  in  cases  of  cholelithiasis  with  intermittent  fever 
and  chills,  as  has  been  stated  by  F.  Pick,  the  leukocyte  count  may  be 
of  importance,  in  that  the  absence  of  hyperleukocytosis  in  such  cases  is 
against  suppurative  processes  in  the  liver. 

In  the  Clinic  of  Prague,  in  Pick's  case  of  cholelithiasis  with  inter- 
mittent chills  and  rises  of  temperature  up  to  104°  F.,  in  the  course  of 
which  normal  or  subnormal  leukocyte  proportions  were  found  in  a  number 
of  attacks,  he  assumed  an  infection  with  the  bacterium  coli.  It  may  be 
seen  from  our  observation  that  the  cases  of  cholangitis  due  to  infection 
with  staphylococci,  streptococci,  and  particularly  with  diplococci,  run  their 
course  with  marked  leukocytosis. 

In  the  Clinic,  in  an  attack  of  fever  in  a  case  of  cholelithiasis  with 
general  infection  by  diplococci,  a  marked  increase  in  the  fibrin  of  the 
blood  was  found,  besides  leukocytosis. 

PROGNOSIS 

In  reconsidering  what  has  been  stated,  it  is  manifest  that  the  outcome 
of  cholelithiasis  is,  as  a  rule,  favorable.  On  the  other  hand,  in  the  course 
of  the  disease  conditions  may  arise  which,  in  a  comparatively  brief  time, 
cause  death.  In  this  category  belong  those  cases  of  severe  gall-stone  colic 
in  which  death  occurs  from  syncope,  probably  from  abdominal  shock,  or  in 
marantic  individuals  from  cardiac  weakness  with  degenerated  heart  muscle ; 
furthermore,  in  this  group  belong  those  cases  of  acute  cholecystitis  which 
run  their  course  with  high  fever  and  acute  meteorism,  becoming  fatal  either 
from  peritonitis  or  general  infection,  from  hepatic  abscesses,  ulcerative 


504  GALL-STONES 

and  suppurative  inflammation  of  the  biliary  passages  and  the  portal  vein, 
or  empyema  due  to  ordinary  pus  cocci,  or  ichorous  empyemata  with  fetid 
pus  in  which,  as  in  a  case  of  Zuber  and  Leroboulet,  anaerobic  microbes 
were  found.  The  dangers  from  obstruction  of  the  common  duct,  cholemia, 
jaundice  with  hemorrhage  appearing  after  a  short  time,  and  secondary 
acute  liepatic  atrophy,  are  no  less  threatening.  The  more  chronic  conse- 
quences and  complications  are  biliary  induration  and  cirrhosis,  chronic 
suppuration  of  the  peritoneum,  adhesions  with  stenosis  of  the  duodenum 
and  of  the  remaining  parts  of  the  intestine  by  giving  rise  to  gastro-intes- 
tinal  disturbances,  in  some  cases  increased  by  morphinism,  and,  finally, 
cancer  of  the  gall-bladder  and  biliary  passages,  all  of  which  may  cause 
death. 

TREATMENT 

On  account  of  the  many  aspects  of  the  disease  and  according  to  the 
stage  in  which  we  find  it,  the  objects  of  treatment  are  manifold.  At  one 
time  the  colic  most  requires  our  therapy,  in  other  cases  closure  of  the 
cystic  duct  from  stone,  of  the  hepatic  and  common  ducts,  at  other  times 
the  infection  of  the  gall  passages  and  peritoneal  -processes,  or  intestinal 
occlusion,  and,  finally,  it  must  be  our  aim  to  prevent  the  formation  of 
new  gall-stones.  In  the  treatment  of  the  paroxysms  of  pain,  opium  and 
its  preparations  remain  the  sovereign  remedy.  Belladonna,  atropin,  chloro- 
forni  and  ether  are  advised  for  the  same  purpose.  By  some  authorities 
the  use  of  oil  and  glycerin  is  advocated.  Hot  poultices,  hot  cataplasms, 
in  other  cases  the  ice-bag,  leeches,  and  protracted  warm  baths  are  the 
therapeutic  measures  with  which  to  combat  the  pain. 

In  regard  to  diet  there  is  still  great  diversity  of  opinion.  According 
to  experience,  it  appears  that  a  mixed  diet  most  thoroughly  meets  the 
indications.  A  plentiful  intake  of  fluid,  particularly  the  alkaline,  chlorin- 
containing  and  saline  mineral  waters  is  favored  by  practice. 

For  the  relief  of  the  gastric  and  intestinal  disturbances,  as  well  as  the 
jaundice,  Fleiner  has  advised  gastric  lavage,  which  he  believes  to  be  more 
efficacious  than  mineral  spring  cures,  but  in  regard  to  which  I  have  no 
personal  experience.  Fleiner  believes  that  by  the  influx  of  water  into 
the  small  intestine,  as  occurs  in  gastric  lavage,  there  is  resorption  of  the 
same  in  the  portal  veins,  and  thus  the  liver  and  the  entire  body  are  washed 
out.  Lately,  systematic  washings  with  silver  nitrate  solution  at  a  tem- 
perature from  122°  to  131°  F.  (50°  to  55°  C.)  have  been  advised  by 
Ehrlieli. 

These  energetic  procedures  may,  however,  change  a  latent  cholelithiasis 
into  the  actual  stage  of  wandering  of  the  stone.  Stones  which  are  latent, 
or  whicli  produce  only  slight  difficulty,  are  to  be  treated  as  a  noli  me 
tangcrc,  or,  more  correctly,  "  quieta  non  movere."  As  the  danger  consists 
largely  in  the  wandering  of  the  stones,  and  this  wandering  is  sometimes 


TREATMENT  505 

induced  by  a  Carlsbad  cure,  we  must  carefully  consider  whether  it  is  advisa- 
ble to  send  patients  with  slight  symptoms  to  Carlsbad;  in  regard  to  the 
value  of  this  old  and  popular  remedy,  a  Carlsbad  mineral-spring  treatment, 
there  is  far  from  unanimity  of  opinion.  According  to  Riedel,  Carlsbad 
water  alleviates  the  pain  of  cholecystitis  by  its  purgative  effect,  by  reducing 
the  hyperemia  of  the  inflamed  mucous  membrane  of  the  intestine,  but  it 
simultaneously  retards  the  expulsion  of  the  stones.  If  the  stones  are  passed 
while  in  Carlsbad,  this  does  not  occur  because  of,  but  in  spite  of,  Carlsbad. 
[In  the  treatment  of  cholelithiasis  with  infection  of  the  biliary  appara- 
tus and  in  cholangitis  without  stones,  many  clinicians  have  found  salicylic 
acid  of  value.  Salicylic  acid  is  excreted  by  the  liver  cells  or  at  any  rate, 
when  ingested,  it  may  be  found  in  the  bile.  It  is  an  antiseptic.  It  has 
been  used  sufficiently  to  prove  its  usefulness  in  infectious  conditions  of 
the  biliary  apparatus  with  and  without  gall-stones.  It  may  be  used  alone 
or  combined  with  alkalies  and  laxatives.  I  have  used  with  good  results 
the  following: 

I^   Sodii  salicylatis 1.0 

Sodii  phosphatis  Gran 2.0 

Sodii  sulphatis  Exsic 6.0 

Misce ;  signa.  One  teaspoonful  in  hot  water  one-half  hour  before  meals, 
three  or  four  times  a  day. 

Or  one  may  give  phenol  salicylas  0.3  in  pill  three  or  four  times  a  day, 
and  a  sufficient  dose  of  Carlsbad  salts  or  magnesii  sulphas  in  hot  water 
on  the  fasting  stomach  to  act  as  a  brisk  laxative. 

Oleate  of  soda  is  also  excreted  by  the  liver  and  undoubtedly  renders 
the  bile  more  fluid.  It  may  be  given  as  a  soda  soap  in  the  form  of  pills 
or  in  the  form  of  ol.  olivae  in  sufficient  dose  to  act  also  as  a  laxative. 
Free  intestinal  action  is  of  unquestioned  value  in  cholelithiasis  with  in- 
fection. The  "  internal  drainage "  established  by  this  method  probably 
explains  the  frequent  relief  from  cholangitis  with  gall-stones. 

Gall-stone  disease  must  be  recognized  as  a  surgical  disease.  The  physi- 
cian, with  benefit,  may  utilize  prophylactic  measures,  may  reduce  the 
accompanying  pain,  vomiting  and  infection,  but  only  the  surgeon  surely 
may  remove  the  calculus  and  correct  the  consequent  morbid  anatomy 
(adhesions,  etc.).  The  danger  of  cholangitis,  hepatic  abscess,  perigastric 
adhesions,  pancreatitis,  etc.,  occurring  as  a  result  of  gall-stones  is  so  great 
that  even  the  most  conservative  physician  may  well  hesitate  to  take  the 
responsibility  of  non-surgical  treatment.- — Ed.] 

The  greatest  difference  of  opinion  prevails  in  regard  to  the  question 
whether  early  operation  or  conservative  treatment  is  indicated.  In  the 
eases  in  which  the  course  is  unusually  protracted  and  painful  and  there 
is  loss  of  strength,  and  in  which  repeated  mineral  spring  treatments  are 


506  GALL-STONES 

ineffectual,  in  those  cases  in  which  an  empyema,  of  the  gall-bladder  threat- 
ens perforation,  or  an  irreducible  stone  obstruction  of  the  common  duct 
is  present,  no  internal  clinician  will  veto  an  operation.  It  is  different, 
however,  in  regard-  to  our  justification  for  an  operation  as  early  as  possible, 
and  it  would  be  interesting  to  know  whether  the  surgeon  who  is  con- 
vinced of  the  wisdom  of  radical  operation,  and  who  himself  has  gall- 
stones, would  not  prefer  to  give  Carlsbad  a  trial  before  consenting  to  an 
operation.     Certainly  general  rules  cannot  be  laid  down. 

The  method  of  operation  is  indicated  after  minute  weighing  of  all  the 
factors  which  are  decisive  for  the  topical  diagnosis  in  a  concrete  case. 
Where  the  diagnosis  has  been  incorrect,  for  example,  when  cholelithiasis 
has  been  diagnosticated  as  wandering  kidney,  and  the  surgeon,  pursuing 
this  incorrect  diagnosis,  attacks  the  supposed  wandering  kidney  posteriorly, 
and  finds  a  stone  in  the  cystic  duct,  the  uselessness  of  operative  procedure 
in  accordance  with  a  laid-out  program  is  apparent. 

The  specter  fear  of  the  serious  consequences  of  cholelithiasis,  which 
the  surgeons  love  to  oppose  to  a  conservative  treatment,  is  much  weakened 
by  contrary  considerations.  In  the  first  place,  quite  a  series  of  even  des- 
})erate  eases  have  been  known  which  were  nevertheless  cured  in  consequence 
of  perforation.  Moreover,  secondary  stone  formation  in  the  tied  stump 
of  the  cystic  duct  and  in  the  biliary  passages  remains  a  sword  of  Damocles 
even  after  a  successful  operation,  and,  finally,  in  the  cicatrix  of  operation 
a  carcinoma  may  develop  similarly  as  in  the  cicatrix  of  ulcer. 

The  surgery  of  the  biliary  passages  is  yet  too  recent  to  permit  a  con- 
clusive opinion  in  regard  to  the  permanent  results  of  operation,  and  we 
are  forced  to  agree  with  Wolfler,  who  says  that  surgery  of  the  biliary 
passages  has  for  several  years  presented  no  reliable  statistics,  and  holds 
that  those  operated  upon  should  be  observed  for  at  least  a  decade. 

Since  cholesterin  stones,  which  alone  come  into  question  here,  may 
develop  in  any  part  of  the  biliary  passages  in  which  there  is  mucous 
meml)rane  epithelium,  we  can,  in  fact,  speak  of  a  radical  prophylactic 
gall-stone  operation  only  when  it  is  possible  to  eradicate  the  entire  choles- 
terin-forming  mucous  membrane  epithelia. 


ETIOLOGY 

The  treatment  of  cholelithiasis,  particularly  its  prophylaxis,  rests  upon 
an  uncertain  foundation,  principally  for  the  reason  that  accurate  knowl- 
edge of  the  near  and  remote  causes  of  gall-stone  formation  is  completely 
lacking.  At  present  two  theories  chiefly  dominate  the  etiology  of  gall- 
stones, the  humoral  and  the  infectious.  The  champions  of  the  one  regard 
eliolelithiasis  as  a  constitutional  affection,  a  link  in  the  chain  of  that 
diathesis  whose  family  tree  is  arthritis.  They  base  their  opinions  chiefly 
upon  tlie  occurrence  of  gall-stones  in  families  in  which,  simultaneously. 


ETIOLOGY  507 

obesity,  gout,  diabetes,  hemorrhoids,  eczema,  increased  uric  acid  excretion, 
and  oxaluria,  etc.,  are  observed.  The  genesis  of  infection  by  means  of  the 
circulation  or  from  the  intestine  is  constantly  gaining  ground.  This  is 
based  particularly  upon  the  finding  of  the  bacterium  coli,  and  even  upon 
the  typhoid  bacillus  as  the  nucleus  of  gall-stones,  as  well  as  upon  the 
similarity  and  the  length  of  time  the  stones  have  been  in  the  gall-bladder, 
which,  according  to  Naunyn,  may  best  be  explained  by  a  single  bacterial 
infection. 

In  the  humoral  theory,  it  would  be  necessary  to  assume  that  the 
physiologic  composition  of  the  bile,  that  is,  the  relation  between  sodium- 
containing  bile  and  cholesterin,  has  been  altered  in  a  pathological  manner, 
and  that  the  liver,  to  begin. with,  secretes  a  pathologically  altered  bile 
which  readily  forms  a  sediment,  takes  the  shape  of  a  ball,  and  grows  into 
a  clumpy  stone.  In  the  case  of  man,  cholesterin  is  chiefly  important  since 
it  forms  the  principal  mass  of  gall-stones,  while  bilirubin  calcium  is  to  be 
looked  upon  only  as  a  cement.  The  fact  that  cholesterin  forms  the  chemical 
base  of  most  human  gall-stones  is  in  contrast  to  the  stones  of  the  herbivora, 
which  consist  principally  of  bilirubin  calcium,  so  that  the  gall-stones  of 
oxen  form  a  suitable  material  from  which  to  prepare  pure  bilirubin  in 
chemical  laboratories.  The  influence  of  food  and  drinking-water,  which 
is  maintained  by  several  authorities,  would,  therefore,  be  operative  only  in 
the  case  of  bilirubin  stones.  Experienced  cattle-raisers  maintain  that  gall- 
stones are  observed  with  surprising  frequency  in  cattle  and  swine  coming 
from  regions  where  the  meadows  contain  saltpeter,  and  this  frequently 
permits  a  direct  conclusion  as  to  the  regions  from  which  the  animals  come. 
In  the  etiology  of  human  stones,  their  rare  occurrence  with  long-standing 
inspissated  bile  by  the  occlusion  of  the  choledochus  (catarrhal  jaundice) 
is  noteworthy,  and  the  view  is  obvious  that  the  causal  factor  of  gall-stone 
fc^mation  is  to  be  sought  either  in  the  blood  from  which  the  liver  cells 
prepare  bile,  or  in  the  liver  cells  themselves,  which  furnish  a  pathological 
secretion. 

The  chemical  examination  of  the  blood  in  cholesterin  anemia,  as  well 
as  in  regard  to  its  diminution  of  alkalinity  and  the  deficiency  of  sodium- 
containing  biliary  acids,  has  been  negative  up  to  the  present  time.  No 
investigations  have  as  yet  been  made  of  hemoglobin  in  regard  to  its 
solubility,  its  power  of  crystallization,  its  faculty  of  coagulation,  or  its 
hygroscopic  relation.  It  is  possible  that  the  hemoglobin  varieties  of  dif- 
ferent individuals  are  not  identical,  and  that  the  hemoglobin  of  gall-stone 
patients  is  different  from  that  of  a  normal  person;  such  individuals  may, 
perhaps,  secrete  a  bile  which  crystallizes  very  readily,  similarly  as  the 
patient  with  the  urate  or  oxalate  diathesis,  who,  without  showing  symp- 
toms, intermittently  excretes  uric  acid  or  calciimi  oxalate  crystals  in  his 
urine. 

If,  however,  to  this  congenital  or  acquired  abnormality  in  the  quanti- 


508  GALL-STONES 

tative  composition  of  the  bile,  we  add  mechanical  stasis,  corset  liver, 
obesity,  pregnancy,  large  abdominal  tumors,  hepatoptosis,  hindrance  of 
the  diaphragm  action,  senile  atrophy  of  the  musculature  of  the  gall- 
bladder, a  sedentary  mode  of  life,  infrequent  meals,  or  bacterial  infection, 
it  is  easy  to  conceive  that,  similarly  as  when  uric  acid  stones  are  present, 
here  also  an  agglomeration  of  cholesterin  precipitate  may  result  in  gall- 
stones. In  this  sense,  cholelithiasis  may  be  regarded  as  a  diathesis  of 
the  tissues. 

By  analogy,  we  might  suppose  that  not  the  blood,  but  the  liver  cells 
themselves  are  affected,  and  that  in  their  decomposition  they  furnish 
cholesterin,  the  possibility  of  which  is  admitted  by  Naunyn.  In  opposition 
to  this  is  my  personal  experience,  according  to  which  gall-stones  do  not 
occur  in  alcoholic  cirrhosis.  It  therefore  follows  that  the  destroyed  liver 
coll,  damaged  by  alcohol,  furnishes  bile  which  is  not  a  suitable  material  for 
gall-stone  formation  although  in  its  quantity,  external  appearance,  color 
and  consistence  it  does  not  decidedly  deviate  from  the  normal.  Reports 
of  microscopic  and  chemical  examinations  of  bile  in  such  cases  are  not  at 
hand,  and,  so  far  as  I  know,  have  not  been  made. 

Some  of  the  factors  are  also  in  opposition  to  the  theory  of  an  infectious 
origin.  In  a  general  affection  of  the  biliary  passages  the  excretion  of 
pathogenic  bacteria  is  frequently  observed.  The  presence  of  typhoid  bacilli 
in  the  gall-bladder  as  the  only  bacterial  flora — which  makes  an  invasion 
by  way  of  the  intestine  very  unlikely,  but  which,  on  the  other  hand,  favors 
the  introduction  by  way  of  the  circulation — is  an  ordinary  finding  in  the 
course  of  enteric  fever.  Bacteriemia  is  frequent  in  ulcerative  tuberculosis, 
while  gall-stones  in  tuberculosis,  as  well  as  after  a  general  bacterial  in- 
fection, are  seldom  observed.  Even  in  the  cholelithiasis  which  follows 
these  maladies  an  absolute  relation  between  the  diseases  cannot  be  proven. 

To  explain  acute  serous,  rapidly  retrogressing  cholecystitis,  which  ae- 
velops  a  sterile,  transparent  dropsy  of  the  gall-bladder  by  an  infection 
from  the  bacterium  coli  in  which  the  latter  organism  has  been  killed, 
appears  to  me  somewhat  far-fetched,  if  we  take  into  consideration  that 
infections  from  the  bacterium  coli,  as,  for  example,  in  cystitis  or  in  pyelitis, 
are  by  no  means  of  such  short  duration.  Why  should  the  gall-bladder 
in  particular  be  so  slightly  injured  by  the  bacterium  coli,  especially  since 
it  has  been  proven  that  bile  is  an  excellent  culture  medium  for  this  bac- 
terium? In  other  mucous  membranes  we  are  familiar  with  acute  swelling 
and  increased  secretion  which  cannot  be  regarded  either  as  inflammation 
or  as  infection.  I  refer  here  particularly  to  coryza  vasomotoria  and  to 
bronchial  asthma,  which  cannot  be  regarded  as  infectious  mucous  mem- 
brane inflammations,  either  from  a  bacteriologic  or  clinical  standpoint. 

Some  forms  of  cholelithiasis  marked  by  the  sudden  disappearance  of 
decided  and  painful  tumors  of  the  gall-bladder  with  all  of  their  accom- 
])anying  symptoms  remind  us  of  the  turbulent  catarrhal  symptoms  with 


ETIOLOGY  609 

which  bronchial  asthma  runs  its  course,  a  true  "  parturiunt  montes " 
which,  as  Kehr  remarked  of  infectious  cholecystitis,  "  often  resembles  a 
fire  of  straw  that  blazes  up  but  once  and  is  rapidly  extinguished."  I 
presume  that  at  least  many  forms  of  this  gall-stone  colic  which  have  been 
explained  as  abortive  infections  belong  to  the  group  of  neuroses  of  secretion, 
and  are,  therefore,  in  fact,  catarrhal  asthma  of  the  biliary  passages.  For 
the  gall-stone  quiescent  in  the  gall-bladder  only  occasionally  assumes  the 
role  of  a  provocative  agent  for  the  development  of  colic,  as,  for  example, 
nasal  polypi  in  the  development  of  bronchial  asthma.  Besides  the  abnor- 
mal secretion  which  is  peculiar  to  asthma,  spasm  of  the  bronchial  muscle 
is  a  prominent  symptom;  the  accompanying  fulminant  nervous  signs  are 
analogous  to  those  of  gall-stone  colic  in  which  the  secretion  stored  in  the 
gall-bladder  forms  a  motive  power  for  the  wandering  stone.  In  acute 
serous  dropsy  of  the  gall-bladder,  which  at  first  is  sterile  but  which  by 
irritation  of  the  foreign  body  and  secondary  bacterial  infection  may  lead 
to  cholecystitis,  the  effect  of  the  operative  removal  of  stones  may  be  com- 
pared to  that  of  the  extraction  of  nasal  polypi  in  asthma.  Just  as  infec- 
tious bronchitis  and  lobular  pneumonia  may  develop  in  the  course  of 
bronchial  asthma,  so  secondary  infections  of  the  biliary  passages  play  an 
important  role  in  the  pathology  of  cholelithiasis.  Although  it  is  evident 
that,  in  most  cases,  these  infections  merely  change  the  latent  to  the  actual 
stage  of  cholelithiasis,  I  am  inclined  to  believe  that  quite  a  number  of 
cases  of  gall-stone  colic  are  neither  inflammatory  nor  infectious.  The 
capricious  behavior  of  some  cases,  with  a  latency  sometimes  lasting  for 
years,  an  eruptive  appearance  after  psychical  emotion  and  a  sudden  dis- 
appearance, the  rapid  sequence  of  relapses,  the  long  intervals  of  health — 
these  peculiarities  are  not  readily  explained  by  the  assumption  of  a  transi- 
tory infection,  and  therefore  I  regard  these  cases  which  run  their  course 
with  acute  dropsy  of  the  gall-bladder  as  neuroses  of  secretion,  parallel 
to  those  observed  in  catarrhal  asthma. 

Rokitansky  ^  points  out  that  pure  cholesterin  stones  may  be  excreted 
without  bile  in  consequence  of  the  pathological  secretion  of  transparent 
synovial-like  fluid  in  dropsy  of  the  gall-bladder,  in  complete  occlusion 
of  the  cystic  duct.  This  opinion  was  first  clearly  formulated  by  Naunyn 
who  also  found  stones  in  a  diverticulum,  "  surroimded  by  mucous  mem- 
brane," which  for  a  long  time  had  precluded  the  presence  of  bile.  Choles- 
terin is,  however,  produced  by  the  mucous  membrane  itself,  while  bilirubin 
stones  are  formed  only  where  bile  is  found. 

These  findings  of  Rokitansky  and  Naunyn  alone  favor  the  assumption 
that  calculus  formation  is  a  local  product  of  the  epithelia  of  the  gall- 
bladder, that  is,  of  the  epithelia  of  the  biliary  passages,  and  that  the  bile, 
as  such,  has  no  action  in  the  original  formation  of  the  stones.     Naunyn 


Handbuch  der  speciellen  pathologischen  Anatomic,"   1842-1844. 


510  GALI^TONES 

directly  proved  this  latter  fact  by  microscopic  investigation;  he  showed 
that  the  original  pulp  of  the  gall-stone  consists  of  structureless,  soft 
clumps  of  cholesterin  which  project  from  the  epithelium  of  the  biliary 
passages  and  subsequently  crystallize. 

This  is  suggestive  of  the  formation  of  Charcot's  crystals  which  are  the 
product  of  the  crystallization  of  pre- formed  eosinophilic  cells;  it  is  proven 
chiefly  by  the  fact  that  the  contents  of  pemphigus  vesicles  sometimes 
consist  only  of  eosinophilic  cells  which  on  being  subjected  to  a  low 
temperature  permit  us  to  recognize  the  direct  transformation  of  the  de- 
composed cells  into  Charcot-Leyden  crystals.  The  subject  is  an  interesting 
one;  in  the  surroundings  of  the  parasite  in  the  intestine  eosinophilic  cells 
form  in  large  numbers,  and  by  their  subsequent  decomposition  furnish 
Charcot-Leyden  crystals.  The  process  appears  to  be  similar  in  the  mucous 
membrane  of  the  biliary  passages.  The  cholesterin  nuclei  which  originate 
from  decomposed  epithelia  are  perhaps  themselves  the  product  of  a  path- 
ologic secretion,  analogous  to  that  in  bronchial  asthma,  and  in  their  fur- 
tluT  course  as  foreign  bodies  they  probably  cause  a  local  irritation  which 
produces  this  pathologic  secretion  of  the  mucous  membrane.  In  a  wide 
sense  a  peculiar  crystallizing  catarrh  is  certainly  present,  but  the  etiology, 
tlie  primum  movens,  of  this  catarrh  is  not  bacterial  infection.  The  latter 
may  occur  subsequently,  and  is  often  an  undesirable  complication.  It  is, 
however,  not  the  cause,  but  the  consequence,  of  stone  formation. 

It  is  possible  that  the  entire  epithelium  of  the  biliary  passages  is  not 
involved,  but  that  only  those  layers  which  differ  biologically  and  morpho- 
logically furnish  the  material  for  the  excretion  of  cholesterin. 

These  considerations  suggest  fresh  problems  in  the  study  of  chole- 
lithiasis, further  examinations  of  the  liver  and  bile,  and  particularly  also 
of  the  blood  in  order  to  ascertain  its  power  of  crystallization  and  the 
coagulation  of  hemoglobin;  they  also  show  the  importance  of  an  exact 
microscopic  examination  of  the  secretion  in  cases  of  sterile  dropsy  of  the 
gall-bladder,  especially  in  those  instances  in  which  there  is  no  infection 
from  the  bacterium  coli,  therefore,  above  all  others,  an  examination  of  the 
fresh  secretion  of  the  gall-bladder  in  operative  cases. 

At  the  present  time  we  are  still  under  the  dominating  influence  of  the 
two  theories  that  have  been  described,  the  humoral  and  the  infectious, 
and  although  neither  is  in  all  respects  satisfactory,  we  cannot  be  entirely 
inde])endent  of  these  so  long  as  we  possess  no  positive  knowledge  upon 
wliicli  to  base  other  views  of  the  etiology  of  gall-stones. 


DISEASES  OF  THE   INTESTINES 


34 


ACUTE    DIFFUSE    PERITONITIS,    APPEN- 
DICITIS,   AND    PERITYPHLITIS 

I.     DIFFUSE  AND   CIRCUMSCRIBED   PERITONITIS 
By  O.    VIERORDT,    Heidelberg 

ACUTE   DIFFUSE   PERITONITIS 

As  an  introduction  to  the  discussion  of  our  present  views  of  acute 
peritonitis  I  will  relate  the  following  clinical  history: 

Case  I. — A  previously  healthy  merchant,  aged  31,  was  taken  ill  after  a  few  days 
of  vague,  dull  pain  in  the  right  side  of  the  abdomen  which  he  had  disregarded,  and 
upon  the  20th  of  October,  about  midday,  he  was  seized  with  very  severe  pain  in  the 
right  lower  abdominal  region  which  compelled  him  to  seek  his  bed;  soon  afterward 
he  had  chilly  sensations  which  increased  to  marked  chills;  there  was  also  nausea, 
eructation  and  vomiting,  first  of  food  and  then  of  bilious  mucus;  a  little  later  tenes- 
mus appeared,  the  patient  first  voiding  small,  compact  feces,  followed  by  scant,  thin 
dejecta.  Within  a  few  hours  the  abdomen  had  become  tympanitic,  the  pains  con- 
tinued with  exacerbations  upon  motion,  after  eructations,  and  on  talking;  the  entire 
abdomen  was  very  sensitive.  Strangury  with  the  frequent  discharge  of  scant  urine 
was  observed. 

Toward  evening  the  physician  found  the  patient  extremely  ill,  immovable  in  the 
active  dorsal  decubitus,  with  an  anxious  facial  expression,  reddened  cheeks,  cautious, 
superficial  respiration  with  a  low,  hushed  voice;  he  complained  of  continuous,  also 
occasionally  of  marked  tearing  and  contracting,  pains  in  the  entire  abdomen,  most 
severe  upon  the  right  side  low  down;  the  temperature  was  103.2°  F.,  the  pulse  was 
112,  full,  somewhat  tense,  regular  and  even. 

The  lips  were  dry,  the  tongue  markedly  coated;  fostor  ex  ore  was  present;  pain- 
ful eructations  were  frequent,  also  singultus,  complete  anorexia  and  extreme  thirst. 
The  respirations  were  superficial,  quite  rapid,  and  purely  thoracic;  the  diaphragm 
was  slightly  raised;  the  pulmonary  liver  border  was  in  the  right  mammillary  line 
at  the  lower  border  of  the  fifth  rib;  upon  anterior  examination  the  thoracic  organs 
appeared  normal ;  the  examination  of  the  back  was  not  then  imdertaken. 

The  entire  abdomen  was  uniformly  tympanitic,  everywhere  very  sensitive  to  the 
slightest  pressure,  but  more  so  upon  the  right  side  than  upon  the  left.  There  was 
also  pain  upon  pressure  in  the  lumbar  region. 

Signs  of  abdominal  respiration  were  absent.  Careful  palpation  showed  a  uniform, 
drum-like  resistance,  otherwise  nothing  abnormal.  The  percussion  note  over  the 
abdomen  upon  light  tapping  (and  only  this  could  be  borne)  revealed  no  decided 
difference,  and  nowliere  any  dulness;  upon  prolonged  continued  auscultation,  high- 
pitched  intestinal  murmurs  were  here  and  there  heard. 

513 


514      ACUTE  PERITONITIS,  APPENDICITIS,  AND  PERITYPHLITIS 

Retraction  of  the  thighs  produced  diffuse  abdominal  pain,  more  marked  upon 
the  right  side  than  upon  the  left;  careful  examination  of  the  hernial  rings  gave  a 
negative  result. 

Upon  careful  digital  exploration  per  rectum  in  the  dorsal  decubitus,  nothing  ab- 
normal was  noted  except  pain  in  the  floor  of  the  pelvis;  the  rectum  was  empty. 

Since  morning  neither  feces  nor  flatus  had  been  passed;  the  patient  complained 
of  strangury  which,  however,  he  rarely  attempted  to  relieve  because  he  feared  to 
aggravate  the  pain  which  shot  downward  and  radiated  into  the  urethra.  The  urine 
was  of  high  color,  clear,  and  contained  a  trace  of  albumin  and  large  amounts  of 
indican. 

The  physician  in  charge  of  the  case  diagnosticated  acute,  diffuse  peritonitis,  the 
origin  of  which  was  not  quite  clear;  very  likely  it  was  in  the  appendix.  He  ordered 
absolute  rest,  that  the  urine  and  feces  be  voided  in  the  recumbent  posture;  that, 
for  the  present,  only  small  quantities  of  ice  be  taken  by  the  mouth ;  that  two  bags 
filled  with  ice  be  applied  to  the  abdomen,  and  be  suspended  from  a  hook  if  tliey 
could  not  be  borne  directly  upon  the  abdomen.  Furthermore,  at  first  every  two 
liours,  later  somewhat  less  frequently,  0.03  of  opium  purum  in  powder  form  was  to 
be  taken  in  a  little  water. 

In  the  following  forty -eight  hours,  with  irregular  variations  and  a  slight  ten- 
dency to  rise,  the  temperature  ranged  between  102.2°  and  105.3°  F.  The  pulse 
became  more  frequent  but  remained  strong  and  uniform;  the  respirations  were  un- 
altered in  character  but  increased  in  frequency  to  48.  The  patient,  unless  under  the 
iiilluence  of  opium,  was  sleepless,  his  mind  was  clear,  and  he  gave  us  the  impression 
of  being  extremely  ill,  although  not  in  collapse.  The  pains,  eructation  and  vomiting 
Mere  decidedly  relieved  by  the  opium ;  but  ice-bags  for  a  time  were  not  well  borne 
and  cold  Priessnitz  compresses  were  substituted.  Vomiting  was  rare,  was  invariably 
bilious  and  coarse-grained;  neither  feces  nor  flatus  were  discharged;  the  urine  was 
as  before,  the  diazo-reaction  negative. 

Distention  of  the  abdomen  and  the  area  of  diffuse  resistance  increased;  sensi- 
tiveness to  touch  appeared  to  be  dulled  by  the  opium ;  in  the  ileo-cecal  region,  how- 
ever, it  was  constantly  severe  and  lancinating.  The  liver  dulness  below  decreased; 
tlie  pulmonary  liver  border  extended  to  the  upper  border  of  the  fifth  rib;  on  the  right 
side  of  the  abdomen  between  the  navel  and  the  anterior  superior  spine  of  the  ilium 
a  circumscribed  slight  dulness  was  observed.  There  was  great  nausea  and  burning 
thirst. 

Ithignosis:  Acute  diffuse  appendicular  peritonitis,  probably  also  perforation;  cir- 
cumscribed perityphlitic  abscess. 

Operation  was  considered  but  not  performed.  Removal  to  the  hospital  for  the 
l)urpose  of  an  operation  was  absolutely  declined  by  the  patient. 

I  saw  him  upon  the  following  day,  the  fourth  of  the  disease.  In  general  the 
severity  of  the  clinical  picture  had  increased,  especially  some  of  the  individual 
symptoms:  Severe,  markedly  febrile  general  condition;  temperature  about  104°  F. 
and  showing  moderata  remissions ;  pulse  120  to  136,  moderately  full,  regular.  There 
was  insonmia  with  occasional  opium  slumber;  otherwise  the  mind  was  clear  but 
anxious.  The  tongue  was  thickly  coated,  the  lips  were  dry,  there  was  tormenting 
thirst.  The  cheeks  were  red.  The  patient  maintained  the  dorsal  decubitus  with 
feebly  flexed  legs  and  hushed  voice;  the  hands  moved  but  slightly  and  trembled. 
Occasionally  there  were  spontaneous  attacks  of  severe,  tearing,  abdominal  pain, 
starting  posteriorly  in  the  lower  right  side.  The  abdomen  was  very  tympanitic  and 
tense,  and  could  scarcely  be  touched ;  nevertheless,  it  was  possible  to  determine  upon 
the  rinlit  side  low  down  an  area  of  dulness  about  the  size  of  a  hand  with  increased 
resistance;    otherwise   the   note   was   tympanitic  upon   percussion.      The   diaphragm 


ACUTE  DIFFUSE  PERITONITIS  515 

was  raised;  except  for  a  small  zone  liver  dulness  was  absent.  Now  and  then  there 
was  grass-green  vomitus  which,  the  last  time,  contained  a  few  brownish  granules 
and  had  a  fecal  odor.     Urine  unchanged;   micturition  very  painful;  no  feces. 

Opium  at  first  decidedly  influenced  the  condition;  the  patient  took  daily  0.5  to 
1.8,  and  since  yesterday  morphin  subcutaneously  0.02  at  a  dose.  Ice-bags  were 
not  well  borne,  and  Priessnitz  compresses  were  used  continuously.  The  intake  of 
food  was  reduced  to  almost  nothing. 

With  a  sharply  circumscribed  perityphlitic  abscess  there  could  be  no  doubt  of 
the  diagnosis  of  diffuse  peritonitis  nor  of  the  indication  for  operation  on  account 
of  the  long  continuance  of  the  severe  symptoms.  But  neither  this  proposition  nor 
that  of  an  exploratory  laparotomy,  the  result  of  which  might  have  induced  the 
patient  to  yield,  was  accepted. 

Morphin  was  ordered  subcutaneously,  Priessnitz  compresses  to  the  abdomen,  pel- 
lets of  ice  and  meat  jelly  by  mouth;  eventually  gastric  lavage. 

Upon  the  sixth  day  of  the  disease  the  picture  changed:  The  complexion  became 
sallow,  the  face  elongated,  the  eyes  hollow;  the  pulse  was  140,  small,  but  quite 
regular;  the  temperature  was  101.3°  F. ;  there  was  clammy  perspiration  and  a  cool 
skin,  the  hands  were  cold;  frequently  slight  eructations  occurred  and,  now  and  then, 
ineffectual  or  mild  paroxysms  of  vomiting  of  a  greenish  yellow  material  with  a 
slight  fecal  odor.  The  mind  was  clear;  there  was  little  pain.  The  abdomen  became 
somewhat  softer,  much  less  painful,  and  was  readily  palpated  and  percussed;  there 
was  a  distinct  resistance  about  the  size  of  a  hand,  quite  firm,  and  not  fluctuating, 
and  accompanied  by  marked  dulness,  around  McBurney's  point  and  downward,  and 
only  in  this  region  severe  stabbing  pain;  in  other  areas  no  dulness. 

The  symptoms  were  those  of  moderately  severe  peritoneal  collapse;  the  prognosis 
was  very  grave  although  not  positively  hopeless.  Treatment:  Small  quantities  of 
alcohol,  to  be  followed  by  camphor. 

This  condition  lasted  nearly  twenty-four  hours ;  then  a  very  large  and  hard  stool, 
followed  by  a  thin  one  of  hemorrhagico-purulent  character  was  discharged  and  simul- 
taneously a  decided  change  took  place:  The  appearance  and  pulse  improved;  the 
abdomen  became  softer  with  the  exception  of  the  marked  resistance  upon  the  right 
side  low  down,  and  the  fever  slightly  remittent,  its  maximum  101.1°  F.  Vomiting 
did  not  recur;  the  patient  moved  about  somewhat  in  bed  and  slept  several  hours 
in  a  half -lateral  posture.     Meat  jelly  and  cold  beef  tea  were  swallowed. 

Upon  the  next  day  there  were  several  hemorrhagico-purulent  stools,  the  urine 
was  profuse  and  voided  without  pain.  Nevertheless,  a  firm,  flat  resistance  was  still 
felt  in  the  lower  right  side  and  upon  pressure  there  was  lancinating  pain ;  no  fever. 

There  could  be  no  doubt  that  the  perityphlitic  abscess  had  ruptured  into  the  in- 
testine, and  that  in  consequence  of  this  the  diffuse  peritonitis  had  at  once  been 
relieved. 

Treatment:  Warm,  followed  by  hot,  flax-seed  poultices;  rest;  freshly  expressed 
meat  juice  or  beef  tea,  in  all  200  grams;  thin  gruel  made  with  milk,  200  grams; 
wine,  100  grams  in  twenty-four  hours,  small  portions  to  be  taken  every  two  hours; 
no  drugs. 

This  improvement  continued  for  several  days  and  even  became  more  marked.  The 
abdomen  returned  to  the  norm  with  the  exception  of  the  ileo-cecal  region ;  there  was 
a  small  stool  daily  without  recognizable  pus;  no  fever. 

Upon  the  tirclfth  day  of  the  disease  vomiting  suddenly  recurred,  with  severe, 
diffuse  abdominal  pain,  marked  meteorism,  and  fever  to  about  102.2°  F. ;  the  symp- 
toms increased  in  severity,  and  changed  during  the  night.  The  next  morning  I  found 
the  patient  in  collapse,  his  temperature  97.3°  F.,  pulse  160,  thready,  uneven;  con- 
spicuous   facies    hippocratica ;    no    pain;    a   slightly    comatose    condition,    mod<^rate 


516      ACUTE   PERITONITIS,   APPENDICITIS,  AND  PERITYPHLITIS 

meteorism,  no  movement  of  the  bowels.  Stimulants  were  without  effect;  subcuta- 
neous saline  infusion  revived  the  patient  but  only  for  a  short  time,  and  death  occurred 
the  following  morning  upon  the  fourteenth  day  of  the  disease. 

Autopsy:  Normal  condition  of  the  serosa  above  the  omentum;  the  appendix  sur- 
rounded by  adhesions  embedded  in  fecal  pus,  gangrenous  toward  its  terminal  portion, 
and  showing  perforation;  fecal  calculus  in  the  pus;  appendix  movable  toward  the 
cecum.  Agglutinated  point  of  rupture  at  the  median  periphery  of  the  cecum  near 
thn  ileo-cecal  valve.  The  perityphlitic  pus  appeared  to  be  sacculated  by  adherent 
intestinal  coils,  but  beyond  the  adhesions  in  the  free  abdominal  cavity  below  the 
oniontum  there  was  diffuse,  fresh,  fibrinous  peritonitis  and  distributed  here  and 
there  small  quantities  of  thin,  putrid  pus  (many  bacteria,  large  quantities  of  strep- 
tococci and  coli  bacilli).  The  peritoneum  was  injected,  of  a  delicate  rose-red  color, 
here  and  there  covered  with  fine,  mucus-like  pseudo-membranes.     Heart  flabby. 

This  clinical  history  is  in  every  respect  typical  and  instructive. 

It  shows  us  the  origin  of  peritonitis  which  is  by  far  the  most  common : 
in  a  diseased  appendix.  At  the  autopsy  this  was  found  necrotic  and  per- 
forated. It  is  questionable  whether  the  perforation  existed  from  the  onset 
of  the  disease;  it  is  possible  that  at  first  an  ulcer  extending  to  the  serosa 
caused  an  infection  of  the  peritoneum ;  at  all  events  this  occurred  acutely, 
and  produced  the  sharply  defined  disease.  The  clinical  abdominal  symp- 
toms in  the  first  period  of  the  malady  pointed  to  the  fact  that  at  the 
onset  there  had  been  a  diffuse  inflammation  of  the  peritoneum,  and  that 
later  by  the  adhesions  to  the  appendix  which  were  found  at  the  autopsy 
an  early  encapsulation  of  pus  had  taken  place  in  the  ileo-cecal  region; 
this  produced  a  purulent  softening  in  the  wall  of  the  cecum  and  led  to 
the  favorable  rupture  of  pus  into  the  intestine  and  to  an  immediate  ameli- 
oration of  the  acute  peritonitis.  The  point  of  rupture,  however,  then 
closed,  and  partly  to  this  circumstance,  partly  perhaps  to  the  action  of 
fresh  infectious  and  toxic  material,  perhaps  only  to  the  perforation  of 
the  appendix,  may  be  ascribed  the  exacerbation  of  the  peritonitis,  that  is, 
a  renewed  attack  which  caused  the  death  of  the  patient.  In  regard  to 
the  fulminant  symptoms  at  the  onset  of  the  disease,  however,  it  is  more 
likely  that  even  then  perforation  had  already  occurred,  and  that  the  final 
and  fatal  exacerbation  was  in  consequence  of  adhesions  formed  in  the 
first  period  which  were  powerless  to  resist  the  entrance  of  organisms 
producing  inflammation.  The  pus  finally  broke  through  the  adhesions, 
and  produced  diffuse  peritonitis. 

Moreover,  the  bacterial  finding  of  streptococci  and  coli  bacilli  in  the 
perityphlitic  abscess  is  typical,  and  the  limitation  of  the  diffuse  peritonitis 
to  areas  below  the  omentum  is  also  instructive.  This  simultaneously 
prevented  the  invasion  of  organisms  producing  inflammation  into  the 
serous  surfaces  above. 

This  strong  man,  aged  31,  had  previously  regarded  himself  as  per- 
fectly well.  Nothing  indicated  the  danger  in  which  he  found  himself  and 
which  had  existed  since  the  appearance  of  the  fecal  calculus,  the  time 


ACUTE   DIFFUSE   PERITONITIS  517 

when  this  had  formed  being  impossible  to  determine.     The  disease  ap- 
peared acutely  with  fulminant  symptoms. 

Severe  abdominal  pain  with  tense  abdominal  walls,  fever  and  vomiting 
form  the  characteristic  triad  in  the  first  phase  of  the  disease;  less  rapidly 
does  meteorism  appear.  This  depends  upon  the  fact  whether  the  inflam- 
mation of  the  serosa  quickly  spreads  or  remains  local.  Peritoneal  meteor- 
ism is  peculiar.  The  abdomen  is  uniformly  distended,  balloon-like;  the 
muscles  as  well  as  the  rest  of  the  abdominal  walls  are  tense.  It  must  be 
added,  however,  that  in  spite  of  the  excruciating  pain  upon  touch  there 
is  no  sign  of  contraction  of  the  abdominal  muscles,  of  the  "  muscular  re- 
sistance" {defense  musculaire)  which  is  so  common  on  pressure  in  other 
forms  of  abdominal  pain,  particularly  when  circumscribed.  The  same  is 
true  of  the  diaphragm;  it  is  forced  upward,  the  muscles  are  therefore 
elongated  and  tense;  but  there  is  no  evidence  of  active  contractions.  Ab- 
dominal respiration  ceases;  gradually  then,  as  may  be  recognized  by  the 
limits  of  percussion,  increasing  loss  of  muscle  tonus  is  added.  In  this 
case  the  autopsy  showed  that  the  peritonitis  had  not  advanced  up  to  the 
serosa  of  the  diaphragm. 

The  excessive  abdominal  pain,  increased  by  movement  and  on  the 
slightest  pressure,  caused  the  patient  to  remain  motionless  upon  his  back 
and  to  avoid  the  slightest  movement  of  the  abdomen  either  by  speaking 
or  coughing. 

At  the  start  the  temperature  was  uniformly  high,  but  later  remissions 
in  the  pus  fever  were  recognized.  The  pulse  from  the  onset  was  com- 
paratively frequent,  regular,  and  somewhat  tense. 

The  vomitus  was  at  first  composed  of  the  gastric  contents,  then  bile 
of  a  peculiarly  pure,  grass-green,  biliverdin  color  mixed  with  a  yellowish 
chyme-like  material,  and  in  the  later  stages  of  the  disease  showed  thin 
masses  having  a  fecal  odor  (ileus  paralyticus).  In  regard  to  the  dejecta, 
the  two  passages  at  the  onset  of  the  disease  pointed  to  increased  peristalsis ; 
this  was  of  short  duration,  soon  changing  to  the  opposite  condition,  and 
until  the  rupture  of  the  perityphlitic  abscess  absolute  constipation  existed. 

Among  these  signs  pain,  either  spontaneous  or  upon  touch,  a  rise  in 
temperature,  increased  frequency  of  the  pulse  and,  in  general,  the  signs 
of  severe  illness,  are  to  be  looked  upon  as  the  local  and  general  symptoms 
of  a  severe  septic  inflammation ;  vomiting,  at  least  in  the  first  stages  of 
peritonitis,  was  due  to  decided  reflex  irritation  of  the  numerous  branches 
of  the  peritoneal  nerves ;  the  fecal  discharges  at  the  onset  may  be  explained, 
but  by  no  means  invariably,  as  due  to  peristalsis  acting  reflexly.  The 
constipation  which  followed  this,  however,  as  well  as  the  meteorism,  must 
be  attributed  to  a  hypotonia  and  paralysis  of  the  musculature  of  the  intes- 
tine by  collateral  edema. 

Pain  upon  urination  and  strangury  were  due  to  inflammation  of  the 
peritoneal  coat  of  the  bladder,  in  which  a  noticeable  irritation  was  pro- 


518       ACUTE   PERITONITIS,   APPENDICITIS,   AND  PERITYPHIJTIS 

duced  by  slight  distention  as  well  as  by  contraction  of  the  bladder.  The 
albuminuria  was  the  well  known  infectio-toxic  "  febrile "  form ;  indi- 
canuria  was  in  proportion  to  the  fecal  stasis. 

In  the  course  of  the  next  few  days  a  new  symptom  was  added  to  this 
group:  Exudation,  which  was  demonstrable  both  by  palpation  and  percus- 
sion. It  was  the  natural  consequence  of  inflammation  of  the  peritoneum, 
and  was  both  of  diagnostic  value  as  indicating  general  peritonitis  and 
of  special  value  in  that,  more  definitely  than  the  pain,  it  pointed  to  the 
original  seat  of  the  affection,  which,  according  to  present  indications, 
could  only  have  been  an  internal  incarceration  following  right-sided  in- 
guinal hernia,  or  femoral  hernia,  or  appendicitis.  As  neither  the  history 
nor  the  general  status  (normal  condition  of  the  hernial  rings)  furnished 
any  points  of  support  for  the  first  view,  only  the  diagnosis  of  appendicitis, 
that  is,  of  perforation  of  the  appendix,  could  be  made  with  that  degree 
of  certainty  attainable  in  diseases  of  the  abdominal  cavity  in  general. 

After  the  appearance  of  these  symptoms,  a  more  or  less  firmly  adherent 
but  limited  perityphlitic  abscess,  and  a  less  intense  although  well  devel- 
oped peritonitis  in  this  region,  were  assumed;  tTie  latter,  notwithstanding 
the  general  painful  meteorism,  was  not  necessarily  diffuse  in  the  strict 
sense  of  the  term;  the  omentum  often  protects  the  upper  abdominal  cavity 
from  infection,  as  was  proven  in  this  case  at  the  autopsy.  It  is  possible 
that  this  diffuse  peritonitis,  which  did  not  in  the  early  period  of  the 
affection  extend  beyond  the  limited  local  focus,  was  not  due  to  the  intes- 
tinal contents  and  to  bacteria,  but  chiefly  to  bacterial  toxins  which  arose 
from  the  circumscribed  original  focus.  This  fact  is  pointed  out  by  the 
prompt  retrogression  of  the  diffuse  peritoneal  symptoms  after  rupture  of 
the  abscess;  the  diffuse  peritonitis  of  this  first  stage  might  then  be  desig- 
nated a  non-bacterial  "  chemical "  inflammation,  according  to  the  termi- 
nology now  in  vogue ;  finally,  it  was  positively  a  bacterial  infection,  although 
the  post  mortem  finding  of  bacteria  in  the  distant  folds  of  the  peritoneum 
is  not  proof  of  this;  we  know  that  during  the  terminal  agony  or  after 
death  these  may  wander  a  long  distance  from  the  perityphlitic  focus. 

After  the  symptoms  of  local  and  general  inflammation  with  their  sec- 
ondary signs  in  the  stomach  and  intestine  had  lasted  for  six  days,  sud- 
denly a  complete  change  took  place:  The  nervous,  anxious,  extremely 
distressed  patient  became  feeble  and  scarcely  complained  at  all;  his  for- 
merly congested  face  was  pale  and  elongated,  the  nose  pointed  and  cool; 
tlu>  skin  lost  its  turgescence  and  warmth,  and  was  covered  with  a  cold 
sweat;  the  bodily  temperature  also  fell,  the  pulse  -became  small  and  fre- 
quent but  remained  quite  regular,  the  abdomen  became  softer  and  to  a 
great  extent  lost  its  sensitiveness ;  the  vomiting  decreased  to  a  few  painless 
attacks,  and  singultus  disappeared:  A  picture  which,  to  a  certain  extent, 
is  a  combination  of  collapse  and  narcosis  although  not  to  the  degree  of 
profound  loss  of  consciousness,  being  the  picture  of  an  intoxication  in 


ACUTE   DIFFUSE  PERITONITIS  519 

sharp  contrast  to  the  preceding  febrile  state.  Just  as  the  affection  had 
suddenly  developed  to  its  full  height  at  the  onset  of  the  disease,  and  much 
more  swiftly  than,  for  example,  is  the  case  in  phlegmon  of  the  external 
walls,  so  with  extraordinary  rapidity  did  the  clinical  picture  assume  a 
new  type.  In  this  respect  we  must  consider  the  very  great  area  of  the 
peritoneal  folds,  their  numerous  lymphstomata,  and  their  intimate  relation 
to  the  circulation,  and  we  are  impressed  with  the  fact  that  fluids  and 
soluble,  as  well  as  formed,  products  are  rapidly  absorbed  by  the  peri- 
toneum. 

Somewhat  less  rapidly  than  this,  but  nevertheless  in  the  course  of  a 
few  hours,  another  change  took  place,  a  favorable  turn  following  the  rup- 
ture of  pus  into  the  intestine.  Here  we  were  dealing  with  a  well  known 
and  familiar  phenomenon;  if  this  occurs  in  the  peritoneum  the  effects  are 
particularly  well  marked;  similarly  as  in  the  case  of  a  phlegmon  which 
rapidly  disappears  with  the  discharge  of  pus  even  although  the  inflam- 
mation extend  beyond  the  pus  focus,  the  symptoms  of  diffuse  peritonitis 
promptly  disappeared  after  the  rupture.  Very  likely,  as  has  already  been 
stated,  the  symptoms  of  diffuse  peritonitis  in  the  first  stages  of  the  disease 
are  to  be  referred  to  a  chemical  inflammation  of  the  serosa,  i.  e.,  one  due 
to  toxins  and  without  the  ingress  of  bacteria;  and  it  must  be  remembered 
that  the  clinical  picture  of  this  chemical  peritonitis  cannot  be  differen- 
tiated from  that  of  the  severe  bacterial  form.  With  the  rupture  of  the 
abscess,  the  entrance  of  poisons  into  the  free  peritoneal  cavity,  and  their 
resorption  by  the  extensive  peritoneal  surfaces,  as  well  as  the  vomiting  and 
the  intestinal  paralysis,  ceased.  The  taking  of  nourishment  again  became 
possible. 

The  point  of  rupture  formed  adhesions,  the  natural  drainage  of  the 
peritoneal  ichorous  focus  ceased,  perhaps  a  new  influx  of  inflammatory 
material  from  the  perforated  appendix  also  took  place.  There  was  a  fresh 
relapse  of  the  local  peritonitis  which  extended  beyond  the  boundaries  of 
the  limiting  adhesions,  and  permitted  the  invasion  by  bacteria  of  the 
free  abdominal  cavity.  This  time  the  severe  toxic  picture  of  collapse 
immediately  followed,  and  with  marked  decrease  in  cardiac  strength  led 
to  death. 

Doubtless  the  patient  might  have  been  saved  in  the  first  stages  of  the 
disease  by  the  evacuation  of  the  abscess;  the  incision  would  at  first  have 
acted  similarly  to  spontaneous  rupture  into  the  intestine,  but  the  relapse 
would  have  been  prevented  by  permanent  drainage,  and  a  radical  cure 
might  have  been  brought  about  by  the  immediate  or  subsequent  removal 
of  the  appendix. 

Opium,  no  doubt,  had  a  favorable  effect  upon  the  affection.  By  re- 
lieving intestinal  irritability,  and  by  bringing  about  a  mild  degree  of  nar- 
cosis, the  patient  was  kept  quiet  and  this  materially  assisted  in  limiting 
the  severe  perityphlitic  suppuration  in  the  first  stage  of  the  disease.     If, 


520      ACUTE  PERITONITIS,   APPENDICITIS,   AND  PERITYPHLITIS 

as  it  unfortunately  happened,  the  point  of  rupture  had  not  immediately 
closed  again,  if  it  had  remained  open  until  suppuration  ceased  and  con- 
traction and  healing  of  the  perforated  appendix  had  taken  place,  opium 
would  have  been  regarded  as  instrumental  in  saving  the  patient,  and  un- 
questionably, at  least  to  some  extent,  justly  so.  Among  other  factors  in 
the  treatment,  the  relief  to  the  intestine  by  the  suspension  of  nourishment 
was  of  paramount  importance.  The  subcutaneous  saline  infusions  had 
an  obvious  but,  naturally,  only  a  transitory  effect. 

I  have  described  this  case  in  detail  because  it  is  calculated  to  exhibit 
to  a  great  extent  the  present  status,  and  our  views,  of  the  processes  in 
acute  peritonitis.  The  case  occupies  a  middle  groimd  between  the  very 
acute  and  the  extremely  gradual  cases  of  perforating  peritoneal  inflam- 
mation ;  according  to  the  valuable  classification  of  Mikulicz  it  should  be 
placed  midway  between  an  acute  diffuse  purulent  and  a  progressive  puru- 
lent peritonitis.  The  infection  of  the  peritoneum  at  the  onset  was  gradual, 
and  not  due  to  a  gross  perforation,  for  it  may  be  assumed  that  the  adhe- 
sions \\hicli  paved  the  way  for  the  favorable  process  in  the  severely  in- 
fected region  formed  from  the  beginning,  probably  before  the  actual  ap- 
pearance of  the  affection,  and  therefore  were  unnoticed  even  by  the  patient 
himself. 

The  rapidity  with  which  the  peritoneum  is  invaded  by  the  chemical 
l)aeterial  infection  and  the  general  toxic  action  of  the  masses  dominate 
to  a  preponderant  degree  the  course  of  perforating  peritonitis.  In  indi- 
vidual cases  the  virulence  of  the  bacteria  is  naturally  very  different,  and 
without  doubt  it  has  the  greatest  influence  upon  the  intensity  and  extent 
of  the  inflammation,  upon  the  quantity  of  toxins  absorbed,  and  therefore 
upon  the  course  of  the  affection;  but  in  many  cases  it  is  probably  only 
a  secondary  factor,  for  we  know  that  the  virulence  of  bacteria  to  a  great 
degree  depends  upon  the  conditions  under  which  they  develop. 

If,  following  this  case  which  occupies  a  middle  position,  we  consider 
some  others  which  in  an  unfavorable  as  well  as  favorable  sense  more 
properly  belong  at  the  end  of  a  series,  the  importance  of  this  fact,  that 
infectious  processes  in  the  peritoneum  rapidly  implicate  its  surroundings, 
will  become  still  more  evident. 

I  shall  first  quote  a  very  characteristic  case  of  Mikulicz's.* 

Case  II. — A  man,  between  25  and  30  years  of  age,  was  brought  to  the  hospital 
in  profound  collapse;  his  speech  was  an  idiom  very  difficult  to  comprehend,  and 
only  after  great  eflfort  was  it  learned  that  for  seven  years  he  had  suffered  from  an 
affection  of  the  stomach,  but  had  suddenly  become  very  ill  only  a  few  hours  before. 

His  face  was  sunken,  the  extremities  were  cool,  the  pulse  was  120  and  moderately 
full.  He  repeatedly  vomited  masses  having  the  odor  of  wine.  The  abdomen  was 
uniformly  distended  and  tense,  painful  upon  palpation,  with  distinct  signs  of  tym- 
panites.    A  trial  puncture  by  means  of  a  fine  cannula  permitted  the  escape  from 

»  Volkmann's  Vortr.  1885,  Nr.  262. 


ACUTE   DIFFUSE   PERITONITIS  521 

the  abdominal  cavity  of  gas  which  was  inflammable  and  had  the  odor  of  alcohol; 
after  the  puncture  subcutaneous  emphysema  occurred  in  the  surroundings  of  the 
opening. 

According  to  all  the  signs,  a  diagnosis  of  perforating  peritonitis  was  hardly 
questionable,  but  the  origin  was  not  clear. 

The  same  evening  laparotomy  was  performed.  Incision  was  made  in  the  median 
line  from  the  navel  to  the  symphysis ;  upon  opening  the  peritoneum  gas  and  a  great 
quantity  of  fluid  of  a  coffee-brown  color  and  with  the  odor  of  wine,  also  undigested 
rice  granules,  escaped.  The  entire  abdominal  cavity  was  filled  with  this  fluid;  the 
intestine,  except  for  isolated  superficial  ecchymoses,  was  of  normal  appearance. 
Fluid  oozed  from  the  gastric  region,  and,  after  enlarging  the  incision,  a  slit-like 
opening  6  to  8  cm.  in  extent  was  found  in  the  lesser  curvature  of  the  enormously 
dilated  stomach  near  the  cardia. 

The  stomach  was  emptied,  the  opening  closed,  the  abdominal  cavity  washed  with 
thymol,  and  the  intestines  cleansed. 

Collapse  followed  the  operation  and,  in  spite  of  stimulation,  death  occurred  three 
hours  later. 

At  the  autopsy  a  greatly  distended  and  flabby  stomach  was  found,  with  normal 
mucous  membrane  borders  around  the  previously  mentioned  slit-like  opening  which 
had  been  sewed  up;  no  ulcer;  in  the  vicinity  of  the  posterior  upper  angle  of  the 
wound  a  striated  cicatrix  about  the  size  of  a  ten  cent  piece,  and  having  no  con- 
nection with  the  wound. 

The  peritoneum  everywhere  was  smooth. 

Here,  in  the  course  of  a  few  hours,  the  severe  picture  of  collapse  devel- 
oped, resembling  that  of  our  first  case,  with  positive  local  signs  of  diffuse 
peritonitis.  The  operation,  which  was  certainly  indicated,  may  have  slightly 
hastened  the  end,  but,  even  without  this,  life  would  have  terminated  in 
the  course  of  a  few  hours.  Eupture  of  a  dilated  stomach  in  the  neighbor- 
hood of  an  old  cicatrix,  undoubtedly  due  to  a  former  ulcer,  was  found. 
There  was  no  gradual  inflammation  continuing  from  the  serosa,  but,  on 
the  contrary,  a  sudden  rupture  into  a  previously  perfectly  normal  perito- 
neum, perhaps  due  to  the  cicatrix  of  an  ulcer,  with  immediate  and  over- 
whelming flooding  of  the  peritoneal  cavity  with  the  gastric  contents. 

In  rapid  sequence  was  a  painful  distention  of  the  abdomen  with  ac- 
companying fulminant  symptoms  which  clinically  resembled  peritonitis 
and  which,  if  life  had  continued,  might  without  doubt  have  been  considered 
the  precursors  of  this  affection,  also  an  immediate  and  very  grave  general 
condition  which  the  earlier  physicians  designated  as  "  reflex  "  or  "  nervous  " 
shock,  and  the  newer  school  is  inclined  to  attribute  to  a  "septic"  intoxi- 
cation; to  this  a  third  fundamental  condition  was  probably  added:  Con- 
gestion of  the  vessels  in  the  splanchnic  area  in  consequence  of  congestive 
hyperemia  of  this  vascular  region.  -^- 

The  designation,  "  perforative  peritonitis,"  is  naturally  unsuited  to  a 
case  of  this  kind,  for  the  patient  died  before  the  appearance  of  inflamma- 
tion, consequently,  not  as  its  result;  the  most  recent  designation,  "peri- 
toneal sepsis,"  according  to  what  has  been  above  stated,  is,  in  our  opinion, 
too  one-sided.     We  are  evidently  dealing  with  a  most  unusual  case  of 


522      ACUTE   PERITONITIS,   APPENDICITIS,  AND  PERITYPHLITIS 

accidental  perforation  into  the  free  peritoneal  cavity,  with  masses  of  dele- 
terious products  distributed  over  the  surface  of  the  peritoneum  which  is 
capable  of  such  enormous  absorption,  these  products  being  the  probable 
result  of  a  purely  chemical  and  local  effect,  as  in  the  circulation,  for  there 
had  scarcely  been  time  for  microorganisms  to  develop  to  any  extent. 

It  may  appear  remarkable  that,  in  such  a  case,  the  cleansing  of  the 
abdominal  cavity  and  the  closure  of  the  death-producing  rent  should  offer 
no  cliance  for  improvement.  But  the  operation,  without  doubt,  adds  to 
the  first  shock  another,  it  produces  a  fresh  congestion  of  the  abdomen 
with  increased  internal  hyperemia,  and  even  to-day,  when,  as  far  as  these 
dangers  are  concerned,  laparotomies  are  performed  with  every  possible 
precaution,  similar  cases  constantly  demonstrate  that  it  is  frequently  im- 
possible to  bring  about  a  favorable  result. 

In  contrast  to  this  case  I  shall  give  briefly  the  notes  of  a  perforation 
of  the  appendix  running  an  acute  course,  and  dating  from  a  previous 
attack  in  which  less  favorable  results  were  obtained  by  operation: 

Case  III. — A  boy,  aged  13,  previously  well,  was  taken  ill  late  at  night  after 
a  cold  bath  with  severe  abdominal  pain  upon  the  right  side  anteriorly  and  low  down 
and  witli  fulminant  vomiting;  the  abdomen  began  to  swell  and  there  was  no  fecal 
movement.     The   physician   called   during  the  night  ordered  opium   and   ice. 

The  next  morning  the  boy  was  admitted  to  the  hospital :  The  patient  was  pale, 
the  mind  clear;  the  temperature  was  100.9°  F.,  the  pulse  120,  very  small  and 
regular;  there  was  considerable  abdominal  pain,  particularly  on  the  right  side, 
low  down.  The  abdomen  showed  a  uniform,  drum-like  swelling,  which  was  ex- 
tremely sensitive  and  most  marked  in  the  ileo-cecal  region ;  no  tumor  or  dulness, 
hernial  rings  free,  no  bowel  movement.  The  urine  was  scant,  caused  pain  when 
voided,  was  very  dark  in  color,  and  contained  much  indican. 

Diagnosis:  Perforation  of  the  appendix.  Treatment:  Opium,  ice  locally,  pellets 
of  ice  by  mouth,  and  camphor. 

In  the  course  of  the  afternoon  the  patient  frequently  vomited  small  quantities 
of  grass-green  material ;  collapse  appeared ;  the  bodily  temperature  fell  to  normal, 
the  pulse  was  140.  Respiration  became  .difficult,  the  diaphragm  rose  very  high,  the 
al)domcn  became  still  more  swollen,  and  Vas  now  enormously  distended. 

During  the  night  the  patient  became  unconscious  (opium  was  discontinued). 
Toward  morning  the  mind  was  again  clear;  there  were  a  few  attacks  of  vomiting, 
hut  no  longer  any  complaints;  the  abdomen  again  became  soft,  the  face  still  more 
sallow,  the  pulse  imperceptible.  Now  and  then  delirium  with  hallucinations  was 
present.     Death  occurred  upon  the  third  day  of  the  disease. 

Autopsy:  Gangrene  and  perforation  of  the  appendix;  fecal  calculus.  Fresh  dif- 
fuse peritonitis  with  scant,  turbid,  serous  exudate  and  the  finest  fibrinous  deposits. 
No  sign  of  adhesions  about  the  cecum. 

Hero  the  conditions  are  similar  to  those  of  the  preceding  observation 
of  Mikulicz's;  the  perforation  was  into  the  free  abdominal  cavity,  at  once 
produced  severe  pain  and  fulminant  vomiting,  and,  by  the  rapid  distribu- 
tion of  putrid  masses  upon  the  serosa,  early  symptoms  of  peritoneal  col- 
lapse which  within  forty  hours  caused  death.  The  autopsy  showed  peri- 
tonitis to  be  present,  but  only  in  its  first  stages. 


ACUTE  DIFFUSE  PERITONITIS  623 

Proceeding  from  these  cases  we  next  meet  with  those  in  which  well 
developed  peritonitis  takes  place,  but  in  which  a  limitation  to  the  imme- 
diate surroundings  of  the  point  of  origin  is  out  of  the  question.  A  classical 
example  of  this  form  of  acute  diffuse  peritonitis  is  the  following: 

Case  IV. — A  saleswoman,  aged  21,  previously  healthy,  a  primipara,  was  attacked 
upon  the  second  day  after  a  quite  severe  but  non-instrumental  labor  (small  lacera- 
tion of  the  perineum,  decided  hemorrhage  ex  utero)  with  a  chill,  vomiting,  and 
moderately  severe,  diffused,  abdominal  pain. 

Upon  the  evening  of  this  day  the  patient  was  very  ill,  the  mind  was  clear  but 
showed  excitement;  the  temperature  was  105.4°,  the  pulse  120,  the  respirations 
frequent  and  somewhat  labored;  there  was  repeated  and  distressing  greenish  vomit- 
ing, also  singultus.  The  diaphragm  was  very  high,  the  abdomen  greatly  distended, 
balloon-like,  and  very  sensitive.  Careful  percussion  elicited  a  tympanitic  note 
throughout,  no  liver  dulness;  some  few  splashing  intestinal  murmurs  were  observed; 
during  the  examination  diarrhea  with  tenesmus-like  pain.  Hernial  rings  were  free, 
nothing  abnormal  was  observed  about  the  genitalia,  and  the  same  was  true  of  the 
discharges.     Much  indican  and  some  albumin  were  present  in  the  urine. 

During  the  night  collapse  occurred  with  cold  sweat  and  a  temperature  of  97° ;  the 
pulse  was  140  and  very  small.  The  patient  did  not  rally  from  this  collapse:  At 
the  beginning  she  was  still  very  excited  and  delirious,  but  gradually  became  more 
quiet;  most  of  the  time  her  mind  was  clear.  There  was  pallor,  the  internal  tem- 
perature gradually  rose  to  101.8°,  but  the  extremities  remained  cool;  the  abdomen 
became  softer  and  less  sensitive.  About  thirty-six  hours  after  the  onset  of  the 
attack  deep  percussion  of  the  lower  lateral  region  on  both  sides  showed  small  areas 
of  dulness.     The  uterus  was  moderately  contracted  and  very  sensitive. 

The  dj'spnea  increased;  during  the  second  night  the  patient  was  periodically 
restless,  threw  herself  about,  was  somewhat  delirious;  she  vomited  with  effort  and 
in  paroxysms,  particularly  when  fluid  was  administered,  ejecting  greenish-yellow 
masses ;  two  thin,  scant,  friable  bowel  discharges  were  evacuated  in  the  bed.  The 
patient  had  no  pain,  lucid  intervals  alternated  with  delirium;  there  was  extreme 
pallor,  facies  hippoeratica ;  dyspnea  was  slight,  the  abdomen  was  quite  soft,  the 
pulse  scarcely  perceptible.  In  the  succeeding  night  death  resulted  from  cardiac 
weakness  after  a  duration  of  the  illness  for  not  quite  three  days. 

Autopsy  revealed  a  diffuse  infra-omental  peritonitis  with  moderately  profuse 
thin  pus  and  slight  adhesions  of  some  intestinal  coils.  In  the  corpus  and  collum 
uteri  numerous  pus  foci,  some  of  which  extended  to  the  peritoneal  coat.  No  pyemic 
foci  in  other  organs.     No  bacteriologic  investigation  was  made. 

In  this  case  pus  foci  in  the  wall  of  the  infected  puerperal  uterus  pro- 
duced a  very  acute  peritonitis  with  peculiar  signs  of  intoxication  in  that 
these  foci  spread  to  the  peritoneum  without  producing  extensive  perforation, 
a  condition  which  we  partially  recognized  in  the  first  two  observations. 
Here  we  are  dealing  with  a  typical  picture  of  peritoneal  sepsis.  The  peri- 
toneal symptoms  were  clear,  they  made  an  early  diagnosis  possible;  there 
was  no  doubt  as  to  their  origin.  It  was  either  in  the  uterus  or  in  its 
adnexa.  A  striking  feature  of  the  pathologic  picture  was  the  early  col- 
lapse wliieh  was  probably  in  part  to  be  attributed  to  labor  which  had 
just  taken  place.     The  diarrhea  in  this  case  was  conspicuous,  and  this  is  a 


524      ACUTE   PERITONITIS,  APPENDICITIS,   AND  PERITYPHLITIS 

characteristic  of  puerperal  peritonitis  to  which  various  authors,  and  re- 
cently Nothnagel,  have  called  attention. 

At  the  time  in  which  this  case  occurred,  and  for  such  cases,  surgical 
treatment  was  seldom  resorted  to;  in  the  case  in  question  it  could  have 
been  of  little  avail.    Internal  treatment  was  entirely  without  effect. 

These  peritoneal  inflammations  which  start  from  the  point  of  invasion 
and  rapidly  implicate  large  areas  of  the  peritoneum  are  in  contrast  to  other 
forms  in  which  there  is  a  more  or  less  conspicuous  tendency  to  limitation. 
I  shall  first  quote  a  classical  case  reported  by  Mikulicz.^ 

Case  V. — A  school-boy,  aged  15,  was  attacked  without  prodromes  by  severe  ab- 
dominal pain  and  vomiting;  in  the  next  few  days  the  abdomen  became  distended 
and  there  was  moderate  fever.     A  fecal  evacuation  occurred  daily. 

Upon  the  fifth  day:  Pulse  100,  quite  strong,  temperature  somewhat  elevated. 
Abdomen  uniformly  distended  and  everywhere  sensitive  to  pressure,  particularly  in 
the  ileo-cecal  region,  where  there  was  increased  resistance  and  limited  dulness  ex- 
tending from  two  to  four  fingerbreadths  from  the  crest  of  the  ilium  and  reaching 
up  to  the  lumbar  region. 

Incision  in  tliis  region  was  followed  by  the  discharge  of  200  c.c.  of  thin  fluid 
pus  from  a  cavity  limited  by  loosely  adherent  intestinal  coils  and  omentum.  The 
cavity  was  packed  with  iodoform  gauze  and  opium  and  moist  heat  were  ordered. 

No  noteworthy  improvement  followed  this,  but  the  dulness  increased; -there  was 
bilious  vomiting,  no  flatus.  For  this  reason  upon  the  following  day,  the  seventh 
day  of  the  disease,  the  first  incision  was  extended  downward  and  toward  the  median 
line.  Ichorous  pus  exuded  from  every  area  limited  by  fibrino-purulent  adhesions  of 
tlie  appendix,  several  coils  of  the  small  intestine  and  the  omentum ;  the  appendix, 
which  was  8  cm.  in  length,  showed  a  perforation  at  its  middle  and  adjacent  to  this 
a  fecal  calculus.  The  operation  consisted  of  resection  of  the  appendix,  intestinal 
suture,  careful  cleansing   (boric  acid  solution),  and  packing  with  iodoform  gauze. 

The  meteorism  and  the  sensitiveness  slowly  decreased ;  flatus  and  later  a  fecal 
movement  were  discharged,  but  vomiting  still  persisted.  The  temperature  remained 
at  100.4°;  the  pulse  was  somewhat  lower,  104  to  116. 

This  improvement  continued  for  six  days  and  up  to  the  twelfth  day  of  the  dis- 
ease, when,  with  a  slight  rise  in  temperature  and  increase  in  pulse  rate,  a  new  area 
of  dulness  with  resistance  and  pain  upon  pressure  appeared  over  Poupart's  ligament 
on  the  left. 

Upon  the  fifteenth  day  of  the  disease  another  incision  was  made:  A  half  liter  of 
foul-smelling  pus  was  evacuated  from  a  cavity  between  adherent  intestinal  coils  which 
extended  into  the  false  pelvis.  The  cavity  was  irrigated  and  drained,  and  improve- 
ment followed. 

Upon  the  nineteenth  and  also  upon  the  thirty-third  day  of  the  disease,  accom- 
panied by  mild  febrile  symptoms,  two  new  exudates  appeared,  the  first  anteriorly 
in  the  median  line  between  the  navel  and  the  symphysis,  the  second  upon  the  right  in 
the  true  pelvis,  and  this  could  be  reached  from  the  opening  of  the  second  incision. 
Both  were  incised  and  discharged  pus.     Drainage. 

Later  still  there  was  a  small  pleural  exudate  upon  the  right  side  which  healed 
spontaneously,  the  patient  leaving  his  bed  after  three  months;  there  was  still  a  fine 
intestinal  fistula  originating  from  the  stump  of  the  appendix;  it  soon  closed.  A 
few  attacks  of  colic  occurred,  then  convalescence  and  restoration  to  health  followed. 

1  Mil:ulic:z,  "  LTeber  die  operative  Behandlung  der  Perforationsperitonitis."  Terh. 
der  dinlschen  Gesellschaft  fiir  Chirurgie,  1889. 


ACUTE   DIFFUSE   PERITONITIS  525 

This  is  the  case  which,  if  I  am  not  mistaken,  Mikulicz  denominated 
as  a  so-called  progressive  purulent  form  of  perforating  peritonitis.  Here 
we  may  assume  that,  prior  to  the  manifestations  of  the  affection,  toxins 
or  isolated  bacteria  entered  the  wall  of  the  already  changed  appendix  and 
produced  a  mild  plastic  peritonitis  encircling  it.  The  rupture  of  the 
appendix,  with  which  the  obvious  symptoms  appeared,  occurred  in  a  region 
preformed  by  adhesions;  the  adhesions,  however,  were  not  close  enough 
for  chemical  poisons,  perhaps  were  not  even  sufficiently  invulnerable  to 
microbes ;  this  is  proven  by  the  immediate  symptoms  of  general  peritonitis ; 
we  have  here  the  typical  picture  of  attenuated  general  peritonitis  (either 
chemical  or  bacterial)  in  the  area  surrounding  a  focus  of  intense  inflam- 
mation not  sufficiently  limited  by  adhesions.  We  may  consider  that  this 
diffuse  attenuated  inflammation  was  due  to  toxins  which  constantly  trav- 
ersed the  actual  focus  composed  of  pseudo-membranes,  and  that  later  bac- 
teria also  now  and  then  penetrated  this  wall  and  produced  the  various 
fresh  suppurations  some  of  which  extended  to  distant  regions  of  the  ab- 
dominal cavity.  It  is  also  possible  that  bacteria  were  present  from  the 
onset,  and  gradually,  in  isolated  areas,  found  especially  favorable  soil  for 
their  growth.  At  all  events  there  was  but  a  moderate  local  and  general 
toxic  effect,  and  this  is  obvious  from  the  fact  that  with  slight  interruptions 
feces  and  flatus  were  discharged,  that  the  fever  was  not  high,  and  that 
not  the  slightest  sign  of  peritoneal  sepsis  was  ever  observed. 

The  peculiar  features  of  plastic  inflammation,  which  in  itself  produces 
resistance,  but  which  may,  under  some  circumstances,  be  again  overcome 
by  the  toxins  of  the  disease,  we  shall  meet  again  in  a  more  distinct  form 
and  running  a  much  slower  course  in  the  description  of  tubercular  peri- 
tonitis. In  this  case  everything  occurred  in  very  rapid  tempo.  Anatomi- 
cally it  is  especially  interesting  to  note  the  important  role  which  the 
omentum  plays  in  limiting  inflammations  in  the  abdomen. 

As  an  aid  to  the  diagnosis  continuous,  persistent,  deep  palpation  (also 
per  rectum!)  is  very  valuable,  as  is  also  deep  percussion  of  the  entire 
abdomen  in  the  prompt  recognition  of  pus  foci.  The  focal  treatment  of 
the  affection  is  very  interesting;  the  radical  procedure  of  loosening  the 
adhesions  at  the  onset,  with  the  toilet  of  the  entire  abdominal  cavity, 
could  hardly  in  this  case  have  produced  such  brilliant  results. 

This  case,  in  fact,  proved  to  be  conspicuously  "progressive."  This 
progression  may  also  take  place  after  apparent  consolidation  of  a  local 
perityphlitis,  and  with  such  rapidity  that  a  sudden  rupture  of  the  pus 
focus  is  simulated. 

An  observation  of  Sonnenburg's  is  a  characteristic  illustration  of  such 
a  course:  y 

Case  VI. — An  apprentice,  aged  16,  previously  well,  was  attacked  with  severe 
pain  and  vomiting.  Upon  the  third  day  he  was  quite  ill.  The  temperature  was 
101.7°,  there  was  congestion  with   increased   respiration,  and  a  full  pulse  of   100. 


526       ACUTE   PERITONITIS,   APPENDICITIS,   AND  PERITYPHLITIS 

Upon  the  fourth  day  an  area  of  resistance  about  the  size  of  a  plate  with  dulness 
below  the  right  arch  of  the  ribs  amounting  to  two  flngerbreadths  and  moderately 
sensitive  to  pressure  was  observed;  the  rest  of  the  abdomen  was  soft  and  only 
slightly  sensitive;  examination  per  rectum  negative;  urine  only  upon  catheteriza- 
tion. The  temperature  had  fallen  to  100.8°  and,  after  a  careful  emptying  of  the 
rectum  by  means  of  a  glycerin  suppository,  gradually  fell  to  99.3°;  simultaneously 
the  tenderness  of  the  abdomen  entirely  disappeared  but  the  resistance  and  dulness 
upon  the  right  side  remained  unchanged;  the  pulse  was  normal,  the  appetite  better, 
the  subjective  condition  excellent.  Upon  the  following  night  and  the  evening  of  the 
sixth  day  of  the  disease  the  picture  of  severe  diffuse  acute  peritonitis  suddenly  devel- 
oped with  rapidly  rising  temperature,  a  pulse  of  140,  and  great  restlessness;  the 
next  morning  the  patient  was  in  collapse,  the  entire  abdomen  was  sensitive,  dulness 
was  distributed ;  at  midday  the  temperature  and  pulse  fell,  the  abdomen  became 
softer;  during  the  night  the  condition  became  worse  and  death  occurred  early  upon 
the  eighth  day  of  the  disease. 

Sonnenburg  assumes  in  this  patient,  who  declined  operation,  the  rup- 
ture of  a  perityphlitic  abscess  into  the  free  abdominal  cavity,  and  he  is 
probably  correct. 

The  patient  was  not  operated  upon  in  the  first  stage  of  the  disease, 
the  time  chosen  in  by  far  the  majority  of  all  cases  of  perforating  peri- 
tonitis which  from  the  onset  show  a  definite  localization,  in  which  the 
rest  of  tlie  abdomen  is  not  implicated,  and  in  which  the  general  symp- 
toms steadily  improve.  A  further  limitation  and  a  transition  into  a  rela- 
tively non-irritating  chronic  stage  or  even  a  cure  was  expected.  That, 
however,  we  cannot  count  upon  this  with  certainty  is  demonstrated  by  this 
case;  and  it  proves  how  difficult  it  is  to  prognosticate  the  course  of  such 
an  affection.  Such  cases  are  calculated  decidedly  to  bias  the  opinion  of 
those  who  see  them  as  to  the  advisability  of  operative  interference. 

Fortunately,  however,  such  cases  are  infrequent. 

In  comparison  I  shall  relate  the  brief  clinical  history  of  a  case  of 
moderate  circumscribed  perityphlitis,  and  one  that  remained  such.  This 
closes  the  series  of  the  forms  of  peritonitis  arising  from  inflamed  neigh- 
boring organs,  the  series  beginning  with  the  severest  cases  and  ranging 
to  the  mildest. 

Case  VII. — H.  G.,  a  robust  student,  aged  22,  in  the  last  five  years  suffered  three 
times  from  "  appendicular  inflammation  "  of  brief  duration,  the  last  time,  according 
to  report,  accompanied  by  a  chill  and  high  fever.  He  was  seized  in  the  evening 
after  a  fatiguing  bicycle  ride  with  a  chill,  followed  by  fever,  repeated  vomiting,  and 
severe  pain  in  the  right  side  of  the  abdomen ;  the  next  morning  the  temperature  was 
103.2°,  the  pulse  120,  the  general  condition  moderately  severe,  violent  pain;  he 
vomited  bile,  there  was  no  fecal  movement. 

The  tongue  was  thickly  coated;  between  the  navel  and  the  spine  of  the  ilium 
an  enormously  sensitive  area  of  resistance  about  the  size  of  a  small  apple  was  found. 
Tlie  surrounding  parts  were  also  sensitive  to  pressure  as  well  as  the  posterior  lumbar 
region.  The  hernial  rings  were  free;  no  bladder  symptoms.  The  rest  of  the  abdo- 
men was  soft  and  not  sensitive  to  pressure.  The  treatment  was  by  ice,  small  doses 
of  opium ;  no  food  allowed. 


ACUTE   DIFFUSE  PERITONITIS  527 

Upon  the  second  and  third  dajs  of  the  disease,  while  the  vomiting  had  ceased, 
the  temperature  remained  between  100.4°  and  102.2°,  the  tumor  had  enlarged  to 
the  size  of  a  small  plate,  was  flat,  coarse,  very  sensitive,  immovable,  with  a  dull 
note  upon  percussion;  no  fluctuation.  No  fecal  movement,  great  thirst.  The  rest 
of  the  abdomen  was  not  involved.  The  patient  was  quite  ill  and  in  severe  pain, 
iloderate  amounts  of  opium  were  ordered. 

Early  upon  the  fourth  day,  the  temperature  was  100.2°,  in  the  evening  101.1°; 
there  was  no  further  enlargement.  In  the  evening  a  compact,  dark-brown  stool  was 
voided,  and  in  the  night  another,  of  pappy  consistence,  which  was  not  seen.  The 
pain  was  slight;  the  temperature  had  fallen  to  normal;  a  general  improvement  in 
the  condition  was  noted. 

From  this  time  there  was  no  fever,  the  bowels  moved  daily  without  recognizable 
pus  or  blood,  and  the  tumor  steadily  decreased  in  size;  hunger  reappeared,  and 
within  eight  days,  except  for  a  deep-seated  indistinct  resistance  over  McBurney's 
point,  all  the  symptoms  had  yielded.  This  resistance  was  demonstrable  for  some 
time;  then  it,  too,  disappeared. 

It  had  been  my  intention  to  propose  an  operation  after  the  attack  abated,  but  I 
relinquished  this  plan  in  consequence  of  the  complete  disappearance  of  the  symptoms. 

From  this  time  the  patient  continued  perfectly  well  for  six  years. 

This  case  belongs  to  the  extremely  full  category  of  moderately  severe 
cases  of  limited  perityphlitis.  Perforation  is  here  most  unlikely.  The 
condition  is  probably  due  to  chronic,  paroxysmally  exacerbating  attacks  of 
appendicitis  without  fecal  calculus,  but  perhaps  a  slight  stricture.  In  the 
last  attack  (whether  in  the  former  is  questionable)  a  purulent  periappen- 
dicitis surrounded  the  isolated  appendix  to  which  adhesions  had  long  since 
formed,  and,  according  to  the  position  of  the  tumor,  probably  also  the 
medial  side  of  the  cecum.  The  quite  fulminant  discharge  of  pus  in  the 
following  days  did  not  rupture  the  barrier,  but  only  strengthened  it.  There 
was  no  fluctuation.  The  change  in  the  condition  was  probably  due  to  a 
rupture  into  the  colon  which  rapidly  drained  the  abscess,  and  in  conse- 
quence healing  soon  took  place.  Subsequently  the  fresh  inflammatory  for- 
mation was  absorbed,  and  the  appendix — as  for  six  years  nothing  abnormal 
could  be  felt,  there  was  no  sensitiveness,  and  no  relapse  occurred — was 
probably  obliterated,  ♦ 

A  favorable  course  was  looked  for,  although  it  could  not  be  prognosti- 
cated with  certainty  because  two  milder  attacks  had  preceded  this,  the 
disease  setting  in  with  moderately  fulminant  symptoms,  without  implica- 
tion of  the  rest  of  the  abdomen,  and  without  any  signs  of  peritoneal 
collapse,  and  because  a  tumor  at  once  appeared  which  was  very  coarse 
and  slowly  increased  in  size.  The  probability  of  a  favorable  course  became 
still  greater  upon  the  fourth  day  when  it  was  observed  that  the  tumor  no 
longer  increased  in  size  and  the  fever  declined;  but  even  then  the  prog- 
nosis could  not  be  regarded  as  quite  certain,  and  the  disappearance  of  the 
fever  and  the  return  of  a  feeling  of  well-being  did  not  remove  our  anxious 
fear  ef  a  relapse,  possibly  of  a  still  more  serious  character.  This,  however, 
was,  according  to  general  clinical  experience,  to  a  high  degree  unlikely. 
85 


528      ACUTE   PERITONITIS,   APPENDICITIS,  AND  PERITYPHLITIS 

I  am  strongly  tempted  to  present  as  complete  a  picture  as  possible  of 
the  numerous,  varieties  of  peritonitis  by  quoting  still  other  pathologic 
pictures.  This  temptation  must  be  resisted  for  it  would  lead  us  too  far 
from  our  subject;  to  be  exhaustive  in  any  sense  it  would  be  necessary 
to  cite  so  many  isolated  cases  that  the  result  would  be  confusion  instead  of 
clearness. 

Neither  is  it  my  object  to  present  a  description  uniformly  elaborated 
in  all  directions  like  a  text-book  description.  On  the  contrary,  when 
referring  to  previous  histories,  points  will  be  described  which  are  regarded 
as  essential  to  the  etiology  and  to  the  clinical  picture,  and  which  will 
chiefly  aid  us  in  deciding  upon  the  treatment  that  is  to-day  recognized 
as  fundamental. 

In  clinical  histories  we  have  learned  to  recognize  inflammations  of  the 
appendix,  gastric  and  intestinal  ulcers,  and  septic  infections  of  the  uterus 
as  causes  of  peritonitis;  these  are  partly  caused  by  perforations,  partly  by 
propagation  tlirough  the  lymph-vessels.  We  must  still  mention  other  fre- 
quent sources  of  peritonitis :  The  biliary  passages  whose  sterile  contents 
cause  little  or  no  chronic  inflammatory  irritation,  but  which,  when  in- 
fected and  according  to  the  virulence  of  the  infectious  agent  (mostly 
bacterium  coli)  may  cause  the  severest  acute  peritonitis;  the  duodenal 
ulcer  and  ulcers  of  the  large  intestine,  traumatic  lacerations  of  the  stom- 
ach and  intestines;  also  the  important  strangulations  of  the  intestine, 
particularly  herniae  with  their  sequelae  of  permeability,  infection,  and 
necrosis  of  the  paralyzed  and  inflated  intestinal  coils;  ulcerations  and 
pericystitic  abscesses  of  the  urinary  bladder,  purulent  perinephritis,  pus 
tubes,  abscesses  of  the  spleen,  of  the  liver,  of  the  pancreas,  of  the  lymph- 
glands  of  the  abdominal  cavity;  the  spleen  and  glands  may  also  come  into 
question,  particularly  after  enteric  fever,  the  former  after  severe  malaria. 
In  the  newborn  the  navel  or  the  umbilical  vein  is  sometimes  the  point 
of  origin  for  septic  infection;  in  young  children  ulcerative  prolapse  of 
the  rectum.  Finally,  we  may  mention  inflammations  from  the  pleura  and 
pericardium  by  way  of  the  diaphragm;  here,  particularly  in  infancy,  the 
pneumococcus  frequently  plays  a  role.^ 

Peritonitis  originating  from  the  vessels  has  already  been  mentioned, — 
that  starting  from  the  umbilical  vein  of  the  newborn;  in  a  similar  manner 
septic  thromboses  from  branches  of  the  vena  cava  and  from  the  portal 
vein,  usually  the  direct  result  of  neighboring  suppurations,  may  arise  and 
cause  disease  of  the  peritoneum,  more  rarely  septic  emboli  from  the  mesen- 
teric arteries  in  general  sepsis.  Infection  of  the  peritoneum  by  circulating 
toxins  from  the  blood  without  local  vascular  disease  has  a  special  action, — 
certainly  it  is  extremely  rare.     That  which  was  formerly  confounded  with 

1  O.  Vierordt,  "  Die  Natur  und  Behandlung  der  Pneumokokkenempyerae." 
DiuLsrh.  An  It.  f.  kliti.  Med.,  Bd.  LXIV. 


ACUTE   DIFFUSE   PERITONITIS  529 

it  must  be  due  to  some  neighboring  focus  in  the  peritoneum  that  may 
not  even  be  detected  in  a  careful  autopsy ;  thus  "  typhoid  peritonitis "  is 
explained  by  the  finest  intestinal  perforation,  or  the  permeation  of  the 
serosa  of  the  intestine  without  perforation,  or  by  an  abscess  in  the  lymph- 
gland,  etc.;  malarial  peritonitis  by  a  focus  in  the  spleen,  and  the  septic 
form  by  a  small  vascular  thrombus,  etc.  Only  in  acute  articular  rheu- 
matism does  it  appear  certain  that  the  toxin  passes  from  the  blood  into 
the  peritoneal  cavity  as  well  as  into  the  joints  and  all  the  serous 
cavities. 

Chronic  affections  of  the  abdominal  organs,  such  as  tuberculosis,  actino- 
mycosis, gonorrhea,  will  be  discussed  later. 

A  review  of  this  array  of  dangers  which  threaten  the  peritoneum  re- 
veals to  us  the  extraordinarily  varied  nature  of  the  actual  originators  of 
inflammation:  The  chemically  high-graded  and  toxic  gastric  contents,  the 
intestinal  contents  with  their  chemical  substances  and  putrid  bacterial  ad- 
mixture, from  which,  if  sufficient  time  be  allowed,  pathogenic  microorgan- 
isms are  first  cultivated  in  the  inflammatory  fluid;  the  appendix,  of  which 
almost  the  same  might  be  said,  but  which  also  in  its  wall  or  in  its  lumen 
furnishes  more  or  less  pure  cultures  of  pus  organisms;  the  many  other 
suppurations  in  which  the  attack  sometimes  appears  to  result  from  a 
gradual  change  of  the  bacteria  to  the  highest  degrees  of  virulence.  Among 
the  pyogenic  organisms:  Bacteria  coli  with  their  very  varying  toxicity, 
streptococci  and  staphylococci,  less  frequently  pneumococci,  very  rarely 
gonococci  and  typhoid  bacilli;  furthermore,  however,  bacteria  of  decom- 
position of  all  kinds,  in  part  the  anaerobic. 

Various  as  are  the  products  capable  of  producing  inflammation  of  the 
peritoneum,  and  innumerable  as  are  the  roads  by  which  they  may  reach 
this  tissue,  everywhere,  however,  two  circumstances  especially  influence  the 
severity  of  the  inflammation:  The  activity  of  the  germ  of  inflammation 
and  the  rapidity  with  which  it  reaches  the  peritoneum.  In  regard  to  the 
latter,  except  in  external  trauma,  it  is  nowhere  greater  than  when  one 
of  the  numerous  hollow  abdominal  organs  perforates  into  an  entirely 
unprepared,  that  is,  normal,  peritoneum.  Extreme  examples  of  this  kind 
are  traumatic  lacerations  of  the  stomach  and  intestine^,  ulcer  of  the  stom- 
ach, the  duodenum,  or  small  intestine,  soon  rupturing  into  the  serosa  and 
extending  far  down  into  the  depths  of  the  abdomen,  a  completely  gan- 
grenous appendix  inflamed  by  the  pressure  of  a  fecal  calculus  and  necrotic, 
in  which  rapid  thrombosis  of  the  vessels  has  occurred,  or  an  empyema  of 
the  appendix  or  gall-bladder  rupturing  from  the  pressure  of  the  eroding 
pus.  Here,  usually  large  amounts  of  the  contents  of  these  organs  are 
suddenly  discharged  into  the  free  abdominal  cavity ;  they  unfold  local  and 
general  toxic  effects,  and  produce  such  similar  clinical  pictures  that  their 
differential  diagnosis  may  occasion  the  greatest  perplexity.  And  yet  we 
are  dealing  with  very  different  factors  which  have  entered  the  peritoneum : 


530      ACUTE   PERITONITIS,   APPENDICITIS,   AND   PERITYPHLITIS 

in  perforation  of  the  stomach,  with  the  chemical  constituents  of  the  gastric 
contents  and  an  admixture  of  bacteria  in  which  specific  pathogenic  bacilli 
have  from  the  onset  certainly  not  been  in  the  majority,  and  which — since 
we  are  almost  always  dealing  with  a  preceding  ulcer  of  the  stomach — have 
usually  lost  much  of  their  vitality  and  virulence  under  the  decided  influ- 
ence of  hydrochloric  acid;  in  a  rupture  of  the  appendix  occurring  under 
the  circumstances  just  mentioned,  we  are  frequently  dealing  with  a 
"  putrid "  infection  in  which  besides  the  pathogenic  bacteria  the  sapro- 
phytic also  at  first  play  an  important  role,  and  with  substances  which 
produce  chemical  and  mechanical  irritation.  In  other  cases,  naturally, 
within  the  lumen  of  the  appendix  or  in  its  wall  the  bacterium  coli  or  the 
streptococcus  has  developed  to  a  high  degree  of  virulence,  and  a  more  or 
less  pure  bacterium  coli  or  streptococcus  peritonitis  develops.  If,  on  the 
other  hand,  an  inflamed  purulent  gall-bladder  ruptures,  a  pure  culture  of 
less  virulent  coli  bacilli  enters  the  peritoneal  sac  with  the  pus,  but  never- 
theless this  also  results  in  peritonitis. 

Since  the  well  known  experimental  investigations  of  Wegner,  Grawitz 
and  others,  we  understand  that  the  animal  flora  of  the  peritoneum  renders 
inert  large  numbers  of  microorganisms,  partly  by  the  bactericidal  effect  of 
its  secretion,  partly  by  th.e  very  rapid  and  intense  absorption  into  the 
lymph-spaces,  especially  in  the  diaphragm.  We  know  also,  chiefly  from 
the  investigations  of  Grawitz,  that  chemical  or  physical  substances  which 
injure  the  epithelium  diminish  the  protective  power  of  the  serosa,  and  it 
is  this  circumstance  particularly  which  permits  the  development  of  bac- 
terial peritonitis.  These  views  have  been  based  upon  experiments  and 
pathologic  conditions  both  in  animals  and  man.  Clinical  experience,  how- 
ever, if  it  be  not  too  strongly  influenced  by  the  suggestive  effect  of  these 
animal  experiments,  cannot  escape  the  conviction  that  in  human  pathology 
the  protective  power  of  the  normal  peritoneum  is  not  great.  Certainly  the 
surgeon,  after  the  necessary  toilet  of  a  fibrino-purulent  intestinal  coil,  sees 
the  peritonitis  disappear.  But  here  we  are  not  exactly  dealing  with  a 
normal  peritoneum  producing  and  absorbing  serum;  but  other  curative 
factors  are  operative :  Adhesions  and  the  action  of  drainage.  On  the  other 
hand,  wherever  in  human  pathology  bacterial  products  of  inflammation 
attack  the  normal  peritoneal  surface,  there  peritonitis  generally  develops 
very  rapidly. 

Valua])le  experiments  by  Silberschmidt  ^  have  shown  that  the  com- 
bination of  deleterious  agents  present  in  non-sterilized  feces  may,  in  from 
twelve  to  eighteen  hours,  cause  the  death  of  the  experimental  animal  by 
purulent  peritonitis.  Only  pathogenic  bacteria  are  capable  of  producing 
a  ra])idly  fatal  diffuse  peritonitis  in  rabbits,  provided  they  do  not  find 
their  way  by  a  single  injection  but,  being  enclosed  in  an  animal  membrane 

1  8ilherscfinii(]t,  M ittheilungen  aus  den  Schweizer  med.  Instituten.  1.  Reihe,  Heft  5. 


ACUTE   DIFFUSE   PERITONITIS  531 

(fish  bladder)  gradually  penetrate  to  the  free  abdominal  cavity.  Wieland  ^ 
has  conducted  experiments  of  this  kind;  they  are  of  great  value  in  the 
study  of  these  conditions;  for  they  show  that  a  minute  change  in 
the  previous  experimental  arrangement  is  sufficient  seriously  to  impli- 
cate the  peritoneum  which  was  at  first  so  resistant,  and  to  destroy  the  life 
of  the  animal;  and,  above  all,  they  have  the  merit,  as  in  Silberschmidt's 
experiments,  of  closely  resembling  the  conditions  in  human  pathology; 
for,  if  highly  virulent  bacteria  gradually  approach  and  penetrate  the 
lymph-spaces  of  the  uterus  or  the  wall  of  the  appendix  and  enter  the  peri- 
toneum, we  actually  have  conditions  similar  to  those  in  Wieland's  tests. 

In  this  connection  let  us  glance  over  the  history  of  Case  No.  3,  that 
of  puerperal  streptococcus  peritonitis !  It  is  a  typical  example  of  a  diffuse 
fatal  peritonitis  due  to  a  pure  bacterial  culture  without  the  aid  of  "  irri- 
tating substances'';  and  if,  in  accordance  with  the  experiments  of  Gra- 
witz  and  Wegner,  we  accept  the  theory  of  the  attenuated  resistance  of  the 
puerperal  organism,  we  cannot  readily  understand  it.  Neither  is  this 
assumption  borne  out  by  the  facts  when  a  phlegmonous,  erysipelatous  in- 
flammation of  the  wall  of  the  appendix  without  perforation  produces  an 
extensive  purulent  peritonitis  in  the  normal  peritoneum  (notwithstanding 
its  undoubted  powers  of  resistance). 

The  result  of  all  this  is  that  we  must  not  estimate  too  high  the  power 
of  the  normal  peritoneum  to  resist  microbes ;  i.  e'.,  above  all,  to  destroy 
them  by  absorption;  if  this  be  regrettable,  it  also  has  something  in  its 
favor.  For  we  know  and  can  prove  by  the  previous  histories  that  a  massive 
absorption  of  toxins  from  the  peritoneum  leads  to  the  severest  form  of 
peritoneal  sepsis,  and  this  we  shall  later  discuss. 

Protection  by  the  normal  absorption  of  the  peritoneum,  therefore,  does 
not  play  the  important  role  in  pathology  which  was  formerly  often  as- 
cribed to  it.  All  the  more  important  are  the  protective  functions  of  the 
inflamed  serosa. 

Before  the  peritoneum  becomes  implicated  by  inflammatory  processes 
in  its  vicinity,  changes  are  produced  which  may  best  be  compared  with  the 
changes  in  the  skin  and  subcutaneous  cellular  tissue  surrounding  a  pus 
focus.  In  the  peritoneum  hyperemia  develop's,  also  a  fluid  exudate  gen- 
erally deficient  in  cells,  which  here,  however,  flows  into  the  free  abdom- 
inal cavity;  this  exudate  may  be  entirely  devoid  of  bacteria,  in  which 
case  to-day  we  speak  of  a  "  chemical  peritonitis " ;  rarely  in  these  cases 
does  the  exudate  become  rich  in  cells,  or  even  purulent.  There  is  no 
doubt  that  these  fluid  effusions  are  of  some  value  in  rendering  inert  the 
phlogogenic  microbes  which  enter  the  abdominal  cavity  from  the  focus 
of  inflammation,  and  eventually  perforate. 

*  E.  Wieland,  "  Experimentelle  Untersucliungen  iiber  die  Entstehung  der  Perito- 
nitis."    Mitth.  a.  d.  Schweizer  med.  Instituten,  Bd.  II. 


532       ACUTE   PERITONITIS,   APPENDICITIS,   AND   PERITYPHLITIS 

But  this  action,  as  already  stated,  must  not  be  estimated  too  high ; 
all  the  greater,  however,  is  the  protective  effect  of  plastic  exudates.  Their 
production  is  the  especial  property  of  the  serous  membranes;  they  may  de- 
velop even  a  few  hours  after  the  beginning  of  an  inflammatory  irritation, 
and  may  appear  as  swelling  and  redness  of  the  skin  surrounding  a  pus 
focus  already  formed  around  an  inflammatory  focus  which  threatens  to 
attack  the  serosa.  These  plastic  exudates,  however,  confer  protection  by 
leading  to  adhesions,  and  later,  by  the  extension  of  these,  to  adhesions 
of  the  serosa  with  neighboring  serous  surfaces.  Preferably  they  unite 
the  anterior  surface  of  the  stomach  with  the  abdominal  wall,  the  greater 
curvature  with  the  colon,  the  gall-bladder  with  the  colon,  etc.;  they  pro- 
duce membranes  which  usually  extend  from  the  intestine  at  a  point  oppo- 
site the  mesenteric  attachment  to  the  abdominal  wall;  they  form  a  sac 
around  the  inflamed  appendix  which,  if  ensuing  perforation  occur,  is 
calculated  to  absorb  the  putrid  masses  and  the  pus  which  these  develop. 

But,  rapidly  as  these  structures  form,  they  nevertheless  require  time 
to  attain  the  necessary  degree  of  firmness. 

Concerning  this  point,  the  clinical  histories  above  cited  should  be 
investigated,  the  autopsy  findings  in  the  rapidly  fatal  cases,  Nos.  2  and  3, 
and  the  findings  at  the  operation  and  at  the  autopsy  in  cases  Nos.  1, 
4,  and  5.  The  great  importance  of  this  circumstance  is  obvious,  and 
since  adhesions  which  exist  before  the  rupture,  if  firm,  afterward  become 
stronger,  sometimes  in  a  very  short  time,  we  find  perfectly  firm  encapsu- 
lated pus  cavities  in  various  regions  of  the  abdomen;  these  encapsulated 
pus  foci  are  probably  most  conspicuous  alongside  the  cecum,  behind  the 
stomach  as  subphrenic  abscesses,  and  in  the  true  pelvis. 

It  is  quite  possible  that  occasionally  even  in  perforation, — for  example, 
of  an  ulcer  of  the  appendix  with  a  normal  peritoneum,  therefore,  in  the 
free  abdominal  cavity, — these  adhesions  may  form  rapidly  enough  to  en- 
capsulate putrid  masses;  it  must  here  be  taken  for  granted  that  these  are 
quiescent,  and  this  above  all  presupposes  absolute  quiet  on  the  part  of  the 
patient  and  absence  of  motion  in  the  intestine.  Probably,  however,  these 
adhesions  are  generally  preformed  before  the  perforation;  naturally,  these 
are  facts  beyond  our  knowledge. 

The  more  infectious  the  pus  that  has  formed,  and  the  greater  the 
pressure  under  which  it  develops,  the  tougher  must  be  the  adhesions  to 
protect  the  free  abdominal  cavity. 

Let  us  again  review  cases  Nos.  1,  2,  and  5;  we  see  that  at  first  typical 
encapsulation  took  place;  later,  however,  the  adhesions  were  not  compact 
enough.  They  either  ruptured  mechanically  by  pressure  of  the  pus,  by 
peristalsis  or  other  causes,  or  were  obliterated  by  the  functions  of  the 
white  cells  and  bacteria,  and  thus,  finally,  they  paved  the  way  for  the  en- 
trance of  inflammatory  products  into  the  free  abdominal  cavity,  provided 
that,  in   the   meantime,  additional   adhesions   had   not  formed.     In   the 


ACUTE   DIFFUSE   PERITONITIS  533 

former  case  a  general  peritonitis  secondarily  developed,  in  the  latter  case 
there  was  a  relapse  of  circumscribed  peritonitis.  In  both  cases  we  see 
the  condition  which  Mikulicz  has  called  the  progressive  purulent  form 
of  acute  peritonitis. 

The  occurrence  of  such  secondary  ruptures  depends,  therefore,  partly 
upon  the  relation  between  the  internal  pressure  of  the  abscess  and  the 
firmness  of  its  wall,  and  partly  upon  vital  and  chemico-physical  processes 
in  the  wall  itself. 

As  auxiliary  factors  of  decided  importance  the  intensity  of  intestinal 
and  gastric  peristalsis,  possible  external  shock,  etc.,  injury  by  purgatives 
and  enemata  or  even  by  inunction  or  massage,  must  be  considered.  At 
all  events,  it  is  clear  that  the  firmness  of  the  boundaries  is  always  doubt- 
ful, and,  especially  at  the  onset  of  the  disease,  this  can  hardly  bo  looked 
upon  as  certain,  least  so  with  a  closed  abdomen,  and  this  is  of  significance 
in  the  prognosis  of  such  abdominal  abscesses.  The  clinical  history  of  Case 
No.  5  is  an  illustration  of  the  surprises  that  may  be  in  store  for  the 
physician. 

This  point  will  be  further  elucidated  under  the  discussion  of  the 
treatment. 

Chemical  peritonitis  has  been  referred  to;  this  exhibits  all  the  pecu- 
liarities of  sero-fibrinous  peritonitis,  it  may  become  rich  in  cells  and  even 
purulent — but  bacteria  are  absent.  It  is  probably  brought  about  by  bac- 
terial toxins  conveyed  from  a  near  focus;  chemical  peritonitis,  therefore, 
occurs  in  the  surroundings  of  an  insignificant  bacterial  pus  focus  of  the 
abdominal  cavity;  that  is,  from  a  periappendicitis,  a  psoas  abscess,  an 
inflamed  appendix,  an  ulcer  of  the  stomach  or  even  an  inflamed  gall- 
bladder. In  the  latter  case,  as  we  have  seen,  it  is  generally  plastic.  Its 
appearance  in  the  hernial  sac  about  the  incarcerated  intestinal  coil  is 
characteristic  and  instructive;  here,  at  all  events,  the  paralyzed  intestine 
is  permeable  for  the  toxins  of  intestinal  bacteria  and  other  soluble  prod- 
ucts, and  this  is  the  precursor  of  permeability  for  bacteria,  and  leads  to 
necrosis  of  the  intestinal  wall;  similar  conditions  arise  in  severe  trau- 
matic contusion  of  the  intestine. 

CHEMICAL   PERITONITIS  -^^ 

In  chemical  periioniti&.prie.  ihix\g  }^  es.p.ecially  yrteresting  to  the  clin- 
ician :  The  hyperemia  and  resulting  fluid  exudation  appear  and  disappear 
according  to  the  focus  of  origin.  A  circumscribed  periappendicular  ab- 
scess may  produce  a  distributed  chemical  peritonitis  in  its  surroundings; 
this  manifests  itself  by  moderate  or  even  decided  sensitiveness  upon  pres- 
sure and  distention  of  the  abdomen,  and,  perhaps,  by  decreased  but, 
clinically,  often  threatening  symptoms  of  extensive  peritonitis;  if  the 
abscess  is  opened  or  ruptures  spontaneously,  these  symptoms  suddenly 
disappear.     Much  of  that  which  the  clinician,  for  want  of  a  better  term. 


534       ACUTE   PERITONITIS,   APPENDICITIS,   AND   PERITYPHLITIS 

has  designated  as  "  peritoneal  irritation  "  belongs  to  the  realm  of  chemical 
peritonitis.  This  dependence  of  chemical  peritonitis  upon  a  bacterial 
focus  of  origin  is  due  to  the  fact  that  the  process,  being  independent  of 
bacteria,  does  not  generate  new  causes  of  inflammation,  is  not  in  itself 
capable  of  propagation,  or  even  progressive.  This  does  not  preclude  its 
occurrence  as  an  accompanying  process  of  great  intensity  and  extension  and 
directly  or  indirectly  extremely  dangerous  (by  moderate  meteorism,  forc- 
ing upward  of  the  diaphragm,  etc.).  This  form  of  inflammation  differs 
from  the  metastases  containing  bacteria  of  peritoneal  inflammation,  which 
may  spontaneously  disappear  provided  their  action  is  moderate  and  they 
may  thus  be  destroyed  by  the  peritoneum;  on  the  other  hand,  in  many 
cases  they  may  survive  and  continue  to  develop  even  after  the  focus  of 
origin  has  been  removed.  These  points  give  us  important  indications 
for  the  treatment. 

It  is  true  the  plastic  exudates  of  chemical  peritonitis,  as  well  as  those 
generated  by  the  presence  of  bacteria,  may  persist  for  a  long  time;  they 
may  be  organized  into  pseudo-membranes  and  indurations  long  after  the 
source  of  inflammation  has  been  removed.  This  newly  formed  connective 
tissue,  by  its  bulk,  resistance,  and  indistensibility,  even  by  its  cicatricial 
retraction,  may  contract,  deform,  and  limit  motion,  and  in  various  waj's 
may  narrow  and  constrict  the  abdominal  organs  and  cause  adhesions. 
In  the  consideration  of  chronic  peritonitis  we  shall  revert  to  this  sub- 
ject again. 

The  foregoing  description  makes  clear  the  meaning  of  our  statement 
that  the  severity  of  peritonitis  depends  primarily  upon  two  things:  The 
activity  of  the  septic  microorganisms  and  the  rapidity  with  which  they 
reach  the  serosa  from  a  focus  near  the  surface  of  the  peritoneum. 

In  contrast  to  these  numerous  methods  of  infection  from  neighboring 
organs  are  invasions  of  the  peritoneum  by  means  of  the  blood  or  lymph- 
channels,  which  are  certainly  rare.  They  occur  in  acute  articular  rheu- 
matism and  occasionally  in  sepsis.  In  the  cases  in  which  small  encapsu- 
lated empyemata,  particularly  the  metapneumonic,  complicate  a  purulent 
peritonitis,  transmission  by  means  of  the  blood  may  also  sometimes  occur, 
as  I  have  previously  stated.^ 

PATHOLOGY  AND  GENERAL  CLINICAL  PICTURE 

In  regard  to  the  pathology  and  general  clinical  picture  of  acute  diffuse 
peritonitis,  the  clinical  observations  quoted  at  the  beginning  of  this  article 
indicate  distinctly  that  two  different  pathologic  conditions  are  to  be  con- 
sidered :  A  congestive  inflammatory  general  condition  with  speciflc  accom- 
panying symptoms  of  peritoneal  irritation,  and  the  general  picture  of 
collapse.     Mixed  forms  between  these  occur,  although  rarely;  as  a  rule, 

1  0.  Vierordt,  Deutsch.  Arch.  f.  klin.  Med.,  Bd.  LXIV. 


ACUTE   DIFFUSE   PERITONITIS  535 

they  may  be  sharply  differentiated,  but  occasionally  they  rapidly  merge 
into  one  another. 

The  triad  of  symptoms  mentioned  in  the  first  clinical  history, — severe 
abdominal  pain,  fever  and  vomiting, — has  been  sufficiently  described  in  the 
epicrisis  of  the  clinical  histories,  as  well  as  peritoneal  meteorism,  which 
almost  always  occurs  as  a  fourth  symptom.  These  four  symptoms,  while 
not  invariable,  are  found  so  uniformly  in  most  cases  of  acute  diffuse 
peritonitis,  and  they  dominate  the  clinical  picture  to  such  an  extent, 
that  without  a  history  the  status  of  the  patient  frequently  gives  no  clue 
for  the  differential  diagnosis  of  the  origin  of  the  affection.  If  the  history 
does  not  aid  us,  this  question  under  some  circumstances  cannot  be  decided ; 
but,  as  a  rule,  there  are  differential  diagnostic  guides  to  which  we  shall 
later  refer. 

Eegarding  the  second  condition,  the  seeming  collapse,  in  our  clinical 
histories  we  note  its  appearance  under  very  different  circumstances:  In 
Case  1  it  developed  twice  from  the  previously  existing  congestive  inflam- 
mation; the  first  time  it  disappeared  after  the  salutary  rupture  of  the 
periappendicular  pus  into  the  intestine,  and  the  second  time  it  was  the 
cause  of  death;  in  Case  2  (perforation  of  the  stomach)  it  appeared  a  few 
hours  after  the  onset  of  the  affection;  here,  post  mortem,  the  massive  con- 
tents of  the  stomach  were  found  in  the  abdominal  cavity,  and  the  peri- 
toneum was  quite  smooth  and  glistening.  In  puerperal  septic  peritonitis 
collapse  occurs  early,  but  appears  to  be  modified  by  the  delirium  and 
marked  somnolence;  post  mortem  we  find  a  severe,  purulent  streptococcus 
peritonitis,  but  no  perforation,  no  putrid  infection. 

The  symptoms  common  to  these  clinical  pictures  are  severe  cardiac 
and  vascular  weakness,  prostration,  cold  sweat,  lowered  general  and  sur- 
face temperature,  and  comparatively  mild  subjective  symptoms;  in  addi- 
tion to  these  a  severe,  widely  distributed  peritoneal  irritation  is  common, 
and  also  probably  the  absorption  of  toxic  products. 

But,  upon  closer  investigation,  these  conditions  differ  from  each  other, 
and  far  more  etiologically  than  clinically.  In  one  case  we  have  the 
sudden  flooding  of  the  peritoneum  with  the  gastric  contents:  Gastric 
juice  containing  hydrochloric  acid,  albuminates,  peptones,  salts,  etc.,  and 
also  bacteria  which  are  of  diminished  vitality,  consequently  bacterial  toxins 
here  play  no  role.  In  the  two  other  cases  we  have  severe  bacterial  peri- 
tonitis— one  being  a  pure  streptococcus  peritonitis;  in  both,  especially  in 
the  latter,  there  is  profuse  absorption  of  bacterial  toxins:  Sepsis. 

At  the  present  time  these  conditions,  especially  in  Germany,  are  re- 
garded from  too  one-sided  a  standpoint, — usually  as  peritoneal  sepsis, — 
and  their  other  aspects  are  ignored;  namely,  the  effects  of  shock  upon  the 
central  organs,  that  is,  the  cardiac  and  vascular  centers,  originating  from 
decided  irritation  of  the  sensory  end  organs  of  the  sympathetic  in  the 
peritoneum,  not   alone  in  peracute  perforations,  but   also  in  peritonitis 


536      ACUTE   PERITONITIS,   APPENDICITIS,   AND  PERITYPHLITIS 

which  rapidly  becomes  diffuse;  and  secondly,  the  internal  congestion  of 
tlie  enormously  dilated  arteries  of  the  splanchnic  region  which  certainly 
play  an  important  part;  anemia  of  the  rest  of  the  body,  giving  rise  to 
cardiac  and  vascular  weakness,  and  probably  also  to  dryness  of  the  tongue 
and  the  marked  thirst  of  which  these  patients  complain,  is  not  only  due 
to  the  peritoneal  irritation  but  is  produced  by  the  intoxication  itself. 

In  the  treatment  it  is  advisable,  and  sometimes  necessary,  to  observe 
tlic  varying  genesis  and  complicated  nature  of  these  clinical  pictures  at 
tlio  bedside.  Certainly  intoxication,  most  often  the  septic  form,  plays  an 
important  part;  the  picture  produced  by  the  latter  may  also  be  of  high 
substantive  value  in  the  diagnosis;  for  example,  in  acute  intestinal  occlu- 
sion, it  points  to  strangulation,  the  immigration  of  bacteria  through  the 
paralyzed  intestinal  wall,  and  beginning  septic  peritonitis.  But  prolonged 
shock  and  congestion  in  the  splanchnic  area  produce  very  similar  symptoms, 
and  neither  the  state  of  the  sensorium  nor  the  preceding  fever  is  a  positive 
and  unmistakable  guide  to  the  differentiation.  This  can  most  readily 
})c  made  from  the  manner  of  development  of  the  affection  and  from  the 
accoin])anying  circumstances,  and  particularly  from  the  diagnosis  of  the 
origin  of  the  peritonitis. 

The  local  symptoms  of  acute  diffuse  peritonitis  have  been  sufficiently 
described  in  the  epicrises  of  the  clinical  histories.  But  a  few  points 
should  be  emphasized. 

LOCAL  SYMPTOMS 

Meteorism  rarely  develops  at  once;  in  some  cases,  particularly  those 
in  which  gastric  perforation  or  severe  traumatic  intestinal  rupture  occurs, 
also  sometimes  in  duodenal  perforation,  it  may  appear  very  late  or  not 
at  all.  The  abdomen  is  at  first  as  hard  as  a  board,  tense  and  even  re- 
tracted; often  there  is  tearing  pain.  In  the  main,  however,  meteorism 
is  typically  uniform  and  rigid,  individual  inflated  coils  are  nowhere  seen, 
the  dull  tympanitic  note  is  occasionally  uniform,  but  nevertheless  shows 
slight  differences  resembling  those  of  the  lungs  (with  marked  tension!); 
Ave  note  the  high  position  of  the  diaphragm,  and  the  marginal  border  of 
the  liver.  We  must  bear  in  mind  the  necessity  of  frequent  investigations 
for  dulness  so  far  as  the  state  of  the  patient  may  permit ;  auscultation 
often  reveals  absolutely  nothing, — "  death-like  silence  in  the  abdominal 
cavity."  Not  rarely,  however,  soft,  highly  tympanitic,  intestinal  splash- 
ing is  here  and  there  heard,  especially  if  slight  diaphragmatic  respiration 
is  present,  also  soft  friction  sounds  over  the  liver,  the  spleen  and  the  upper 
portions  of  the  intestine. 

In  gastric  and  intestinal  perforation,  air  in  the  peritoneal  sac  is  some- 
times very  easy  to  difi^osticate,  particularly  if  it  rapidly  forms  in  large 
amounts,  distends  the  belly-wall  and  raises  the  diaphragm,  causes  the  liver 
dulness  completely  to  disappear,  and  produces  a  clear,  absolutely  uniform, 


ACUTE    DIFFUSE   PERITONITIS  537 

more  or  less  tympanitic  note  upon  auscultatory  percussion,  with  the  ab- 
sence of  all  signs  upon  auscultation,  or  profuse  splashing  sounds.  Whether, 
owing  to  its  importance  in  the  diagnosis,  we  should  try  by  cautious  move- 
ment of  the  patient  to  obtain  a  succussion  sound,  can  only  be  decided  by 
the  individual  circumstances  and  by  the  physician's  own  conscience.  If 
marked  effusion  is  present,  this  becomes  still  more  obvious  by  its  prompt 
motion  upon  change  of  position.  If  peritoneal  meteorism  develops  slowly 
after  a  preceding,  high-graded,  intestinal  meteorism,  it  is  difficult  to  dis- 
criminate between  these  signs;  a  uniform  percussion  note,  the  disappear- 
ance of  liver  dulness  (even  complete),  the  death-like  silence  which  accom- 
panies the  latter,  the  soft,  faint  splashing,  and  even  the  unmistakable  signs 
upon  auscultatory  percussion  are  manifest  at  quite  a  distance.  The  physi- 
cal signs  in  both  cases  are  very  similar.  The  differentiation  may  be  just 
as  great  when  the  gas  in  the  peritoneum  owes  its  origin  not  to  perforation 
but  to  the  putrid  decomposition  of  a  fluid  exudate. 

Peritoneal  meteorism  which  appears  rapidly  proves  perforation;  in- 
versely, however,  it  may  be  absent  in  perforation;  it  is  most  frequent 
in  the  perforation  of  typhoid  intestinal  ulcers,  and  relatively  rare,  at 
least  at  the  onset,  in  complete  traumatic  intestinal  rupture;  perforation 
of  the  appendix  seldom  causes  the  discharge  of  gas;  in  gastric  perforation 
this  varies  greatly. 

As  has  already  been  stated,  diffuse  peritonitis  is  by  no  means  always 
distributed  evenly  and  '*  diffusely  " ;  the  large  omentum  and  the  transverse 
colon  frequently  act  as  a  barrier ;  appendicular  peritonitis,  peritonitis  of 
the  small  intestine,  and  puerperal  peritonitis  chiefly  originate  beneath 
this  barrier,  gastric  peritonitis  develops  above  it,  and  it  is  therefore  im- 
portant for  us  to  decide  as  to  the  starting-point  of  a  peritonitis,  whether 
it  presents  itself  as  diffused  inferiorly  or  diffused  superiorly.  The  clinico- 
diagnostic  difficulties  of  this  differentiation  will  be  found  great  beyond 
expectation.  The  symptoms  of  subdiaphragmatic  peritonitis,  absence  of 
diaphragm  respiration,  and  singultus  are  not  strictly  confined  to  this 
form.  I  remember  quite  a  number  of  autopsies  in  cases  which  had  shown 
these  symptoms  during  life,  and  the  entire  upper  portions  of  the  peri- 
toneum were  free.  The  persistence  of  diaphragmatic  respiration  might 
be  considered  to  indicate  a  superior  peritonitis,  but  diaphragmatic  respira- 
tion is,  in  fact,  almost  always  absent  from  the  onset  in  the  diffuse  forms. 

The  circumstance  is  very  important  that  in  gastric,  and  partly  also  in 
duodenal,  perforation,  vomiting  is  insignificant  or  may  be  entirely  absent; 
frequently  there  are  eructations.  In  contrast  to  this,  in  deep-seated  peri- 
tonitis urinary  difficulties  and  a  high  degree  of  pain  upon  pressure  are 
observed  during  "  cautious "  vaginal  and  rectal  examinations. 

With  gas  in  the  abdominal  cavity  peritonitis  in  the  upper  part  is 
mostly  diffuse;  gas  everywhere  finds  its  way  upward,  and  promotes  the 
rapid  distribution  of  inflammation. 


538      ACUTE   PERITONITIS,   APPENDICITIS,   AND  PERITYPHLITIS 


DIAGNOSIS 

The  diagnosis  of  diffuse  peritonitis  may  be  easily  made  when  we  con- 
sider the  totality  of  the  symptoms.  In  a  minority  of  cases,  however,  we 
meet  with  differentio-diagnostic  difficulties  which  are  usually  very  great. 

An  acute  peritonitis  without  meteorism,  i.  e.,  with  a  hard  retracted 
abdomen,  with  excruciating  pain  in  the  gastric  region,  but  without  vomit- 
ing or  constipation,  and  in  which  there  is  perhaps  a  history  of  ulcer,  may 
simulate  a  severe  cardialgic  attack  in  a  patient  with  gastric  ulcer;  fever, 
diffused  pain  upon  pressure  in  the  hypochondriac  region,  and  even  in  the 
lumbar  region,  and  the  symptoms  of  collapse  will  favor  peritonitis,  but 
the  diagnosis  may  remain  doubtful  until  meteorism  appears.  The  same 
conditions  are  also  observed  in  ulcer  of  the  duodenum. 

Severe  inflammatory  attacks  of  gall-stone  colic  with  a  distended  abdo- 
men, vomiting,  and  even  fecal  vomiting  and  fever,  may  cause  great  per- 
plexity in  the  differential  diagnosis,  particularly  if  the  anxious  patient 
states  that  the  whole  abdomen  is  painful  upon  pressure.  The  difficulty 
is,  however,  at  least  lessened  by  the  rapid  disappearance  of  meteorism 
when  the  attack  ceases,  and  perhaps  with  the  administration  of 
morphin. 

In  the  majority  of  cases,  however,  it  is  difficult  to  decide  whether 
peritonitis  or  intestinal  obstruction  is  present,  particularly  if  strangulation 
be  suspected,  since  the  latter,  as  is  well  known, "  gradually  produces  peri- 
tonitis. Simple  obstruction  is  readily  differentiated  from  peritonitis  by 
the  absence  of  fever,  by  the  less  painful  meteorism,  by  a  more  or  less  dis- 
tinct local  peristalsis,  by  collapse  which  sets  in  late  or  does  not  appear 
at  all.  The  obstacles  are  even  greater  in  the  diagnosis  of  obstruction 
due  to  strangulation:  Examination  of  the  hernial  rings  (they  must  all 
be  examined,  and  all  symptoms  of  hernia  considered)  by  rectum  will 
sometimes  at  once  decide  the  question  in  favor  of  the  latter;  but  where 
all  these  tests  are  negative  or  uncertain  (as  in  long-standing,  non-incar- 
cerated hernia),  in  the  absence  of  fixed  inflated  coils  (v.  Wahl)  or  of 
peristalsis  above  these  (Schlange) — as  is  unfortunately  frequently  the  case 
— the  differential  diagnosis  at  once  becomes  very  obscure;  early  fever 
favors  peritonitis  (initial  shock  occurs  in  this  condition  as  well  as  in 
strangulation)  and  hemorrhagic  dejecta  indicate  strangulation,  particu- 
larly invagination.  The  longer  the  condition  lasts  the  more  difficult  is  the 
diagnostic  differentiation,  because  peritonitis  is  then  added  to  strangula- 
tion. It  is  obvious  that  under  these  circumstances  the  previous  history 
of  tlic  patient  is  important  and  occasionally  decisive. 

Tlic  same  conditions  are  met  with  in  the  extremely  rare  cases  where 
an  enormous  fecal  accumulation  causes  great  meteorism,  vomiting,  sensi- 
tiveness of  the  abdomen,  eventually  fever,  and  simulates  peritonitis.  Ure- 
mia also  may  lead  to  confusion  when  accompanied  by  severe  vomiting. 


ACUTE   DIFFUSE  PERITONITIS  539 

meteorism,  diarrhea  and  fever,  and  when  the  symptoms  of  nephritis  (acute 
or  chronic)  have  been  insufficiently  observed. 

PSEUDO-PERITONITIS,  PERITONISM 

By  a  pseudo-peritonitis,  peritonism  (Gubler),  we  mean  conditions  in 
which  the  combination  of  abdominal  pain,  vomiting,  a  tense  and  usually 
distended  abdomen,  constipation  and  perhaps  even  fever  depending  upon 
a  hysterical  basis  simulates  peritonitis.  These  cases  usually  occur  in  young 
hysterical  persons,  not  rarely  in  children;  occasionally  the  causes  are  mild 
intestinal  and  genital  affections,  retention  of  urine  and  feces,  slight  trauma. 
The  clinical  picture  may,  at  the  first  glance,  lead  to  confusion ;  but  upon 
careful  observation  a  certain  disproportion  in  the  symptoms  becomes  obvi- 
ous; for  example,  tearing  pain  and  continuous  vomiting  without  a  sign 
of  collapse;  in  one  of  my  cases  there  was  severe  spontaneous  pain  as  well 
as  tenderness  upon  pressure  with  marked  meteorism,  but,  instead  of  lying 
still,  upon  palpation  the  patient  made  energetic  efforts  to  rise;  this  does 
not  occur  in  acute  peritonitis.  Other  characteristics  are  the  abrupt  change 
in  the  symptoms,  the  effect  of  suggestion  particularly  on  the  pain,  the 
absence  of  cardiac  asthenia  (although  Naun}Ti  saw  dyspnea  and  a  poor 
pulse  due  to  the  elevated  position  of  the  diaphragm),  finally,  stigmata  and 
antecedentia  lujsterica  must  be  considered,  both  of  which,  naturally,  may 
be  absent  in  the  young.  Taken  all  in  all,  the  careful  observer  is  liable 
to  be  mistaken  the  first  day  of  the  disease,  but,  upon  the  second,  one  of 
these  signs  will  lead  him  to  a  correct  conclusion. 

In  all  of  these  cases,  in  which,  in  contrast  to  diffuse  peritonitis,  non- 
inflammatory or,  at  least,  not  diffusely  inflammatory  affections  in  the 
abdomen,  or  other  conditions  are  to  be  considered,  a  rise  in  the  rectal 
temperature  (two  or  more  degrees  higher  than  in  the  axilla)  may  be  of 
diagnostic  importance,  but  only  when  the  temperature  is  very  accurately 
taken  by  the  axilla. 

The  diagnosis  of  the  point  of  origin  is  easy,  provided  the  symptoms 
of  the  original  affection  have  been  previously  observed  by  the  physician; 
otherwise,  the  diagnosis  is  generally  the  more  obscure  the  greater  the 
development  of  the  peritonitis.  But  even  then  it  may  often  be  made 
from  the  history — which,  however,  may  be  erroneous  (cardialgia  and  gall- 
stone colic,  ulcer  of  the  stomach  and  ulcer  of  the  duodenum,  an  affection 
of  the  pancreas,  perityphlitis  and  genital  affections,  etc.). 

It  is  most  important  to  determine  the  seat  of  greatest .  tenderness,  and 
there  eventually  to  locate  an  objective  point.  Some  authors  have  recently 
attached  great  significance  to  the  hyperalgic  zones  of  the  skin.  Examina- 
tion of  the  hernial  rings  and  of  the  vagina  should  never  be  omitted;  both 
this  and  rectal  examination  are  generally  necessary  for  the  detection  of 
exudates  into  the  pelvis,  and  to  differentiate  perityphlitis  from  genital  and 
bladder  affections. 


540      ACUTE   PERITONITIS,  APPENDICITIS,  AND  PERITYPHLITIS 

It  must  be  remembered  that  the  individual  abdominal  organs,  particu- 
larly the  appendix,  have  no  fixed  position ;  the  tip  of  a  long  appendix  may 
reach  far  down  into  the  right  iliac  fossa,  as  has  been  previously  remarked. 
A  pericholecystitis  will  occasionally  be  situated  very  near  McBurney's 
point,  or  may  be  also  somewhat  displaced  laterally.  There  is  naturally 
no  positive  seat  for  perforation  of  the  small  intestine,  although  typhoid 
perforation  is  often  found  low  down  upon  the  left  side.  Ovarian  affections 
may  be  widely  distributed,  particularly  toward  the  ileo-cecal  region.  The 
pancreas  and  duodenum  have  fixed  locations,  but  here  the  differentiation 
from  the  stomach  is  difficult. 


CIRCUMSCRIBED  ACUTE  PERITONITIS  WITH  PARTICULAR  REF- 
ERENCE  TO   PERITYPHLITIS 

PATHOLOGY 

Circumscribed  peritonitis  is  prone  to  develop  when  bacteria  find  in- 
gress to  the  abdominal  cavity  and  penetrate  to  regions  preformed  by 
adhesions.  We  have  previously  seen  that  in  perforation  the  severity  of 
the  infection  of  the  abdominal  cavity  depends  upon  the  amount  of  material 
discharged  into  it  from  the  stomach  and  intestines,  upon  the  entrance 
of  pyogenic  organisms  from  the  lymph-tracts,  upon  the  virulenc6  of  the 
pathogenic  pure  cultures  which  have  been  previously  produced  in  the  tis- 
sues. Now,  if  the  perforation  be  very  minute  or  the  virulence  but  moderate, 
if  it  take  place  in  an  area  favorable  for  deposit  (the  ileo-cecal  region,  the 
pelvis,  the  subphrenic  space),  on  the  cessation,  spontaneous  or  induced, 
of  intestinal  peristalsis  and  when  the  patient  remains  very  quiet — it  cer- 
tainly happens  that  a  previously  normal  peritoneum  without  adhesions 
will  produce  direct  epithelial  or  fibrinous  adhesions  of  its  walls,  and,  in 
the  meantime,  will  absorb  a  certain  amount  of  the  poison  and  in  this 
manner  localize  the  process.  The  individual  parts  of  the  abdominal  cavity 
joined  to  the  mesentery  form  a  fan-like  structure  which  aids  us  here. 
Tlie  clinical  picture  depends  upon  how  rapidly  encapsulation  takes  place, 
whether  it  be  complete  or  partial,  whether  the  toxins  do  not  produce 
(although  their  agents  themselves  do  not)  a  diffuse  chemical  peritonitis 
beyond  the  protective  wall,  and  upon  the  density  of  the  adhesions,  the 
firmness  of  their  hold,  and  their  further  course.  Naturally  it  also  depends 
upon  the  reaction  of  the  entire  organism  to  the  irritation  of  the  peri- 
toneum and  to  the  intoxication. 

From  the  different  forms  of  circumscribed  peritonitis  I  shall  single 
out  perityphlitis,  and  describe  this  affection  in  detail.  This  is  the  disease 
which,  in  the  majority  of  cases,  presents  itself  to  the  family  physician, 
and  it  has  l)Gcome  a  mooted  question  whether  it  does  not,  from  the  very 


PERITONITIS  WITH   REFERENCE  TO  PERITYPHLITIS  541 

onset,  belong  to  the  realm  of  surgery.  Besides,  it  shows  the  greatest 
variations,  and  therefore  best  illustrates  all  of  the  conditions  which  play 
a  part  in  circumscribed  peritonitis.  ^^ — 

We  have  seen  from  the  history  of  these  cases  that  circumscribed  peri- 
typhlitis may  be  absent  clinically  and  anatomically  (Case  3)  in  the 
severest,  i.  e.,  in  the  most  acute  cases  of  perforation  of  the  appendix ; 
that  it  may  sooner  or  later  develop  in  diffuse  perforation  of  the  appendix 
(Case  1),  and  may  even  appear  simultaneously  with  this  or  may  precede 
it;  that  an  accompanying  general  peritoneal  irritation  may  dominate  the 
clinical  picture;  that,  finally,  and  fortunately  in  the  majority  of  cases, 
it  may  occur  alone  and  exclusively  in  an  otherwise  normal  belly.  In  its 
course  this  focal  affection  may  extend  to  the  surrounding  portions  of  the 
abdominal  cavity.  It  has  just  been  mentioned  that  perityphlitis  may 
appear  gradually  as  the  actual  nucleus  of  a  distributed  peritonitis,  and 
when  the  peritonitis  disappears  may  dominate  the  picture;  inversely,  from 
the  originally  circumscribed  affection  one  or  more  serious  relapses  may 
unexpectedly  occur,  perhaps  with  fatal  result. 

AVhieh  of  these  extraordinarily  different  clinical  pictures  will  develop 
depends  chiefly  upon  the  nature  of  the  appendicitis  which  has  produced 
the  pdritoneal  inflammation  (skolikoiditis  is  the  designation  proposed  by 
iSTothnagel) ;  this  collective  name,  however,  includes  jnany  varieties.  If 
we  leave  out  of  consideration  the  tubercular,  the  typhoid,  and  the  actino- 
mycotic affections  of  the  appendix,  most  of  the  non-specific  cases  may  be 
referred  to  two  large  groups  of  causal  changes  in  the  appendix:  To  fecal 
impaction,  and  to  certain  chronic  inflammatory  and  also  acute  "  relapses  " 
of  the  wall  of  the  appendix. 

Proceeding  from  the  most  dangerous  to  the  mildest  diseases  of  the 
appendix,  we  first  distinguish  an  acute  distributed  gangrene  of  the  organ 
with  immediate  perforation  and  putrid  flooding  of  the  surrounding  area; 
next,  the  milder  cases,  i.  e.,  those  with  gradual  onset  and,  at  least  in  the 
beginning,  less  extensive  putrid  infection  of  the  peritoneum  by  the  per- 
forating, gangrenous  or  non-gangrenous  ulcer.  These  lesions  are  almost 
always  due  to  the  greatly  dreaded  fecal  conerement,  although  it  may 
certainly  be  absent.  We  recognize  also  a  gangrenous  inflammation  of  the 
appendix  without  fecal  calculus,  particularly  in  stenosis,  followed  by  the 
rupture  (which  may  be  gradual)  of  an  empyema  of  an  appendix  which  is 
closed  at  the  cecal  end  by  stricture,  but  also  by  empyemata  and  suppura- 
tions of  the  wall  of  an  appendix  which,  without  a  gross  rupture,  permits 
the  passage  of  pus  cocci ;  nearly  all  of  these  eases  are  due  to  collections 
of  bacteria  (Tavel  and  Lanz),  among  which  pathogenic  microbes  that 
have  previously  attained  decided  virulence  are -found  to  predominate  (al- 
most invariably  bacterium  coli).  But  simple  phlegmonous  or  erysipel- 
atous inflammations  of  the  mucosa  of  the  appendix  may,  without  them- 
selves being  purulent,  produce  a  suppurative  perityphlitis  usually  charac- 


542      ACUTE   PERITONITIS,  APPENDICITIS,   AND  PERITYPHLITIS 

terized,  at  least  at  first,  by  a  benign  form,  i.  e.,  with  slight  toxic  action 
and  a  tendency  to  limitation. 

Passing  from  the  severer  to  the  milder  forms,  we  note  that  the  appendix 
is  frequently  the  seat  of  "  chronic  catarrh  "  of  the  mucous  membrane  and 
its  numerous  glands  and  follicles  (angina  of  the  vermiform  appendix, 
Salili),  in  itself  not  serious,  but  also  of  deeper  chronic  inflammation  of 
its  connective  tissue  (appendicitis  granulosa,  Eiedel).  These  changes  may 
be  the  starting  point  of  the  above  mentioned  severe  forms  of  inflammation, 
either  directly  or  by  causing  secondary  changes:  Stenosis  and  stricture  by 
loss  of  epithelium,  the  formation  of  cicatrix,  adhesion  of  the  surfaces 
of  mucous  membranes  lying  opposite  each  other, 

A  factor  of  great  significance  in  the  development  of  these  forms  of 
appendicitis  is  that  the  serosa  of  the  appendix,  and  also  its  mesenteriolum, 
often  early  implicate  the  wall  of  the  organ,  even  by  mild  chronic  inflam- 
matory changes.  In  these  instances  the  serosa,  as  we  learn  from  early 
surgical  operations,  is  rarely  quite  normal,  but  is  usually  reddened,  per- 
meated by  numerous  vessels,  more  or  less  thickened,  often  unevenly,  by 
the  formation  of  constrictions  of  the  appendix;  frequently  the  mesen- 
teriolum is  also  implicated,  being  shortened,  thickened,  bent  and  torn, 
causing  immovability  of  the  contractile  organ.  Often  the  entire^  mass 
early  becomes  embedded  in  new  connective  tissue,  or  the  appendix  at 
its  end  or  at  some  other  part  of  its  length  adheres  to  the  cecum,  the  iliac 
fossa,  the  ovary  or  the  bladder. 

There  can  be  no  doubt  that  these  inflammations  of  the  mucous  mem- 
brane and  the  early  changes  in  the  serosa  indicate  severe  disease.  If  we 
remember  that  the  appendix  is  comparatively  long  and  thin,  a  hollow, 
secreting  organ,  it  is  not  difiicult  to  realize  that  even  a  moderate  diminu- 
tion of  the  elasticity  of  its  enclosing  serosa,  a  slight  induration  of  the 
same,  but  still  more  an  external  stenosis  and  kinking,  may  very  readily 
check  the  flow  of  its  secretion,  as  well  as  lead  to  circulatory  disturbances 
in  its  walls.  Moderate  stricture  may  act  like  a  narrowed  foramen  upon 
catarrh  of  the  frontal  bone;  desquamation  and  serous  transudation  of  its 
tissue  may  also  cause  venous  stasis;  the  finding  of  a  penis-like  thickening 
of  the  process,  but  even  more  the  microscopic  findings  of  Eiedel  (round- 
cell  accumulation,  disappearance  of  the  glands  and  hemorrhages)  must 
increase  this  presumption.  But  these  processes  take  place  in  the  neigh- 
borliood  of  products  which  mechanically  and  toxically  injure  them,  and 
in  tlie  presence  of  putrid  collections  of  bacteria;  doubtless  in  the  latter 
case  the  ])athogenic  bacteria  which  are  always  present  frequently  gain  the 
upper  liand.  We  must,  therefore,  on  the  one  hand,  attribute  to  the  con- 
dition of  the  secretion,  and  on  the  other  hand,  to  stasis  combined  with 
the  aljove  circumstances,  a  part  in  the  genesis  of  all  mild  and  severe  forms 
of  periappendicitis  which  develop  without  fecal  calculi;  but  also  the 
severest  forms,  for  the  remarkable  finding  of  acute  gangrene  without  fecal 


PERITONITIS  WITH  REFERENCE  TO  PERITYPHLITIS  543 

calculus  may  be  plausibly  explained  by  a  free  desquamation  of  the  organ 
with  limited  distensibility,  by  immediate  severe  stasis  in  the  region  of 
the  fine  venous  branches  of  the  interior,  and  by  gangrene  from  the  influ- 
ence of  bacteria  constantly  ready  to  develop. 

The  most  vital  point  here  is  the  intimate  relation  of  comparatively 
mild  changes  in  the  appendix  which  cause  no  apprehension  to  the  most 
severe  and  most  dangerous.  This  is  probably  due  to  the  fecal  calculus 
which  may  remain  a  varying  length  of  time  in  the  appendix  without 
producing  symptoms  (in  some  cases  large  fecal  calculi  have  been  discovered 
accidentally  without  resultant  effect),  and  then,  as  a  rule  suddenly,  ex- 
hibits decided  activity.  On  the  other  hand,  it  may  be  due  to  the  previously 
mentioned  chronic  inflammatory  conditions.  In  regard  to  the  latter  we 
are  indebted  to  Riedel  for  having  systematically  paved  the  way  to  the 
recognition  of  their  relations  to  perityphlitis.  He  has  shown  that  chronic 
appendicitis  is  in  some  cases  a  comparatively  mild,  in  others  an  exceed- 
ingly grave,  affection.  He  relates  his  observations  and  results  of  investi- 
gation so  clearly  that  I  cannot  refrain  from  quoting  his  remarks  on  the 
point  in  question:  "  In  one  case  the  disease  (appendicitis  granulosa)  leads 
insidiously  and  painlessly  in  the  course  of  years  to  obliteration;  in  an- 
other, one  or  several  inflammatory  relapses  occur  and  obliteration  results; 
in  a  third  the  appendix,  notwithstanding  several  relapses,  remains  in  the 
state  of  appendicitis  granulosa;  in  a  fourth,  the  lymph-glands  become 
infected;  in  a  fifth,  a  periappendicular  abscess  forms  which  may  later 
be  absorbed  without  a  trace  of  pus  appearing  in  the  appendix;  finally,  in 
a  sixth,  the  acute  inflammatory  paroxysm  begins  with  suppuration,  even 
with  gangrene;  here  appendicitis  granulosa  forms  the  basis  for  the  acute 
suppurative  attack,  usually  without  fecal  calculus,  so  that  frequently  the 
pus  is  but  slightly  or  not  at  all  putrid ;  with  gangrene  that  sets  in  at  once 
it  is  usually  putrid,  but  not  invariably." 

If  we  consider  what  has  long  been  known  of  fecal  calculi,  and  what 
has  become  obvious  from  the  conditions  just  described,  we  come  to  the 
conclusion  that  in  by  far  the  majority  of  cases  of  severe  appendicular 
peritonitis  dangerous  to  life  the  disease  has  existed  for  a  longer  or  shorter 
time.  For  the  clinician,  however,  the  important  questions  at  once  arise: 
Can  these  preceding  changes  be  clinically  recognized,  or  can  we,  at  least, 
approach  more  nearly  to  their  recognition?  These  questions  we  will  dis- 
cuss later. 

If  suppuration  occurs  in  any  of  the  previously  mentioned  regions  out- 
side of  the  appendix,  the  development  and  course  depend  upon  various 
circumstances.  The  most  malignant  forms  are  the  putrid  infections  and 
those  from  highly  virulent  and  more  or  less  pure  pyogenic  agents  (bac- 
teria coli.  streptococci  and  staphylococci),  the  former  occurring  in  gan- 
grene with  or  without  fecal  calculus,  but  usually  without,  the  latter  less 
frequently  in  a  few  cases  of  empyema  and  phlegmonous  appendicitis. 
"^30 


544      ACUTE   PERITONITIS,   APPENDICITIS,   AND  PERITYPHLITIS 

An  important  and  usually  decisive  factor  is  the  eventual  presence  and 
the  strength  of  the  adhesions;  coarse  ones  resist  the  mechanical  and  vital 
influence  of  pus,  weaker  ones  succumb.  As  auxiliary  conditions  we  must 
mention  the  position  of  the  abscesses  as  related  to  the  cecum :  Those  medi- 
ally situated  soon  penetrate  into  the  free  abdominal  cavity,  those  laterally 
situated  toward  the  sacral  hollow  of  the  pelvis  are  most  readily  limited. 
Suppuration  between  the  layers  of  the  mesenteriolum  appendicis  frequently 
extends  to  the  retrocecal  space  and  occasionally  along  the  colon  as  far  as 
the  descending  colon;  thus  it  may  give  rise  to  paranephritis  either  dextral 
or  sinistral,  subphrenic  abscess,  empyema  upon  the  right  or  left  side; 
and  these  may  apparently  be  produced  paroxysmally.  Suppuration  low 
down  in  the  median  line  readily  finds  its  way  to  the  pelvis.  It  is  obvious 
that  when  pus  is  found  in  this  locality  the  original  position  of  the  appen- 
dix has  a  decided  influence. 

Periappendicular  suppuration,  even  when  not  very  extensive,  produces 
desquamation  and  serous  transudation  of  the  surroundings:  of  the  serosa 
of  the  cecum  and  appendix,  the  preformed  adhesions  and,  possibly,  the 
adherent  parietal  peritoneum  in  this  region,  perhaps  also  of  some  of  the 
mesenteric  glands;  in  some  cases  the  connective  tissue  of  the  retrocecal 
space  becomes  involved;  all  this  occurs  to  a  varying  extent,  and  produces 
the  perityphUtic  tumor  in  the  interior  of  which  suppuration  is  found 
which  resembles  the  purulent  nucleus  of  a  furuncle  (Sahli).  If  the  pus 
becomes  more  profuse  the  tumor  may  show  fluctuation;  it  may  become 
enlarged  by  an  accumulation  of  feces  in  the  paralyzed  cecum,  by  reflex 
action  of  the  inflammation  or  by  the  intestinal  paralysis  which  may  be 
very  extensive,  and  by  vomiting.  Occasionally  it  may  produce  distant 
efTecis:  Engorgement  and,  not  rarely,  serous  exudation  ("chemical  peri- 
tonitis") of  the  free  abdominal  cavity  which  is  usually  the  result  of 
a  general  toxic  action,  namely,  fever. 

As  Ave  have  just  seen,  non-purulent  inflammatory  processes  in  the 
appendix  cause  external  suppuration,  mild  irritative  conditions  in  the 
vermiform  process  cause  thickening  of  the  serosa  and  adhesions.  These 
mild  irritations,  especially  the  relapses  of  appendicitis  granulosa,  are  prob- 
ably capable  of  producing  relapsing,  that  is  paroxysmal,  serous  transu- 
dation and  serous  or  sero-fibrinous  exudates  (Sonnenburg)  in  the  sur- 
roundings without  the  formation  of  pus,  and  these  are  clinically  observed 
as  tumors;  they  are  characterized  by  their  brief  duration,  their  rapid 
disappearance,  sometimes  by  their  sequelae  of  marked  thickening  and 
adhesions. 

Tlie  variety  of  conditions  produced  by  circumscribed  perityphlitic  sup- 
puration is  partly  illustrated  by  clinical  histories;  left  to  themselves,  after 
more  or  less  time  they  are  prone  to  rupture,  generally  into  the  intestine, 
especially  into  the  colon,  and  then  heal;  they  may  also  rupture  exter- 
nally,— llirough  the  skin,  into  the  bladder,  into  the  rectum,  into  a  pleural 


PERITONITIS   WITH   REFERENCE  TO   PERITYPHLITIS  545 

cavity  and  perhaps  into  the  lung;  or  they  penetrate  to  a  greater  or  less 
extent  within  the  free  abdominal  cavity  and  immediately  cause  an  acute 
diffuse  peritonitis,  or,  in  case  adhesions  were  preformed,  a  progressive 
purulent  peritonitis  (compare  clinical  history  N"o,  4) ;  in  the  series  of  re- 
lapses they  may  produce  here  and  there  a  number  of  new  foci  which 
result  in  a  more  or  less  rapid  destruction  of  the  organism.  But  metastatic 
suppurations  may  also,  particularly  by  rupture  through  the  intestine,  force 
their  way  outward,  and  surprising  recovery  has  been  observed  even  in  the 
severest  cases;  in  the  first  stages  of  progressive  peritonitis,  however,  we 
often  note  a  sudden  halt  in  the  process,  it  ceases  everjrwhere  except  in 
the  perityphlitic  center,  and  even  here  it  finally  runs  a  favorable  course 
or  becomes  chronic. 

Besides  this  unexpected  change  for  the  better  there  may  be  an  un- 
looked-for change  for  the  worse;  a  perityphlitic  abscess  which  has  previ- 
ously been  circumscribed  may,  at  any  time,  after  days  or  weeks,  rupture; 
general  peritonitis,  sepsis,  and  death  follow.  Doubtless  this  occurrence  is 
most  frequent  in  recent  encapsulation,  i.  e.,  in  perityphlitic  abscesses  which 
have  existed  only  three  to  five  days.  The  longer  this  period  and  the 
firmer  the  encapsulation,  the  more  unlikely  is  a  fatal  rupture;  but  it  can 
never  be  excluded  with  certainty  while  pus  is  present  in  the  abdominal 
cavity.  It  is  in  putrid  suppuration  that  this  condition  is  always  most 
to  be  feared. 

There  can  be  no  doubt  that  on  partial  discharge  of  the  pus,  for  exam- 
ple, after  surgical  operation,  the  remaining  pus  is  absorbed,  even  if  the 
wound  be  imperfectly  drained.  Consequent  upon  operation  special  condi- 
tions are  present;  congestive  hyperemia  probably  acts  by  vitalizing  all 
important  processes,  the  absorbent  as  well  as  the  bactericidal.  Therefore 
in  the  general  application  of  these  observations,  particularly  when  we  have 
the  condition  of  a  closed  belly,  we  must  be  cautious;  prior  to  operation, 
such  a  condition  is  extremely  difficult  to  distinguish.  What  appears  to 
be  absorption  may  very  likely  be  an  unperceived  rupture  into  the  intestine. 
Even  more  than  in  the  normal  peritoneum,  we  must  avoid  over-estimating 
the  absorptive  activity  of  the  peritoneal  pseudo-membranes.  "We  have  little 
certain  knowledge  regarding  these;  all  is  conjecture. 

Of  other  complications  produced  by  pus,  only  septic  thromboses  of 
venous  trunks  in  the  portal  vein  system,  or  of  branches  of  the  iliac,  or 
of  this  vessel  itself,  are  to  be  mentioned.  The  latter  may  lead  to  septic 
embolism  of  the  pulmonary  artery,  and  pulmonary  abscess  (not  always 
fatal).     These  thromboses  usually  result  in  general  sepsis  and  death. 

SYMPTOMS 

In  considering  the  clinical  symptoms  of  circumscribed  perityphlitis,  we 
must  again  review  the  clinical  liistories:  Acute  illness  with  severe  pain 
in   the   ileo-cecal   region,   vomiting,    a   varying   temperature   and   usually 


546      ACUTE  PERITONITIS,  APPENDICITIS,  ANt)  PEHITYPHLITIS 

rapidly  rising  fever,  but  rarely  fulminant  symptoms;  frequently,  at  first, 
a  few  thin  fecal  movements,  followed  by  constipation  which  depends  upon 
intestinal  paralysis,  and  then  the  appearance  of  a  painful,  more  or  less 
immovable  tumor  in  the  region  of  McBurney's  point,  which  at  first  in- 
creases in  size,  is  coarse  upon  palpation,  but  rarely  fluctuates  markedly; 
the  inguinal  glands  are  occasionally  swollen;  flexing  the  right  leg  often 
produces  deep-seated  pain  in  the  belly;  if  this  be  very  severe  it  favors 
paratyphlitis.  This  is  the  typical  picture  to  which,  under  some  circum- 
stances, the  more  or  less  intense  symptoms  of  a  diffuse  peritoneal  inflam- 
mation or  "  peritoneal  irritation  "  are  added. 

The  case  is  not  always  so  simple;  in  all  similarly  located  affections  the 
possibility,  and  even  the  likelihood,  of  perityphlitis  will  come  into  mind 
because  this  disease  is  so  frequent.  But  the  symptoms  will  often  necessi- 
tate careful  inquiry;  under  some  circumstances,  nothing  more  can  be 
found  than  an  indistinctly  limited  resistance  deep  in  the  belly  and  cov- 
ered by  an  intestine  containing  gas, — occasionally  not  even  this.^  To 
ensure  certainty  from  the  onset  in  the  differential  diagnosis  an  examina- 
tion must  always  be  made  of  the  hernial  rings,  of  the  vagina,  as  well  as 
of  the  rectum;  vaginal  as  well  as  rectal  examination  is  usually  to  be 
repeated  in  the  further  course  (to  solve  the  question  of  possible  descent 
into  the  pelvis). 

Pain,  fever  and  resistance  are  the  principal  symptoms. 

Pain. — The  pain  in  the  majority  of  cases  at  once  correctly  indicates 
the  location;  as  a  rule  it  is  spontaneously  severe  and  upon  pressure  un- 
bearable; it  is  situated  near  McBurney's  point  or  often  somewhat  below  it. 
At  the  onset  it  may  be  diffuse,  or  may  be  complained  of  in  a  paradoxical 
region  (upon  the  right  above,  upon  the  left  below,  etc.)  ;  but,  among  all 
the  acute  abdominal  affections  with  pain,  it  should  be  remembered  that 
perityphlitis  is  the  most  frequent;  it  should  always  be  borne  in  mind. 
The  position  and  the  radiation  of  the  pain  from  the  median  line  down- 
ward, and  often  associated  with  dysuria  (indicating  inflammation  toward 
the  pelvis),  to  the  lateral  and  posterior  lumbar  region  (inflammation  in 
the  retrocecal  and  retrocolic  space)  are  only  briefly  mentioned.  Psoas 
pain  upon  flexure  of  the  right  side  certainly  occurs  in  perityphlitis  without 
decided  paratyphlitis.  Painful  flexure  contraction  of  the  thigh,  however, 
and  the  impossibility  of  extending  it,  point  with  great  positiveness  to  the 
retrocecal  connective  tissue.  Lancinating  pain  upon  pressure  points  to 
pu.s,  dull  pain  does  not  exclude  it.     Very  severe  spontaneous  pain  and 

1  After  this  article  was  finished  I  read  an  excellent  publication  by  B.  v.  Beck 
upon  "  \\'eitore  Erfahrungen  iiber  operative  Behandlung  der  diffusen  eitrigen  Peri- 
tonitis "  {Beitrdge  zur  klinischen  Chirurgie,  1902),  from  which  I  see  that  v.  Beck, 
in  the  diagnosis  of  the  point  of  origin  of  peritonitis,  attaches  importance  to  the  pre- 
viously mentioned  circumscribed  hyperalgic  zones  of  the  skin ;  he  looks  upon  them 
as  a  valuable  indication.    In  regard  to  this  symptom,  I  have  as  yet  no  experience. 


PERITONITIS   WITH   REFERENCE  TO   PERITYPHLITIS  547 

pain  upon  pressure  with  only  a  small  tumor  and  mild  general  symptoms 
are  not  rarely  observed  in  empyema. 

Fever.— In  regard  to  the  fever,  I  should  like  to  state  briefly  that  in 
my  experience  high  fever,  according  to  its  duration  and  type,  enables  us 
to  arrive  at  positive  diagnostic  and  prognostic  conclusions.  But  the  ab- 
sence of  fever,  or  a  fall  in  the  temperature,  must  be  utilized  with  a 
certain  reserve.  A  glance  at  the  clinical  history  shows  that  high  fever, 
setting  in  abruptly  with  chills,  with  a  parallel  increase  in  the  pulse  rate, 
here,  as  well  as  frequently  in  pathology,  indicates  pus;  yet  it  may  occur 
without  pus,  particularly  in  the  inflammatory  relapses  of  appendicitis 
granulosa  (Eiedel)  ;  less  rarely  is  vomiting  absent  in  either  case.  High 
fever  with  a  very  rapid  small  pulse,  excruciating  pain,  and  severe  vomit- 
ing usually  points  to  perforation.  It  will  be  remembered,  too,  that  the 
symptoms  of  septic  collapse  and  the  general  abdominal  signs  of  perfora- 
tion occur  conjointly  with  immediate  diffuse  peritonitis  or  peritoneal 
sepsis;  when  the  exudate  is  limited,  severe  septic  collapse  is  absent  and 
the  abdominal  symptoms  are  slight,  or,  in  case  they  are  well  developed, 
they  decline  in  one  to  three  days,  usually  with  a  fall  in  temperature.  But 
cases  midway  between  this  latter  picture  and  that  of  acute  septic  peri- 
tonitis are  not  rare.  The  fever  course  which  indicates  rapid  limitation  is, 
therefore,  that  which  gradually  declines  for  three,  five  or  more  days  after 
the  initial  height.  The  local  signs  accompanying  this  are  usually  those  of 
concentration  upon  the  perityphlon.  A  change  at  this  time  with  rise  of 
fever  and  still  greater  distribution  of  the  process  is  serious,  but,  fortu- 
nately, infrequent.  Gradual  limitation  corresponds  to  a  sub-continuous 
range  with  diffuse  abdominal  symptoms  lasting  several  days,  the  fever 
disappearing  by  lysis  when  the  limitation  has  been  reached ;  but  even  com- 
plete circumscribed  peritonitis  sometimes  gives  rise  to  high  fever  continu- 
ing for  a  week  or  longer.  If  collapse  is  not  present  sudden  decline  of 
the  fever  almost  always  indicates  perforation  of  the  abscess  into  the  intes- 
tine, or  one  of  the  other  directions  indicated.  The  feces  and  urine  should 
be  watched ! 

A  milder  type  of  fever  usually  accompanies  slight  perforations  of  the 
appendix  or  purulent  periappendicitis  without  perforation,  but  also  appen- 
dicitis simplex  with  slight,  non-purulent  implication  of  the  serosa.  Em- 
pyema of  the  appendix  presents  a  varying  temperature,  usually  not  high 
fever,  occasionally  none  at  all ;  sometimes,  however,  chills  and  great  eleva- 
tion of  temperature  are  observed. 

In  the  later  course  a  sudden,  sharp  rise  without  symptoms  of  sepsis 
points  to  an  increase  of  the  purulent  inflammation;  that  is,  in  accordance 
with  the  conditions  present  and  the  accompanying  local  sjnnptoms,  to 
progressive  purulent  peritonitis,  to  an  extension  of  the  process  along  the 
colon,  or  to  subphrenic  abscess,  empyema,  etc. ;  another  decided  rise  with 
immediate  septic  symptoms  which  at  first  may  be  only  latent,  indicates 


548      ACUTE   PERITONITIS,   APPENDICITIS,   AND  PERITYPHLITIS 

threatening  diffuse  peritonitis.  But  even  here  there  are  also  intermediate 
forms:  For  example,  rapid  and  progressive  distribution  of  the  disease 
without  septic  collapse. 

The  long-continued,  progressive  purulent  forms  naturally  exhibit  a 
long-continued  febrile  state  with  great  variation  in  temperature,  chills,  a 
sub-continuous  course  during  renewed  encapsulation,  a  decline  with  pos- 
sible rupture,  etc. 

I  cannot  go  beyond  these  general  remarks;  it  is  easy  to  construct  me- 
diiim  courses  as  types;  Rotter  and  others  have  no  doubt  constructed  these 
by  carefully  utilizing  their  numerous  observations.  From  a  didactic  stand- 
point these  types,  which  are  exemplified  only  in  a  certain  number  of  cases, 
are  always  questionable,  because  the  reader  who  does  not  bear  in  mind 
the  multiplicity  of  exceptions  is  always  inclined  to  adhere  closer  to  the 
type  than  does  the  author  himself. 

Tumor. — The  tumor  varies  greatly  in  size,  varies  in  position  according 
to  its  mode  of  attachment  to  the  appendix  and  its  length,  varies  in  con- 
sistency according  to  the  manner  of  its  production.  Its  walls  may  be 
pcrceptil)le  or  may  be  overlapped  by  intestinal  coils,  and  in  the  latter 
case,  if  meteorism  be  present,  may  be  completely  obscured.  Palpation  as 
well  as  deep  percussion  ^  is  restricted  by  the  pain  of  the  patient,  as  well 
as  by  prudence.  Experience  has  often  revealed  to  surgeons  empyemata 
and  abscesses  which  were  at  the  point  of  rupture.  Usually,  however,  it 
suffices  for  the  diagnosis  if  we  discover  resistance  over  the  cecum,  or 
medially  or  laterally  related  to  it.  We  may  be  fully  assured  of  a  firm 
limitation  when  a  coarse  but  slightly  painful  tumor  is  found,  and  also 
when  a  large  tumor,  with  a  parallel  retardation  of  the  other  symptoms, 
daily  becomes  smaller  and  more  compact;  yet  these  findings  afford  no 
guarantee  against  secondary  perforation. 

Vomiting. — Vomiting  is  due  to  reflex  irritation  of  the  peritoneum; 
in  the  malignant  infections  which  are  rapidly  and  widely  distributed,  it 
is  often  severe  with  the  ejection  of  grass-green  masses;  in  high-graded 
intestinal  paralysis  obstruction  occurs  under  some  circumstances,  usually 
with  the  symptoms  of  collapse. 

These  forms  are  typical  of  acute  diffuse  peritonitis.  In  the  circum- 
scribed form  the  vomited  material  is  rarely  grass-green,  but  the  vomiting 
is  frequently  severe  and  distressing,  and  often  bears  a  certain  relation 
to  the  intensity  of  the  inflammation.  Vomiting  usually  accompanies  re- 
lapses of  appendicitis,  and  especially  when  they  run  their  course  without 
purulent  inflammation  of  the  serosa;  this  symptom  is  met  with,  therefore, 
in  many  cases  when  all  other  signs  of  implication  of  the  peritoneum 
are  absent. 


1  According  to  Weil,  I  understand  by  deep  percussion  that  form  in  which  the 
pleximeter  or  the  pleximeter  finger  is  pressed  deeply  into  the  belly. 


PERITONITIS  WITH   REFERENCE  TO  PERITYPHLITIS  549 

TTrine. — The  urine  varies^  but  these  variations  do  not  always  correspond 
to  the  severity  of  the  disease;  in  the  severer  cases,  particularly  those  with 
high  fever,  it  often  contains  albumin  and  indican;  in  children  these,  as 
well  as  aceto-acetic  acid,  are  found  much  more  frequently  and  often  in 
decided  quantities.  Dysuric  symptoms  depend  upon  implication  of  the 
lower  portion  of  the  abdominal  cavity;  they  may  be  temporarily  observed 
when  no  other  symptom  points  to  the  areas  surrounding  the  bladder. 


DIFFERENTIAL  DIAGNOSIS 

1.  The  Differentiation  of  Perityphlitis  from  Other  Conditions. — In  case 
we  find  a  distinct  tumor  between  the  umbilicus  and  the  anterior  superior 
spine  of  the  ilium  the  question  of  a  fecal  tumor  comes  into  consideration. 
It  must  be  remarked  that  this  may  be  an  accompanying  symptom  of  peri- 
typhlitis, and,  if  accompanied  by  severe  pain  and  vomiting,  must  always 
be  borne  in  mind.  A  mere  accumulation  of  feces  also  occurs  here,  but  is 
much  rarer  in  ordinary  constipation  than  in  local  conditions  which  cause 
stasis,  stenosis  of  the  colon  low  down  (tumor  of  the  left  flexure,  chole- 
cystitis with  adhesion  to  the  transverse  colon),  or  stenosis  at'  the  cecum 
itself  from  old  adhesions  or  thickening  of  the  serosa,  i.  e.,  residues  of  a 
former  perityphlitis;  such  a  fecal  tumor  is  moderately  sensitive,  movable, 
circular,  usually  compressible,  and  disappears  after  a  bowel  evacuation  (as 
a  matter  of  caution  this  had  better  be  produced  by  enemata). 

Neoplasms  of  the  cecum  or  colon  may,  under  some  circumstances,  also 
cause  tumors  in  this  region ;  these  are  also  movable  at  first,  are  very  coarse, 
non-sensitive  or  slightly  painful.  Here  attacks  resembling  perityphlitis 
are  very  rare;  paroxysmal  marked  stasis  is  produced  much  more  readily; 
during  the  attack  the  diagnosis  may  occasionally  be  difficult  on  account 
of  insufficient  preceding  observation. 

The  latter  is  also  true  of  acute  intestinal  occlusion  in  this  region, 
particularly  that  due  to  strangulation;  invagination  of  the  ileum  into  the 
cecum  causes  at  first  a  characteristic  tumor,  later  hemorrhagic  dejecta; 
the  condition  cannot  be  readily  mistaken. 

Tuberculosis  and  actinomycosis  of  the  cecum  and  appendix,  particu- 
larly in  the  earlier  stages,  may  lead  to  extreme  differentio-diagnostic 
perplexity. 

Besides  appendicitis,  other  pathologic  conditions  produce  painful  at- 
tacks in  the  vicinity  of  McBurney's  point,  pain  upon  pressure,  vomiting 
and  fever,  and  these  are:  Cholelithiasis  or  cholecystitis,  right-sided  renal 
colic,  particularly  when  combined  vfWh  a  dislocated  kidney,  inflammatory 
disease  and  tumors  of  the  ovaries  and  of  the  tubes,  gravitation  abscess 
from  the  psoas.  Here  a  careful  history  is  of  great  value;  not  rarely  the 
diagnosis  can  be  made  at  once ;  a  large  liver  and  the  respiratory  movability 
of  a  tumor  that  may  be  present  favors  pericholecystitis;  we  must  be 


550       ACUTE   PERITONITIS,   APPENDICITIS,  AND  PERITYPHLmS 


cautious,  however,  in  the  consideration  of  moderate  jaundice,  since  it  also 
occurs  in  perityphlitis;  gall-stones  are  rarely  found  in  the  feces,  but,  if 
present,  they  aid  in  the  decision.  This  differential  diagnosis  is  sometimes 
difficult  or  even  impossible.  If  the  kidneys  are  implicated,  it  will  be 
evident  from  the  well  known  manifestations  of  a  dislocated  kidney  as  well 
as  the  examination  of  the  urine  (nephrolithiasis).  The  question  of  disease 
of  the  female  genitalia  will  usually  be  decided  by  a  vaginal  examination 
which  should  never  be  omitted  in  any  case;  naturally  this  is  not  always 
decisive,  and  especially  when  there  is  implication  of  the  serosa  of  the 
pelvis  in  perityphlitis,  or  in  case  of  simultaneous  disease  of  the  adnexa  and 
perityphlitis.  When  considering  gravitation  abscess,  the  vertebral  column 
and  the  sub-inguinal  region  should  be  carefully  examined;  the  history 
is  of  value  in  this  instance  as  well  as  in  all  others. 

The  most  difficult  cases  are  those  in  which  no  resistance  is  present 
and  the  pain  can  scarcely  be  localized,  or  where  pain  and  resistance  are 
present  in  a  paradoxical  area,  as  in  the  case  of  a  very  long  appendix 
adherent  at  its  apex;  here  the  focus  may  be  under  the  liver,  in  the  pelvis, 
oven  upon  the  left  side  of  the  abdomen,  and  the  diagnosis'  of  appendicitis 
may  cause-  the  greatest  perplexity.  In  all  such  instances,  if  the  accom- 
panying symptoms  point  to  appendicitis,  this  affection  should  be  first  con- 
sidered as  it  is  relatively  the  most  frequent.  In  late  childhood  it  is  of 
especial  importance,  as  disease  of  the  biliary  passages  and  gastric  ulcers 
seldom  arise  in  these  subjects ;  they  occur  at  the  end  of  the  second  decade 
of  life,  but  do  not  often  occasion  symptoms  that  resemble  appendicitis. 
From  the  thirtieth  year  upward  the  frequency  of  appendicitis  diminishes 
(i.  e.,  of  the  first  attack!)  and  after  the  fortieth  year  the  disease  is  rare. 
Hernia  and  internal  incarceration  must  invariably  be  thought  of:  History 
and  local  examination  including  that  per  rectum! 

2.  The  diagnosis  of  the  form  of  perityphlitis  is  the  most  difficult 
part  of  this  entire  subject. 

I  must  first  emphasize  that  appendicitis  in  itself,  particularly  that 
form  with  but  slight  implication  of  the  serosa  and,  at  all  events,  without 
purulent  implication,  is  very  difficult  to  differentiate  from  periappendicitis. 
The  affection  begins  with  mild  fever  of  brief  duration,  sometimes,  however, 
with  a  decided  rise  in  temperature  and  ileo-cecal  pain;  nausea  and  vomit- 
ing invariably  point  to  implication,  or  at  least  to  congestion,  of  the 
serosa;  constipation  may  also  be  present.  Local  examination  reveals  pain 
upon  pressure  and  in  some  of  the  cases  a  tumor,  corresponding  to  the 
swollen  appendix,  globular  in  shape  and  often  distinctly  movable,  sharply 
circumscribed,  or  apparently  embedded  in  a  firm  mass — serous  exudation 
in  the  serosa,  in  which  case  implication  of  the  peritoneum  may  be  assumed 
with  certainty.  This  condition  has  long  been  recognized  but  was  more 
accurately  studied  in  the  operations  which  Riedel  performed  early  in  his 
cases,  and  he  explains  it  as  an  inflammatory,  phlegmonous,  or  erysipela- 


PERITONITIS   WITH   REFERENCE  TO  PERITYPHLITIS  551 

tous  relapse  of  chronic  appendicitis  granulosa  hemorrhagica.  It  is  often 
the  precursor  of  well  developed  attacks  of  perityphlitis.  The  diagnosis 
may  be  made  with  great  probability  when,  besides  the  symptoms  already 
enumerated,  no  sign  of  severe  general  implication,  no  special  meteorism, 
no  symptoms  attributable  to  the  lower  portion  of  the  abdominal  cavity 
are  present,  and  no  large  tumor  has  formed.  It  is  well  constantly  to 
bear  in  mind  that  a  perforative  peritonitis  may  set  in  insidiously,  and  for 
this  reason  the  patient  must  be  carefully  watched. 

From  what  has  been  stated  the  difficulty  of  the  differential  diagnosis 
of  the  forms  of  perityphlitis  may  be  imagined.  Clear  clinical  diagnoses 
which  include  the  anatomical  condition  of  the  appendix,  the  cecum,  the 
peritoneum,  etc.,  and  besides  convey  an  idea  as  to  what  may  develop,  can 
only  be  made  in  exceptional  cases.  For  the  present  we  must  be  content 
with  a  diagnosis  which  is  made  principally  from  the  practical  standpoint 
of  prognosis  and  therapy;  and  here  the  burning  question  always  is:  Is 
the  process  localized,  and  will  it  remain  so? 

If  no  pus  is  present  the  attack  as  such  may  be  looked  upon  as  mild 
— with  rare  exceptions  which  shall  at  once  be  mentioned.  I  believe  it 
likely  that  in  the,  fortunately,  very  rare  cases  in  which  a  severe,  diffuse, 
septic  perforative  peritonitis  (with  fecal  stone  always  present)  sets  in 
with  a  stage  of  several  days  of  mild  fever,  pain,  and  moderate  vomiting — 
in  these  cases  in  the  "  prodromal  stage  " — nothing  more  is  present  than 
a  simple  appendicitis  preceding  gangrene.  These  are  exceptional  cases 
which  we  are  unable  to  recognize  by  any  method  of  our  art.  In  general 
the  law  holds  good:  If  there  is  no  pus  the  case  is  mild,  if  pus  is  present 
it  is  serious,  and  when  the  pus  is  putrid,  situated  around  or  in  the 
appendix,  the  condition  is  extremely  serious,  i.  e.,  immediately  dangerous 
to  life;  in  the  latter  case  perforation  almost  invariably  takes  place,  and  is 
usually  due  to  fecal  calculus;  rarely  does  a  putrid  empyema  form. 

The  question,  therefore,  arises:  Can  we  diagnosticate  the  presence  of 
pus,  and  can  we  recognize  it  as  putrid? 

Not  long  ago  the  answer  to  this  first  question  appeared  to  be  greatly 
simplified  by  the  assumption  that  every  perityphlitic  exudate  contained  a 
purulent  nucleus  (Sahli) ;  it  appeared  simplified — yet,  from  the  practical 
standpoint  of  prognosis  and  from  the  treatment  which  was  to  be  under- 
taken or  rejected  it  nevertheless  was  not  so — because  the  presence  of  pus 
is  of  very  varying  importance  (compare  page  544).  But  we  are  not 
always  dealing  with  pus:  We  learn  from  the  early  operations,  above  all, 
those  of  Eiedel,  that  there  may  be  a  serous,  or  sero-fibrinous,  periappendi- 
citis, and  a  recently  inflamed  appendicitis  surrounding  this. 

Therefore,  in  an  acute  attack  of  appendicular  disease,  we  are  con- 
fronted by  the  question:  Is  pus  present  or  not? 

A  fluctuating  tumor  appearing  acutely  in  this  region  always  indicates 
pus;  a  small  tumor  will  by  its  resistance  at  least  permit  us  to  assume 

JOLLEuE   OF    :■-  1  L 


552      ACUTE   PERITONITIS,   APPENDICITIS,   AND  PERITYPHLITIS 

its  fluid  contents,  although  exploratory  puncture  is  very  rarely  permissible; 
if  any  fluid  be  present,  it  is  pus.  But  in  the  majority  of  cases  we  find 
firm  tumors  or  tumors  with  more  or  less  indistinct  resistance.  In  positive 
tumors  Avith  firm  walls  an  exploratory  puncture  may  be  made;  but  it  does 
not  in  all  cases  show  pus;  this  is  only  the  case  when  the  point  penetrates 
to  the  purulent  nucleus.  In  all  cases  of  resistance  and  when  positive 
walls  are  distinctly  perceptible  this  operation  should  in  my  opinion  not 
be  undertaken,  as  the  result  is  usually  negative  and  it  may  disseminate 
the  pus  and  feces;  I  once  saw  a  hole  made  with  a  fine  Pravaz  syringe 
in  tlie  free  wall  of  the  intestine,  which  soon  became  gangrenous,  as  was 
determined  by  an  autopsy  shortly  afterward  conducted. 

As  is  well  known,  the  diagnosis  of  local  suppuration  is  to-day  based 
upon  the  presence  of  leukocytosis.  Concerning  this  I  possess  no  personal 
experience,  and  no  conclusive  opinion  has  been  reached  by  other  authors. 

The  result  of  this  is  that  it  is  frequently  necessary  to  consider  the 
other  symptoms  of  pus.  I  have  previously  mentioned  that  pus  may  be 
suspected  in  perityphlitis  when  fever,  either  continuous  or  remittent,  lasts 
for  a  number  of  days,  three  to  five  or  longer;  chill  at  the  onset  without 
prolonged  fever  is  an  uncertain  symptom;  it  may  be  produced,  like  a 
fever  of  brief  duration,  by  a  non-purulent  appendicitis  and  by  periappen- 
dicitis. Neither  are  violent  vomiting  and  severe  pain  positive  symptoms 
of  pus.  Empyema  of  the  appendix  may  be  diagnosticated  if,  with  chills 
and  high  fever  of  long  duration,  a  very  circumscribed,  round,  excessively 
painful  tumor  appears  in  the  right  lower  abdominal  region. 

Finally,  pus  infection,  and  at  that  the  most  serious  form,  the  putrid, 
is  present  when  the  so-called  symptoms  of  sepsis  or  collapse  become 
noticeable. 

Occurrences  of  this  kind  are  rare;  in  the  majority  of  cases  the  fever 
is  less  intense;  nevertheless,  pus  may  be  present. 

With  a  solid  tumor,  and  even  without  a  recognizable  tumor,  pus  may 
form  in  the  appendix  or  around  it,  and  may  even  be  putrid,  yet  the 
temperature  remain  normal,  and  pain  not  be  excruciating.  These  latter 
cases  naturally  are  rare  exceptions — this  is  the  only  consolation  they 
afford. 

The  absence  of  symptoms  of  pus  does  not  therefore  exclude  the  pres- 
ence of  pus;  but  when  they  are  absent,  when  the  picture  of  appendicitis 
simplex^  as  sketched  above,  and  with  or  without  periappendicular  symp- 
toms, is  present,  it  may  be  excluded  with  a  great  degree  of  likelihood; 
notwitlistanding  this,  we  must  be  on  our  guard. 

Pus  in  the  appendix  is,  moreover,  a  very  varying  condition.  There 
is  a  benign  pus,  particularly  among  the  cases  without  perforation,  and 
with  clearly  defined  limits ;  i.  e.,  it  at  once  causes  a  very  hard,  moderately 
large  tumor  and,  after  a  little  time,  probably  by  rupture  into  the  intestine, 
disappears;  but  among  the  non-putrid  suppurations  there- is  also  a  very 


PERITONITIS  WITH  REFERENCE  TO  PERITYPHLITIS  553 

malignant  form,  usually  seen  in  perforation,  but  also,  although  very  rarely, 
without  this.  Here  also  the  rule  is  operative :  The  malignancy,  i.  e.,  the 
tendency  to  rapid  progression,  is  often  manifest  from  the  typical  symp- 
toms, but  it  cannot  be  excluded  when  milder  symptoms  only  are  present. 
That  the  relative  position  of  the  abscess  and  cecum  is  of  importance 
has  already  been  stated. 

How  may  we  recognize  putrid  infection  which,  in  the  majority  of  cases, 
indicates  fecal  calculus  perforation?  The  symptoms  of  septic  collapse, 
even  when  only  indicated,  must  always  arouse  this  suspicion;  in  a  success- 
ful exploratory  puncture  a  positive  diagnosis  can  at  once  be  made  by  the 
sense  of  smell.  With  chill,  continued  high  fever,  very  severe  pain,  and 
especially  with  pelvic  or  other  severe  local  symptoms  (marked  meteorism, 
singultus),  with  albuminuria  and  very  marked  indicanuria,  this  must 
always  be  thought  of,  particularly,  however,  when  these  decided  symp- 
toms are  contrasted  with  the  absence  of  tumor;  with  mild  symptoms  it 
cannot  be  positively  excluded,  yet  it  is  rare. 

Comprehensively  the  following  may  be  stated: 

1.  As  a  rule,  vomiting,  ileo-cecal  pain,  a  moderate  fever  not  lasting 
longer  than  three  days,  and  very  circumscribed  or  indistinct  resistance  are 
in  favor  of  appendicitis  simplex  (inflammatory  relapse  of  appendicitis 
granulosa  hemorrhagica,  Riedel),  with  non-purulent  implication  of  the 
serosa.  A  moderately  severe  chill  accompanies  this  condition;  very  severe 
pain  upon  palpation  does  not  disprove  it. 

2.  As  a  rule,  the  same  symptoms  with  protracted  fever  reaching  to 
102.2°  F.,  and  with  a  larger,  coarse  tumor  indicate  purulent,  non-putrid, 
circumscribed  periappendicitis;  moderate  meteorism  occurs  at  the  onset, 
but  then  disappears. 

3.  As  a  rule,  an  extensive  tumor  between  the  umbilicus  and  the  ante- 
rior superior  spine  of  the  ilium  with  severe  symptoms  (chill,  frequent 
vomiting,  moderate  meteorism),  but  from  the  third  to  the  fifth  day,  and 
synchronous  with  the  fall  in  temperature  and  cessation  of  the  vomiting, 
a  certain  but  limited  decrease  in  size  favors  perforation  of  the  appendix 
but  with  a  tendency  to  solid  encapsulation  of  the  abscess  which  is  for 
the  most  part  putrid. 

Jf.  A  sudden  onset  with  fulminant  symptoms,  extensive  painful  meteor- 
ism, pelvic  disturbances,  and  the  absence  of  distinct  resistance,  awakens 
the  fear  of  an  insufficient  limitation  of  a  perforative  peritonitis.  Signs 
of  so-called  septic  collapse,  even  the  slightest,  are,  however,  the  positive 
evidence  of  this  condition. 

5.  Retrocecal  and  retrocolic  symptoms  (movements  and  position  of  the 
leg  are  to  be  observed,  pain  in  the  posterior  lumbar  region)  always  favor 
pus,  which  need  not,  however,  be  putrid. 

6.  Chills,  high  fever  (later  declining),  excessive  vomiting,  and  very- 
severe  pain  with  a  circumscribed  round  tumor  from  the  onset  favor  em- 


554       ACUTE   PERITONITIS,   APPENDICITIS,   AND  PERITYPHLITIS 

pyema.    In  the  majority  of  cases  this  is  not  putrid;  for  this  reason  encap- 
sulation of  the  empyema  is  usually  firm. 

7.  As  a  rule,  when  several  relapses  occur,  perforation  hy  fecal  stone 
will  have  been  most  severe  in  the  first  attack;  if,  therefore,  an  attach 
suggestive  of  perforation  have  already  occurred,  the  relapses  are  usually 
milder ;  inversely,  if  attacks  of  non-perforative  periappendicitis  begin  with 
an  appendicitis  granulosa  and  stenosis,  usu/illy  mild  at  first,  and  gradually 
becoming  more  severe,  gangrene  and  perforation  eventually  occur;  the 
preceding  attacks  are  then  u^uully  a  certain  guaranty  of  preceding  adhesions. 

8.  Exceptions  to  all  of  these  rules  occur,  and  in  all  directions.  The 
more  serious  are  those  in  which  malignant  affections  set  in  with  mild 
symptoms.  The  gravest  condition  is  that  of  ichorous  empyema  and 
ichorous  perforating  abscesses  with  mild  initial  symptoms  and  sudden 
rupture  into  the  free  abdominal  cavity.  Neither  occurrence  is  very 
frequent.  Much  more  often  is  a  tendency  to  secondary  distribution 
gradually  revealed  by  more  severe  and  more  distributed  pain,  higher  fever, 
and  more  rapid  pulse,  vomiting  and  mild  meteorism  which  will  be  appar- 
ent to  the  careful  observer.  Usually  with  secondary  distribution  we  are 
dealing  ivith  mild  or  even  moderately  severe  cases  of  progressive  purulent 
peritonitis;  almost  invariably  these  are  due  to  perforation  from  a  fecal 
calculus.  Abscesses  at  the  medial  side  of  the  cecum  are  most  prone  to 
show  this  tendency. 


GENERAL  REMARKS  REGARDING  THE  COURSE  OF  PERITYPHLITIS 

According  to  various  comprehensive  statistics,  particularly  Sahli's  col- 
lective investigations,  it  may  be  stated  that  acute  perityphlitis  without 
operation  is  fatal  in  from  4  to  9  per  cent,  of  all  cases,  and  that  relapses 
occur  in  about  20  per  cent,  of  non-operative  cases. 

Relapses. — These  relapses  must  occupy  our  attention  for  a  moment. 
They  occur  in  perforative,  as  well  as  in  non-perforative  perityphlitis,  but 
even  according  to  previous  statistics  they  are  much  more  rare  in  the 
former;  when  we  consider  the  milder  "relapses"  of  "appendicitis  granu- 
losa," the  greater  proportion  of  relapses  in  the  relatively  benign  forms  will 
become  apparent. 

'I'he  first  relapse  generally  occurs  in  the  first,  less  often  in  the  second, 
year,  and  much  more  rarely  thereafter. 

In  the  perforative  forms,  the  first  attack  is  usually  the  most  severe, 
the  relapses  are  benign,  and  occasionally  show  a  gradually  decreasing 
severity.  The  earlier,  however,  the  first  relapse  occurs  after  the  first 
attack,  the  more  certainly  must  we  reckon  upon  its  malignancy;  one  that 
occurs  after  a  few  weeks  is  not  infrequently  more  serious  and  occasionally 
even  fatal.  These  relapses  may  be  caused  by  various  conditions :  By  a 
propagation  to  the  abdominal  cavity  of  the  pus  which  has  not  yet  dis- 


PERITONITIS  WITH  REFERENCE  TO  PERITYPHLITIS  555 

appeared  (delayed  progressive  purulent  form,  malignant),  to  the  retro- 
colic  tissue,  etc.;  by  the  sudden  occlusion  of  a  perforation  into  the  intes- 
tine before  the  pus  has  fully  discharged;  by  induration  and  adhesions 
which  hinder  the  passage  of  feces.  Accordingly  the  character  and  the 
prognosis  of  the  attack  vary  greatly. 

Chronic  appendicitis  without  fecal  calculus,  and  with  or  without  steno- 
sis, frequently  causes  "  relapses  "  of  gradually  increasing  severity  in  which 
implication  of  the  peritoneum  is  at  first  doubtful,  but  may  be  later  more 
distinct;  finally,  pus  forms  and  meets  with  adhesions  previously  for  a 
long  time  present.  But  in  these  ceises  without  fecal  calculus,  even  when 
the  first  (distinct)  attack  produces  periappendicular  pus  (usually  without 
gangrene,  therefore  without  perforation),  the  course,  according  to  the 
experience  of  Eiedel,  is  generally  favorable:  Absorption  or  rupture — in- 
duration for  a  varying  time,  occasionally  only  amounting  to  days — stenosis 
or,  what  is  most  favorable,  complete  obliteration  of  the  appendix  and 
entire  recovery.  In  rare  cases,  naturally,  the  abscess  persists,  possibly  with 
secondary  complications  (descent,  slow  rupture  into  an  inconvenient  point, 
for  example,  the  bladder,  venous  thrombosis,  etc.) — or  without  this,  with 
chronic  invalidism  associated  with  pain,  occasional  fever,  and  dread  of 
eating.  Or,  indistinct  febrile  attacks  come  on  even  when  the  abscess  has 
disappeared;  some  time  ago,  in  one  of  my  cases  of  this  kind,  a  torpid 
flat  ulcer  was  found  in  the  thickened  appendix  which  was  everywhere 
adherent.  Not  infrequently  attacks  of  gradually  decreasing  severity  are 
observed  for  years;  here  pus  is  no  longer  present,  the  adhesions  and  in- 
durations gradually  disappear;  the  nature  of  the  difficulties  produced  by 
these  conditions  we  shall  soon  refer  to. 

Long-continued  abscesses  usually  give  the  patient  no  rest;  however, 
long  periods  of  latency  (over  a  year)  occur,  exceptionally  even  with  putrid 
abscesses,  and  under  some  circumstances  with  sudden,  severe,  peritoneal 
exacerbations. 

I  recently  observed  an  instructive  case  of  this  kind. 

A  robust  young  man,  22  years  of  age,  had  two  years  previously  a  moderately 
severe  febrile  inflammation  of  the  cecum  which  "  healed  completely " ;  since  that 
time  he  has  now  and  then  suffered  from  indistinct  drawing  pains  in  the  right 
lower  abdominal  region;  lately  he  had  a  mild  relapse,  with  moderate  fever  lasting 
a  day,  violent  pain,  constipation,  and  nausea.  He  was  a  strong,  well  nourished  man. 
A  tumor  about  twice  the  size  of  a  plum,  compact,  round,  and  slightly  movable,  was 
found  below  McBurney's  point.  Slight  pain  upon  deep  pressure  aroused  a  suspicion 
of  pus;  the  conditions  were  otherwise  negative.  Operation:  Old  non-putrid  abscess 
around  a  perforated,  otherwise  markedly  thickened,  appendix;  fecal  calculus. 

If  abscesses,  after  a  prolonged  duration,  finally  rupture  into  any  organ, 
it  may  happen  that,  in  the  meantime,  rigid  cavities  will  have  formed 
which,  even  though  communication  is  open,  do  not  heal;  therefore  the 
result  is  invalidism.     But  even  old,  closed,  rigid  wall  cavities  may  form 


556      ACUTE   PERITONITIS,   APPENDICITIS,   AND  PERITYPHLITIS 


Avhicli  mechanically  act  as  tumors;  my  last  observation  of  this  kind  showed 
in  a  patient  aged  50  a  rigid  tumor,  round  as  a  ball  and  the  size  of  a 
child's  head,  situated  between  the  bladder  and  the  rectum,  and  causing 
great  difficulty  in  defecation. 

If  pus  has  disappeared,  leaving  behind  it  permanent  adhesions  and 
induration,  usually  mild  "  relapses  "  occur — disturbances  which  come  and 
go  and  scarcely  deserve  the  name  of  relapse.  In  part  these  may  consist 
of  difficulty  in  the  passage  of  feces,  and,  depending  upon  the  seat  of  the 
induration,  there  may  be  a  cecal  fecal  stasis  which  may  cause  secondary 
typhlitis  stercoralis.  This  was  probably  the  case  in  the  following  obser- 
vation : 

A  man,  aged  64,  who,  twenty  years  previously,  had  suflFered  from  severe  inflam- 
mation of  the  cecum,  was  subject  from  that  time  on,  at  first  every  year  and  later, 
up  to  the  time  of  death,  every  few  years,  to  relapses,  the  severity  of  which  varied 
but  generally  lessened,  and  constantly  suffered  from  marked  constipation.  Death 
was  due  to  apoplexy.  Autopsy:  Appendix  slightly  adherent  and  obliterated,  trans- 
versely over  the  cecum  in  an  oblique  direction  a  narrow,  constricting  thickening  of 
the  serosa    (compare  Fig.  20). 

But  adhesions  of  the  cecum  without  constriction,  peritoneal  plaques, 
and   adhesions  of  the   appendix  by  torsion   are  also   sufficient  to   cause 

occasional  pain  during  peristalsis.  That  the 
latter  condition  may  give  rise  to  the  retention 
of  secretion  and  further  complications  (see 
above)  by  causing  a  stenosis  of  the  appendix  is 
elf-evident. 

It  has  been  previously  explained,  and  is  re- 
iterated like  a  red-letter  line  throughout  the 
pathology  of  perityphlitis,  that  two  conditions 
are  responsible  for  the  majority  of  cases  of 
perityphlitis:  Fecal  calculus  and  chronic  ex- 
acerbations of  appendicitis.  Can  we  diagnosti- 
cate these  before  they  produce  perityphlitis? 
The  answer  to  this  question  is  scarcely  satisfac- 
tory. 

Fecal  calculus  before  it  produces  inflam- 
mation is  completely  masked ;  of  premonitory  relapses  of  pure  appendicitis 
which  precede  gangrene,  and  of  periappendicitis,  we  know  but  little.  Nev- 
ertheless, in  perityphlitis  we  often  have  a  history  of  slight  drawing  and 
tearing  pains  in  the  ileo-cecal  region. 

Chronic  appendicitis  and  stenoses,  on  the  other  hand,  readily  produce 
tlio  ])ro\  iously  mentioned  "relapses,"  beginning  mildly  and  becoming  more 
severe.  In  tlie  future  these  will  be  more  closely  observed.  For  the  diag- 
nosis of  perityphlitis  it  is  highly  desirable  that  we  should  in  time  obtain 
furtlier  knowledge  of  these  prior  conditions. 


Fig.  20. 


PERITONITIS  WITH   REFERENCE  TO  PERITYPHLITIS  557 

Peritonitis  originating  from  neighboring  organs  in  the  peritoneum,  or 
from  chronic  purulent  circumscribed  peritonitis,  belongs  to  the  realm 
of  diseases  of  these  organs.  I  shall,  therefore,  permit  myself  only  a  few 
general  remarks  in  regard  to  them.  The  points  of  origin  of  circum- 
scribed peritonitis  are  just  as  numerous  as,  or  even  more  so  than,  in  acute 
diffuse  inflammation  of  the  peritoneum.  All  portions  of  the  gastrointes- 
tinal canal,  the  liver,  and  particularly  the  biliary  passages,  the  pancreas, 
the  lymph-glands,  the  female  genitalia,  the  kidneys  and  the  bladder,  and 
finally,  the  actual  surroundings  of  the  abdominal  cavity  (the  diaphragm 
from  the  pleura  or  from  the  pericardium,  the  ribs,  the  vertebral  column 
and  the  pelvis)  must  be  considered. 

These  conditions  are  partly  related  to  specific  (typhoid,  dysenteric), 
partly  to  non-specific  ulcerative  processes,  partly  to  infections  of  normal 
secretions  (bile,  urine),  partly  to  infection  of  the  tissues  of  the  liver,  of 
the  genitalia,  etc.  Occasionally  chronic  processes,  as  echinococcus,  tuber- 
culosis, carcinoma  and  other  neoplasms,  are  behind  the  acute  process,  and 
only  manifest  themselves  on  rupture  into  a  hollow  organ  or  by  preceding 
suppuration. 

Whether  in  these  cases  an  acute,  diffuse,  and  extensive  or  a  limited 
peritonitis  occurs,  depends  upon  the  nature  of  the  inflammatory  agent, 
also  partly  and  chiefly  upon  the  rapidity  with  which  it  reaches  the  peri- 
toneum; the  location  of  the  point  of  rupture  and  whether  or  not  this  is 
favorable  for  encapsulation  also  plays  a  role. 

Gastric  ulcer  sometimes  produces  perigastric  abscesses  when  it  slowly 
approaches  the  serosa  and  forms  adhesions;  but,  even  with  a  rapid  rup- 
ture, if  it  is  situated  in  the  smaller  curvature  or  upon  the  posterior  wall 
of  the  stomach,  circumscribed  peritonitis  below  the  diaphragm  and  sub- 
phrenic abscess  may  develop,  because  here  the  conditions  for  limitation 
are  favorable. 

Infection  of  the  biliary  passages,  as  a  rule,  at  first  causes  mild  and 
then  severe  relapses,  similar  to  the  appendicular  ones,  and  thus  tough 
adhesions  are  produced;  in  consequence  of  this  perforating  or  non-perfo- 
rating pericholecystitic  suppuration  is  for  the  most  part  localized. 

A  perforating  typhoid  ulcer  only  exceptionally  causes  circumscribed, 
but  usually  diffuse,  peritonitis;  on  the  other  hand,  the  dysenteric  ulcer 
which  more  slowly  invades  the  deep  tissues  most  often  produces  local 
inflammation. 

Puerperal  suppurative  processes  of  the  uterus  and  of  the  adnexa  are 
usually  highly  virulent  and  progress  rapidly;  here  we  have,  as  a  rule, 
the  conditions  for  diffuse  peritonitis.  Most  manifold  local  inflammations 
may  arise  according  to  the  virulence  of  the  poison  and  the  rapidity  with 
which  it  enters  the  abdominal  cavity. 

There  can  be  but  few  points  of  preference  for  circumscribed  purulent 
peritonitis  since  it  has  been  found  in  all  regions  of  the  abdominal  cavity. 


558      ACUTE  PERITONITIS,  APPENDICITIS,  AND  PERiTYPHLITIS 

It  is  frequently  noted  in  the  pelvis,  sometimes  originating  from  the 
immediate  surroundings,  and  sometimes  descending  from  the  appendix 
or  from  the  colon.  Another  point  of  preference  is  the  vault  of  the  dia- 
phragm :  Here  the  intraperitoneal  subphrenic  abscess  is  usually  situated, 
particularly  if  it  contains  gas;  pyopneumothorax  subphrenicus  is  usually 
to  the  left  of  the  suspensory  ligament  of  the  liver,  but  also  occasionally 
to  the  right  of  it,  and  rarely  bilaterally.  All  of  the  organs  bordering  on 
the  subphrenic  region  are  implicated  in  the  development  of  these  abscesses : 
The  stomach,  the  liver  (that  is,  the  biliary  passages),  the  duodenum,  the 
pancreas,  the  colon,  the  kidneys,  the  spleen,  the  ribs  and  vertebral  column, 
the  diaphragm  from  the  pleura,  the  lungs  and  pericardium.  The  majority 
of  abscesses  originating  from  the  biliary  passages  are  situated  below  the 
liver;  frequently  they  extend  almost  to  the  ileo-cecal  region,  and  may 
cause  great  difficulty  in  the  diagnosis;  if,  to  aid  us  in  our  decision,  an 
exploratory  puncture  be  risked,  pus  admixed  with  bile,  or  frequently  only 
pus,  is  found.  Abscesses  of  the  colon,  often  of  obscure  origin,  are  occa- 
sionally situated  here,  or  they  may  be  opposite  the  ascending  colon  and  at 
the  flexure;  they  are  usually  circumscribed  and  prone  to  be  chronic. 

The  same  is  true  of  these  abscesses  as  of  the  periappendicular  form: 
They  may  show  firm  encapsulation  and,  particularly  when  small,  may 
remain  latent  for  a  long  time ;  according  to  their  position  they  may  rupture 
in  any  direction,  through  the  abdominal  wall  into  a  hollow  organ,  espe- 
cially into  the  intestine  or  into  the  bladder,  or  through  the  diaphragm 
and  ultimately  into  the  lung;  they  may  by  erosion  force  their  way  into 
a  solid  organ,  as,  for  example,  perigastric  abscesses  and  abscesses  of  the 
biliary  passages  into  the  liver ;  by  rupturing  into  the  free  abdominal  cavity 
they  may  immediately  produce  a  diffuse  peritonitis  or  develop  a  pro- 
gressive purulent  inflammation.  Finally,  they  may  readily  lead  to  pye- 
iiiia,  particularly  by  septic  venous  thrombosis.  If  the  abscess  is  small  and 
insignificant,  situated  deep  and  not  susceptible  to  examination,  a  crypto- 
genetic  septicopyemia  may  develop  clinically. 

To  enter  into  further  details  is  at  this  point  impossible. 


PROPHYLAXIS  AND  TREATMENT 

Prophylaxis. — As  to  the  prophylaxis  of  acute  diffuse  peritonitis,  mod- 
ern asepsis  and  antisepsis  in  the  hands  of  the  surgeon  and  gynecologist 
are  powerful  agents  to  prevent  the  development  of  this  affection  after 
operations  upon  the  abdomen,  in  the  treatment  of  abdominal  injuries, 
and  during  labor.  The  situation  is  more  complicated  when  we  consider 
the  numerous  pathological  conditions  which  expose  the  peritoneum  to  in- 
flammation from  its  surroundings.  Here  it  would  be  well  if  we  could 
decide  in  the  individual  case  whether  the  process  has  been  so  extensive 
as  to  produce  inflammatory  conditions  or  those  that  lead  to  danger  of 


PERITONITIS  WITH  REFERExNCE  TO  PERITYPHLITIS  559 

rupture,  and  also  whether  an  invasion  into  the  ahdominal  cavity  is  likely. 
But,  unfortunately,  this  is  seldom  possible. 

In  round  ulcer  of  the  stomach  and  of  the  duodenum  and  in  enteric 
ulcer  this  is  never  the  case,  and  even  in  the  pancreas  we  are  far  from 
accuracy  in  clinical  judgment.  In  gall-stone  colic  with  fever,  or  even 
with  chills,  serious  consequences  may  more  readily  be  prevented;  appendi- 
citis and  perityphlitis  have  just  been  accurately  described.  In  incarcerated 
hernia,  in  strangulation  and  in  invagination,  surgical  treatment  which 
prevents  peritonitis  plays  an  important  role.  But  upon  this  subject,  and 
also  the  diseases  of  the  sexual  organs,  we  shall  not  now  enter. 

In  not  a  few  of  these  conditions  the  aid  of  the  surgeon  is  needed 
before  there  is  any  thought  of  a  diffuse  peritoneal  complication.  But  even 
where  this  has  been  previously  impossible,  the  family  physician  or  the 
internal  clinician  should  consider  himself  honored  by  inviting  the  surgeon 
in  consultation,  should  he  be  at  hand  and  the  patient  permit  it,  and  in 
obtaining  his  opinion  so.  soon  as  a  diffuse  peritonitis  seems  threatening, 
or  even  before  it  has  developed.    Thereafter  the  case  belongs  to  the  surgeon. 

If  the  physician,  however,  finds  an  acute  diffuse  peritonitis  already 
developed,  the  question  of  treatment  is  directed  primarily  to  the  point  of 
origin;  whether,  and  how,  it  may  be  attacked  is  the  privilege  of  the 
surgeon  to  decide. 

In  many  cases,  from  a  theoretical  standpoint,  we  must  strictly  dis- 
criminate between  bacterial  and  chemical  peritonitis.  I  have  previously 
stated  of  the  latter  form  of  peritonitis  that  it  stands  or  falls  with  the 
bacterial  focus  of  origin;  therefore  this  should  be  immediately  removed, 
when  the  rapid  disappearance  of  the  diffuse  symptoms  may  be  expected. 
Considerations  of  this  kind  will,  under  some  circumstances,  influence  the 
surgeon  as  to  his  manner  of  procedure.  But  it  is  neither  my  object  nor 
my  function  to  enter  into  more  minute  details  in  regard  to  this.  Prac- 
tically, it  is  evident  from  the  foregoing  that  the  clinical  differentiation 
between  malignant  bacterial  and  benign  chemical  peritonitis  (peritoneal 
irritation)  frequently  occasions  the  greatest  perplexity. 

Operative  Measures. — Therefore,  according  to  our  present  standpoint 
of  therapeutic  knowledge,  surgical  relief  is  to  be  sought  in  all  cases  of 
acute  diffuse  peritonitis  except  those  in  which  decided  symptoms  of  severe 
peritoneal  collapse  have  already  appeared.  Mild  and  moderately  severe 
clinical  pictures  of  this  nature  are,  as  a  rule,  not  positive  contraindica- 
tions for  an  operation ;  but  subjective  judgment  as  to  the  patient's  powers 
of  resistance,  particularly  the  condition  of  the  heart  and  the  vasomotor 
system,  as  well  as  the  severity  of  the  other  toxic  phenomena,  leaves  wide 
room  for  doubt;  definite  rules  cannot  be  established.  It  must  always 
be  borne  in  mind  that,  as  a  rule,  operation  at  first  intensifies  the  collapse. 

On  the  whole,  a  comparative  estimate  (in  so  far  as  this  is  possible) 
of  the  results  with  and  without  operation  proves  that  in  perforative  peri- 
37 


560       ACUTE   PERITONITIS,   APPENDICITIS,  AND  PERITYPHLITIS 

tonitis,  if  operation  is  very  early,  i.  e.,  inside  of  twelve,  or,  at  most,  twenty- 
four  hours  after  perforation,  there  is  slightly  more,  but,  nevertheless, 
greater  hope  of  recovery  than  without  operation.  Those  cases  are  naturally 
the  most  favorable  in  which  peritonitis  has  not  yet  developed,  provided 
that  up  to  the  moment  of  operation  there  is  no  peritoneal  collapse.  If  the 
latter  occurs,  the  prognosis  in  laparotomy  is  exceedingly  grave  and,  there- 
fore, it  is  rejected  by  most  surgeons, 

A  relatively  unfavorable  prognosis  after  operation  is  presented  by  those 
cases  in  which  previously  more  or  less  localized  relapses  of  progressive 
peritonitis  have  occurred,  after  which  a  severe  diffuse  picture  is  suddenly 
presented,  and  also  in  those  cases  in  which,  combined  with  a  circumscribed 
peritonitis,  the  indistinct  picture  of  diffuse  peritoneal  irritation  had  some 
time  previously  existed,  this  having  abruptly  changed  to  a  severe  diffuse 
inflammation;  here,  as  a  rule,  there  is  a  massive  secretion  of  pus,  widely 
distributed.  These  occurrences  are  usually  preventable  by  proper  surgical 
treatment  of  the  preceding  circumscribed  peritonitis  (see  below). 

The  conditions  are  likewise  unfavorable  for  surgical  intervention  in 
peritonitis  to  which  a  septic  condition  has  been  added,  or  in  which  this 
already  coexisted,  as  is  so  frequently  the  case  in  the  puerperal  forms. 
Here  also,  for  good  reasons,  the  surgeon  refuses  to  operate. 

For  the  not  infrequent  cases  where  either  a  diffuse  peritonitis  is  certain 
— its  origin,  however,  not  being  quite  clear — or  in  which  the  differential 
diagnosis  between  peritonitis  and  strangulation  or  the  like  cannot  be 
readily  made  with  certainty,  early  surgical  treatment  is  generally  advisable. 
It  is  a  serious  error  to  confound  this  condition  with  coprostasis,  uremia  or 
peritonism,  although  I  can  easily  imagine  isolated  cases  in  which  the 
physician,  and  also  the  surgeon  relying  upon  his  asepsis,  might  with  an 
uncertain  diagnosis  assume  the  responsibility  of  deciding  upon  an  "  ex- 
ploratory laparotomy.'' 

These  criticisms,  which  in  part  extend  into  the  realm  of  surgery,  I 
may  be  permitted  to  make  because  they  indicate  the  cases  in  which  the 
internal  clinician  or  the  house  physician  would  make  a  gross  error  not 
to  consult  a  surgeon,  and  because  they  show  that  the  surgeon's  aid  is 
usually  needed  early,  and  that,  to  avert  danger,  laparotomy  must  speedily 
be  performed. 

From  a  purely  practical  standpoint,  however,  the  conditions  are  such 
that  where  the  surgeon  may  be  readily  obtained  his  opinion  should  be 
sought  in  every  case  in  which  acute  diffuse  peritonitis  appears  to  be  cer- 
tain or  likely,  or  even  possible.  This  cannot  be  emphasized  too  strongly. 
If  he  can  be  reached  only  with  difficulty,  the  internal  clinician  himself 
must  weigh  the  possibilities  and  decide  whether  or  not  the  aid  of  the 
surgeon  is  necessary. 

Internal  treatment  must  be  resorted  to  in  those  cases  in  which  opera- 
tion is  rejected  and  those  in  which  surgical  relief  is  either  unobtainable 


PERITONITIS   WITH   REFERENCE  TO  PERITYPHLITIS  561 

or  cannot  be  secured  at  the  right  time.  These  are  almost  all  lost,  but 
none  of  them  present  an  absolutely  bad  prognosis;  this  must  be  borne 
in  mind.  We  may  see  most  remarkable  recoveries  from  the  severest  clin- 
ical picture,  even  of  peritoneal  collapse,  and  particularly  in  appendicular 
peritonitis;  I  have  known  the  symptoms  to  disappear  after  rupture  and 
recovery  finally  to  take  place  in  cases  where,  without  rupture,  the  heart 
would  have  held  out  but  a  few  hours  longer.  Such  outcomes  are  unfor- 
tunately rare,  but  they  must  stimulate  the  physician  in  each  individual 
case  to  continue  the  battle  to  the  end. 

Internal  Treatment. — We  possess  no  radical  internal  treatment  of 
peritoneal  suppuration,  i.e.,  antitoxic  or  bactericidal,  which  promises 
success. 

Two  principal  indications  are  to  be  met  by  the  internal  treatment  of 
acute  diffuse  peritonitis:  Absolute  rest  of  the  areas  surrounding  the  focus 
of  origin  and  also  of  the  entire  abdomen,  and  the  maintenance  of  the 
strength  of  the  patient  as  long  as  possible.  With  this,  too,  is  the  im- 
portant consideration  of  relieving  the  sufferings  of  the  patient. 

The  first  indication  calls  for  absolute  quiet,  avoidance  of  shock  to  the 
abdomen,  therefore,  above  all,  the  prevention  of  vomiting,  the  stopping 
of  all,  or  nearly  all,  food  by  the  mouth,  the  arrest  of  intestinal  peristalsis, 
psychical  repose. 

The  necessity  for  absolute  quiet  is  often  confronted  by  the  question 
of  moving  the  patient  to  a  hospital;  here,  under  all  circumstances,  the 
individual  case  must  be  considered;  the  issue  cannot  be  discussed  from 
a  general  standpoint.  The  vomiting  is  at  once  somewhat  favorably  in- 
fluenced by  opium  or  morphin;  if  this,  however,  should  not  be  the  case 
careful  lavage  of  the  stomach  with  a  cool  fluid  may  be  employed  soon 
after  a  meal,  particularly  if  we  suspect  a  complicating  ileus  or  a  perfora- 
tion from  ulcer,  and  in  other  isolated  cases  in  which  we  are  under  the 
impression  that  continued  severe  retching  will  be  more  injurious  than 
the  perturbation  produced  by  the  stomach-tube.  In  conclusion,  I  cannot 
advise  the  general  employment  of  the  stomach-tube,  as  some  authors 
have  done. 

Food  by  the  mouth  is  to  be  stopped  at  the  onset;  but,  in  the  course 
of  the  affection,  circumstances  will  not  seldom  compel  us  to  return  to 
this — naturally  when  improvement  begins.  The  first  food  that  may  be 
administered  is  meat  juice  freshly  expressed  (by  means  of  a  meat  press), 
then  cool  bouillon  with  the  addition  of  Plasmon,  Jjeube-Rosenthal's  meat 
solution  and  the  like,  following  this  milk,  cooled  by  ice,  all  to  be  given 
in  teaspoonf ul  or  tablespoonf ul  doses ;  diluted  wine  or  cognac  is  permissible. 
The  subsequent  stage  of  beginning  convalescence  I  shall  pass  over.  Ad- 
ministration of  water  by  the  mouth  should  only  be  stopped  in  the  severest 
cases;  small  pellets  of  ice  may  usually  be  swallowed,  unless  this  increases 
the  vomiting  which  may  occur. 


562      ACUTE  PERITONITIS,  APPENDICITIS,  AND  PERITYPHLITIS 

Administration  of  food  by  the  rectum  is  by  no  means  immaterial;  as 
is  well  known,  it  may  stimulate  peristalsis  in  the  entire  colon.  If  we 
are  forced  by  the  failure  of  strength  to  employ  this  method,  I  advise 
only  eneinata  consisting  of  two  eggs  with  1.0  sodium  chlorid  to  each  egg 
(sodium  chlorid  20.0  to  200,  10  grams  or  one  small  teaspoonful  per  egg). 
If  there  be  temperature,  about  15  cm.  of  this  solution  is  to  be  cautiously 
injected  high  up,  or  milk,  perhaps  with  an  egg  and  about  5  per  cent. 
of  sugar.     Anything  else  will  readily  irritate. 

Water  is  particularly  valuable  for  conserving  the  strength,  and  much 
more  indispensable  than  food.  The  organism  must  not  thirst!  Accord- 
ing to  the  case  and  how  water  is  borne,  it  may  be  given  either  by  rectum 
or  subcutaneously  (in  the  thigh)  in  as  large  quantities  as  possible  (in 
tlie  latter  case  sterile  physiologic  salt  solution  of  the  temperature  of  the 
body,  about  200  at  a  time,  or  by  continuous  infusion). 

Of  course,  if  the  patient  becomes  chilly  he  should  be  made  warm;  that 
is,  external  heat  should  be  applied. 

To  meet  the  indication  for  complete  rest  of  the  intestine,  the  use  of 
opium  in  large  doses,  perhaps  of  morphin,  immediately  at  the  beginning 
of  tlie  disease,  is  recommended.  It  is  true  that  the  bowel  rests  in  conse- 
quence of  the  peritonitis  itself,  although  it  is  questionable  whether  this 
is  invariably  the  case,  for  example,  in  those  cases  associated  with  diarrhea; 
at  all  events  clinical  observation  proves  that  rest  of  the  intestine  is  pro- 
moted by  opium ;  the  decisive  significance  of  which  is  obvious,  and,  in 
comparison,  the  deleterious  effects  of  its  energetic  use  are  unimportant. 
In  this  connection  it  is  urged  that  it  increases  constipation,  masks  the 
course  of  the  disease,  and  acts  unfavorably  upon  the  strength,  particularly 
upon  the  heart.  In  diffuse  peritonitis  I  believe  these  views  to  be  without 
weight.  Constipation  in  diffuse  peritonitis  is  almost  always  unimportant, 
particularly  when  we  consider  the  abstinence  from  food;  what,  however, 
opium  may  be  said  to  conceal  is  not  quite  clear  to  me,  since  the  decrease 
of  pain  and  vomiting  while  other  severe  symptoms  persist  cannot  deceive 
the  physician,  and  the  somnolence  produced  by  drugs  can  lead  to  no 
diagnostic  doubt  regarding  the  true  condition,  provided,  naturally,  that 
actual  intoxication  is  avoided;  finally,  as  regards  the  unfavorable  effect 
of  the  alkaloids  of  opium  upon  the  heart,  this,  as  is  well  known,  is  very 
slight  and  is  readily  compensated  for  by  its  favorable  effect  in  diminish- 
ing pain  and  vomiting. 

Treatment  hy  opium  is  deleterious  to  a  high  degree  when  it  is  the  re- 
source of  those  who  cannot  decide  upon  an  operation;  here  the  anodyne 
and  stupefying  effect  of  the  remedy  is  a  source  of  great  danger.  For  the 
critical  physician,  however,  who  objectively  grasps  the  actual  state  of 
affairs,  no  such  danger  exists;  perhaps  he  may  prefer  to  let  the  patient 
bear  a  little  pain  for  some  time  in  order  to  win  his  consent  to  the  life- 
saving  operation !     I  can  readily  imagine  such  a  state  of  affairs. 


PERITONITIS   WITH   REFERENCE  TO  PERITYPHLITIS  563 

In  a  treatment  with  opium  the  fact  must  be  borne  in,  mind  that  the 
drug  should  be  given  as  early  as  possible  and  in  decided  doses;  with 
continued  employment  its  paralyzing  effect  upon  the  intestines  soon  ceases; 
often  in  the  subsequent  course  of  the  affection,  and  according  to  the  con- 
dition of  the  patient,  the  treatment  must  be  at  times  suspended.  There- 
fore, at  the  onset  a  dose  should  be  given  hourly  or  every  two  hours,  later 
every  three  hours,  and  then  even  more  rarely,  and  when  aggravation 
occurs  increased  doses  of  from  0.03-0.05  of  pure  opium  or  the  extract 
of  opium,  or  six  to  ten  drops  of  tincture  of  opium  are  to  be  administered 
by  the  mouth.  Vomiting  once  or  twice  (pellets  of  ice  to  be  given)  need 
not  cause  the  suspension  of  this  method  of  administration.  If  vomiting 
increases,  the  drug  should  be  used  by  rectum  (enemata  or  suppository) 
or  morphin,  which  unfortunately  does  not  have  the  same  effect,  by  sub- 
cutaneous injection  of  about  0.01  with  the  intermediate  pauses  mentioned 
above.  Naturally,  when  such  doses  are  employed  the  symptoms  of  poison- 
ing must  be  watched  for,  particularly  those  on  the  part  of  the  sensorium 
and  the  pupils,  and  we  must  remember  that  the  pupils  contract  under 
moderate  toxic  action;  when  it  is  very  severe  they  dilate.  Moderately 
narrow  pupils  do  not  contraindicate  the  continued  cautious  use  of  the 
drug.  I  have  never  seen  an  instance  of  the  sudden  cumulative  effect  of 
the  remedy,  which  indicates  that  after  a  period  of  non-absorption  several 
doses  have  suddenly  been  absorbed.  It  is  possible  that  this  occurrence 
as  reported  is  due  to  confusion  with  peritoneal  collapse  and  loss  of  con- 
sciousness ;  however,  these  remarks  are  not  to  be  looked  upon  as  a  criticism 
of  the  reports  just  referred  to. 

Morphin  acts  upon  the  mind  and  the  sensation  of  pain  to  at  least  the 
same  extent  as  opium,  upon  intestinal  peristalsis  and  vomiting  less  in- 
tensely; it  is  therefore  an  imperfect  substitute  for  opium,  which  we  are 
only  to  employ  when  nothing  but  the  subcutaneous  injection  remains, 
or  when  we  wish  to  effect  a  rapid  action,  as  when  pain  is  the  most  promi- 
nent symptom  in  the  case. 

Other  substitutes  are  only  to  be  considered  when,  on  account  of  repeated 
attacks  of  vomiting,  which  are  of  very  serious  import,  or  the  solution  of 
adhesions,  or  the  distribution  of  the  generators  of  inflammation,  trial 
is  made,  of  other  drugs.  Tincture  of  iodin  in  drop  doses  in  a  little  water 
is  an  old  remedy  which  is  occasionally  very  successful;  cocain  is  useless; 
only  gastric  lavage  remains  which  in  such  cases  is  advisable;  naturally 
but  small  quantities  of  water  and  very  slight  pressure  are  to  be  employed. 

Of  cardiac  and  vasomotor  remedies  in  collapse,  above  all  in  threatening 
collapse,  camphor  and  caffein,  subcutaneously  injected,  are  recommended. 

In  very  isolated  cases,  particularly  when  the  fever  disappears,  the  pain 
and  metcorism  have  become  less,  yet  feces  are  not  discharged,  and  there 
is  marked  dulness  of  the  descending  colon,  the  indication  may  arise  to 
evacuate  this  organ  carefully.     I  should  not  do  more  than  use  about  100 


564       ACUTE   PERITONITIS,   APPENDICITIS,   AND  PERITYPHLITIS 

grams  of  olive  oil  by  enema.  The  careful  observation  of  the  state  of 
the  bladder  and,  with  a  prolonged  duration  of  the  disease,  the  prevention 
of  bed-sores,  must  always  be  borne  in  mind. 

CIRCUMSCRIBED    PERITONITIS,  PARTICULARLY 
PERITYPHLITIS 

We  must  consider  also  the  therapeutic  indications  in  perityphlitis. 
First,  because  it  is  the  best  guide  to  the  points  suitable  for  consideration, 
partly  because  it  is  the  more  frequent  affection,  and  also  because  the 
consideration  of  all  other  forms  of  circumscribed  peritonitis  ranks  in 
importance  with  the  treatment  of  all  the  organs  of  the  abdomen  and 
their  surroundings. 

PROPHYLAXIS 

The  prophylaxis  of  perityphlitis  up  to  the  present  time  is  somewhat 
chaotic.  The  apparent  increase  of  this  disease,  particularly  in  the  United 
States,  has  led  to  the  supposition,  which  is  perhaps  most  reasonable,  that 
here  hasty  eating,  insufficient  mastication,  and  constipation  are  certain 
causative  factors;  the  conclusion  is  obvious  that  persons  who  from  a  fear 
of  appendicitis  eat  slowly  and  masticate  thoroughly  may  thus  become 
hypochondriacs.  It  is  much  better  to  relegate  to  general  hygienic  strictures 
all  advice  of  this  kind. 

We  are  dealing  with  tangible  objects  when  we  consider  fecal  calculi 
which  may  certainly  remain  in  the  appendix  a  long  time  before  they 
become  dangerous,  and  also  when  we  consider  chronic  appendicitis  and 
its  exacerbations,  the  "  relapses "  which  we  have  already  described. 

Up  to  this  time  the  latent  fecal  calculus  cannot  be  diagnosticated,  not 
even  with  the  X-rays;  here,  therefore,  is  no  question  of  prophylaxis;  if  it 
were  possible  to  recognize  it,  and  considering  its  danger  and  the  present 
certainty  of  surgery,  no  doubt  it  would  be  well  to  remove  it  with  its 
enclosure,  the  appendix. 

Here  the  indication  would  be  simple.  Much  more  complex  are  the 
conditions  in  that  other  precursor  of  perityphlitis,  chronic  appendicitis; 
here  the  diagnosis  is  clear  if  the  "  relapses "  are  correctly  considered, 
but  it  is  not  at  all  certain  that  mild  "  relapses "  lead  to  purulent  peri- 
appendicitis, or  even  to  necrosis  and  perforation:  The  danger  of  chronic 
appendicitis  is  far  less  than  the  danger  of  fecal  calculus.  The  question 
resolves  itself  into  this,  whether  in  pure  appendicitis  we  should  operate 
to  prevent  a  purulent  perityphlitis,  and  this  is  certainly  worthy  of  serious 
reflection.  We  shall  consider  it  in  common  with  the  operative  treatment 
of  perityphlitis. 


CIRCUMSCRIBED   PERITONITIS,   PARTICULARLY  PERITYPHLITIS    565 


TREATMENT 

In  the  treatment  of  perityphlitis  which  has  either  been  diagnosticated 
with  certainty  or  with  a  great  degree  of  probability,  in  general  the  follow- 
ing facts  are  to  be  weighed:  Under  internal  treatment,  i.e.,  without  re- 
course to  surgery,  from  70  to  80  per  cent,  of  all  cases  entirely  recover, 
a  number  which  is  large  but  which,  naturally,  does  not  comport  with  our 
therapeutic  endeavors ;  in  the  treatment  of  these  cases,  that  therapy  suffices 
which  has  for  its  Alpha  and  Omega  the  keeping  of  the  intestines  and  the 
entire  abdomen  absolutely  at  rest.  Of  the  cases  that  remain,  no  doubt 
nearly  all  might  be  cured  by  timely  operative  measures;  in  the  majority 
of  these  cases,  too,  a  surgical  operation  might  be  performed  if  the  right 
time  were  chosen,  and  the  patient  were  carefully  examined  and  watched. 
In  a  small  proportion  of  these  cases,  however,  it  is  done  too  late,  partly 
because,  without  fault  of  the  physician,  and  without  prodromes,  there  is 
a  sudden  perforation  into  the  free  abdominal  cavity,  but  partly  also  be- 
cause the  case  was  an  apparently  benign  one  which  gave  hope  of  recovery 
by  internal  treatment  yet  it  suddenly  became  dangerous,  or  because  at 
the  beginning  it  appeared  to  improve  and  a  sudden  fatal  relapse  occurred. 
These  last  two  categories  will  always  rest  as  a  weight  upon  the  conscience 
of  the  physician. 

From  the  preceding  observations  it  will  be  noticed  that  the  most 
serious  cases  and  those  requiring  most  speedy  operation  are  the  following: 
1.  Perforation  into  the  free  abdominal  cavity;  2.  Larger  abscesses  which 
usually  perforate,  and  are  characterized  by  an  increasing  tumor  and  a 
tendency  to  further  enlargement,  a  "progressive  condition,"  noted  par- 
ticularly upon  the  inner  side  of  the  colon;  3.  Empyema  without  marked 
adhesions,  especially  the  putrid  form.  In  contrast  to  these  are  the  rela- 
tively mild  conditions:  Non-purulent  periappendicitis;  small  non-perfora- 
tive  abscesses  with  solid  adhesions,  which  terminate  partly  by  absorption 
and  partly  by  rupture  in  the  direction  of  least  resistance,  i.  e.,  toward  the 
intestine ;  finally,  mucus  and  sero-purulent,  moderately  virulent,  non-putrid 
collections  of  secretion  in  the  appendix. 

These  conditions  very  rarely  lead  to  immediate  danger;  but  during 
healing  they  may  produce  strictures  and  kinking,  and  by  relapses  develop 
a  malignant  character — although  this  is  very  rare. 

Midway  between  these  two  categories,  in  regard  to  spontaneous  cure, 
are  the  moderately  large  abscesses  which  sometimes  show  fine  perforation 
and  sometimes  do  not  perforate,  and  in  which  the  danger  depends  upon 
the  continuance  of  preformed  and  fresh  adhesions,  upon  the  virulence 
of  the  pus,  and  upon  the  promptness  of  its  rupture  in  a  favorable  locality. 
These  abscesses  are  rarely  absorbed.  They  form  a  large  proportion  of 
the  total  number  of  cases  of  perityphlitis. 

I  repeat  what  has  already  been  said  elsewhere  in  other  words,  in 


566       ACUTE   PERITONITIS,   APPENDICITIS,   AND  PERITYPHLITIS 

order  to  recall  to  mind  the  general  diagnostic  knowledge  regarding  these 
conditions.  The  most  extreme  cases  of  this  kind  may  nearly  always  be 
readily  diagnosticated;  but  in  the  severe  types,  especially  perforations, 
which  may  simulate  mild  forms,  errors  are  not  rare. 

Even  in  these,  but  still  more  often  in  the  numerous  cases  of  moderate 
severity,  it  is  not  only  difficult  to  decide  exactly  what  condition  is  present 
but,  much  more  so,  what  will  be  its  course. 

Let  us  assume  that  in  all  cases  of  perityphlitis  we  have  a  full  com- 
prehension of  the  anatomical  structure,  the  position  of  the  possible  abscess, 
the  condition  of  the  appendix,  the  adhesions:  Even  then,  in  the  great 
majority  of  cases,  it  will  he  impossible  to  say  that  recovery  will  take  place 
ivithout  surgical  intervention,  and,  if  so,  whether  it  will  he  complete,  or 
whether  the  Imife  will  ultimately  he  necessary.  We  cannot  correctly  esti- 
mate the  resistive  power  of  the  adhesions  to  the  mechanical  influence  of 
the  pus  which  still  has  an  inflammatory  action,  and  whether  this  will 
still  later  be  absorbed,  that  is,  whether  the  lesion  will  heal  by  a  timely 
rupture  into  the  intestine. 

Still  greater,  however,  are  the  practical  actual  difficulties  of  diagnosis 
in  regard  to  prognosis !  What  a  gloomy  outlook  is  there  presented  in 
regard  to  a  future  improvement  in  our  diagnosis,  particularly  as  a 
foundation  for  treatment !  Nevertheless,  we  may  say  to-day  that  in 
by  far  the  majority  of  cases  of  perityphlitis  the  thera])eutic  indica- 
tions are  so  palpable  that  proper  treatment  will  lead  to  a  favorable 
termination. 

The  first  question  in  treatment,  which  must  be  answered  as  soon  as 
possible,  is  this:  Must  we  operate  immediately  and  during  the  attack? 
]\Iost  internal  clinicians  and  surgeons  will  answer  that  we  should  operate 
in  the  following  clinical  forms: 

1.  In  the  acutest  cases  of  perforative  peritonitis  without  tumor,  and 
here  as  speedily  as  possible — every  quarter  of  an  hour  is  of  importance; 
those  cases  of  well  developed  peritoneal  collapse  in  which  an  operation 
can  no  longer  be  borne  mUSt  be  excluded;  it  is  obvious  that  these  furnish 
a  fruitful  field  for  individual  judgment. 

2.  With  secondary  distribution  of  inflammation  to  the  remaining  areas 
of  the  abdominal  caivity  from  an  already  existing  perityphlitic  abscess; 
this  process,  however,  should  be  averted  by  a  timely  early  operation  (in 
regard  to  this,  see  No.  3). 

3.  Tn  a  large,  distinct,  fluctuating  abscess,  as  well  as  in  all  acute 
painful  perityphlitic  tumors,  which,  either  by  a  tendency  to  enlargement 
or  by  a  fever  wliich  increases  for  several  days,  or  by  a  rise  in  temperature 
M'hich  is  continued  for  more  than  five  days,  or  by  a  fresh  exacerbation  after 
a  previous  improvement,  foreshadow  the  danger  of  rapid  progression.  Here 
it  is  our  duty  by  every  possible  means  to  prevent  the  extension  of  the 
peritonitis,  or  even  peritoneal  collapse. 


CIRCUMSCRIBED   PERITONITIS,   PARTICULARLY   PERITYPHLms    567 

4.  When  a  very  painful,  circumscribed,  round  tumor,  appearing  with 
fulminant  symptoms,  indicates  a  putrid  empyema  of  the  appendix. 

In  my  opinion,  and  according  to  the  present  status  of  our  science,  in 
these  cases  there  can  be  no  doubt  as  to  the  indication  for  operation. 

Neither,  after  an  attack  has  passed,  can  there  be  the  least  doubt  in 
regard  to  the  necessity  of  operation  in  the  following  cases: 

1.  When  a  recognizable*  abscess,  even  without  irritation,  persists  for 
weeks. 

2.  When,  after  an  attack  without  operation,  debilitating  relapses  occur, 
and  particularly  when  the  relapses  show  an  increasing  severity. 

3.  When  there  are  permanent  adhesions  and  indurations  which  disturb 
the  appetite,  the  digestion,  and  motion;  when  these  cannot  be  relieved 
in  other  ways  (see  below),  and  prevent  recovery;  and  when  they  manifest 
themselves  either  by  pain  and  slight  inflammatory  relapses  or  by  fecal 
stasis. 

These  are,  as  I  believe,  the  absolute  indications  for  operation;  what 
now  remains,  and  this  should  be  borne  in  mind,  applies  to  the  majority 
of  cases  of  perityphlitis.  These,  as  a  rule,  make  a  good  recovery  without 
operation,  hut  are  nevertheless  subject  to  some  dangers.  These  dangers 
are  of  various  kinds:  First,  are  those  which  arise  from  an  error  in  diag- 
nosis, from  larval  perforation  with  non-recognizable  pus,  etc.;  also  when, 
after  a  correct  diagnosis — for  example,  in  a  well  encapsulated  abscess  with 
a  moderately  severe  appendicitis — a  change  occurs  which  could  not  have 
been  foreseen  (rupture  into  the  abdominal  cavity,  sudden  necrosis  of  the 
appendix,  venous  thrombosis,  etc.). 

If  we  wish  to  protect  ourselves  from  these  eventualities  we  neces- 
sarily face  the  question:  Is  it  not  well  to  operate  in  all  cases,  even  in 
the  mildest  ones?  Should  we  not  even  terminate  the  paroxysmal  exacer- 
bations of  chronic  appendicitis  by  extirpation  of  the  organ  ?  The  surgeon, 
who  usually  sees  only  severe  cases,  and  among  these  many  with  a  severe 
relapse  after  a  first  mild  attack,  in  surprising  contrast  to  the  benign 
onset,  is  confronted  with  this  question  which  must  be  answered  according 
to  his  skill,  his  temperament,  and  the  results  which  he  has  obtained. 
Many  a  one,  however,  later  becomes  conservative. 

In  the  hands  of  the  skilful  surgeon  the  immediate  dangers  of  opera- 
tion, contrasted  with  the  general  dangers  of  perityphlitis  calculated  purely 
by  percentage,  are  decidedly  in  favor  of  the  patient;  however,  here  we 
are  dealing  with  the  personal  methods  of  individual  surgeons,  and  the 
most  skilful  are  not  always  at  hand.  This  must  be  borne  in  mind  by  those 
who  write  regarding  these  conditions.  Besides,  we  must  consider  the  not 
infrequent  sequelae  of  the  operation,  in  spite  of  the  fact  that  modern 
surgery  does  everytliing  possible  to  prevent  them;  we  mean  hernia  of  the 
abdominal  wall  from  diastasis  of  the  cicatrix,  and  weakening  of  the  mus- 
culature by  degenerative  atrophy  in  consequence  of  the  section  of  motor 


568       ACUTE   PERITONITIS,   APPENDICITIS,   AND  PERITYPHLITIS 

nerves.  These  conditions  are  occasionally  of  vital  importance,  especially 
in  the  female  during  labor.  To  this  must  be  added  the  instinctive 
repugnance  of  man  to  mutilation,  which  in  a  mild  illness  makes  it  difficult 
for  liim  to  consent  to  operation  for  an  affection  which  is  usually  only 
slightly  dangerous. 

The  relegation  of  all  forms  of  the  disease  to  the  knife  of  the  surgeon 
will,  therefore,  I  am  firmly  convinced,  never  be  possible;  on  the  contrary, 
on  account  of  the  rare  dangers  which,  however,  can  never  be  completely 
excluded  in  the  individual  case  in  the  milder  forms  of  the  affection,  the 
question  arises  in  how  far  is  operation  necessary. 

On  this  point  opinions  are  far  asunder,  which  is  only  to  be  expected. 
The  perplexity  which  assails  us  in  an  exact  discrimination  of  the  cases 
is  very  great;  aside  from  a  certain  tenacious  adherence  to  the  old,  which 
to  some  extent  still  shows  itself  in  internal  medicine,  and  aside  from 
the  very  prevalent  error  of  the  surgical  author  in  considering  as  the 
normal  whatever  he  is  able  to  do  for  himself,  each  position  has  its 
justification. 

The  question  to  be  put  in  the  "  intermediary  "  cases  is  a  double  one : 
1.  Which  cases  are  to  be  operated  upon  during  the  attack?  2.  Which 
aue  to  be  operated  upon  after  the  attack?  In  regard  to  the  first,  many 
authors  are  of  the  opinion  that  operation  is  to  be  immediately  undertaken 
wlien  pus  is  present  or  when  it  is  likely  to  be  present.  Here  we  must 
face  the  previously  mentioned  diagnostic  difficulties  based  on  the  general 
assumption  that  pus  always  accompanies  acute,  painful,  febrile  tumors, 
a  position  that  can  no  longer  be  maintained;  for  pus  may  be  absent  when 
wo  have  quite  high  fever,  severe  vomiting,  and  a  distinct,  painful  tumor. 
Besides,  the  catchword  "pus"  by  no  means  embraces  everything;  the  dan- 
gerous character  of  a  periappendicular  pus  focus  varies  according  to  the 
position  and  the  length  of  existence  of  the  adhesions,  according  to  whether 
or  not  perforation  takes  place,  whether  or  not  it  is  putrid — and  not  only 
the  local  but  also  the  general  symptoms  are  of  significance;  they  may 
manifest  severer,  or  milder,  conditions  than  those  present.  Finally,  pus 
may  be  absent  in  one  "  relapse  "  and  appear  in  the  next  one. 

I  advise,  in  general,  in  those  cases  in  which  pus  may  be  assumed  and 
in  which  there  is  no  solidity  of  the  tumor,  when  it  decreases  in  size  at 
the  latest  about  the  third  day,  with  a  retardation  of  the  fever  and  im- 
provement in  the  general  condition  and  pulse,  all  of  which  point  to 
cnod  encapsulation — in  such  cases,  a  consultation  with  a  surgeon  and, 
if  possible,  the  consideration  of  an  operation.  When  the  previously 
mentioned  symptoms  of  encapsulation  appear  there  will  rarely  be  an 
augravation  of  the  condition,  and,  should  this  occur,  it  will  almost  always 
show  itself  by  certain  symptoms  (enlargement,  meteorism  with  moderate 
pain  upon  pressure,  renewed  rise  in  pulse  and  temperature,  tendency  to 
vomiting,  dysuria,  etc.),  so  that  operation  may  still  be   undertaken   in 


CIRCUMSCRIBED   PERITONITIS,   PARTICULARLY   PERITYPHLITIS    569 

good  time.  For  this,  however,  it  is  necessary  carefully  to  watch  the 
patient,  and  this,  in  fact,  should  be  done  as  conscientiously  as  possible; 
where,  however,  it  is  impossible,  the  list  of  operative  cases  will  be  en- 
larged. In  these  intermediate  cases  the  question  whether  or  not  the  patient 
can  he  watched  has  a  strong  hearing  upon  the  question  whether  or  not 
we  shall  operate  in  the  attack. 

In  many  of  these  cases,  if  we  do  not  operate  during  the  attack,  the 
question  of  operation  may  again  arise  in  a  few  weeks,  and  invariably 
if  there  is  a  suspicion  of  persisting  pus. 

Operation  after  an  attack  has  advantages  and  disadvantages  in  contrast 
to  those  of  operation  during  an  attack.  I  shall  not  enter  upon  the  pros 
and  cons,  as  this  is  a  purely  surgical  question.  Whoever  rejects  operation 
during  the  attack  must  naturally  take  account  of  the  risks.  Here,  too, 
watching  the  patient  is  specially  important. 

Neither  can  I  answer  the  question  as  to  the  method  to  be  chosen, 
whether  immediate  removal  of  all  the  pathologic  conditions,  or  the  open- 
ing of  the  abscess  and  the  subsequent  extirpation  of  the  appendix. 

It  is  not  my  function  to  discuss  the  surgical  indications  in  slowly 
progressing  cases  with  the  appearance  of  new  pus  foci  in  the  abdominal 
cavity,  in  the  belly  wall,  or  in  the  pelvis  behind  the  colon  (examining 
the  lumbar  region!),  in  the  subphrenic  tissues,  or  in  the  pleura.  But 
it  is  the  duty  of  the  physician  on  the  slightest  sign  of  complication  of 
this  kind,  for  which  search  should  be  made  in  all  cases,  to  call  in  the 
surgeon.  Prior  to  this,  however,  these  cases  have  usually  come  under 
surgical  treatment. 

Non-operative  Treatment. — I  have  previously  stated  that  the  Alpha  and 
Omega  of  treatment  in  those  cases  of  perityphlitis  and  also  of  appendicitis 
itself  in  which  an  operation  is,  or  appears  to  be,  unnecessary,  or  is  not 
permissible,  is  to  keep  the  intestine  and  the  whole  abdomen  quiet. 

The  indications  are  primarily  the  same  as  in  diffuse  peritonitis:  Rest 
(great  care  in  transportation  to  a  hospital),  no  administration  of  nourish- 
ment by  the  mouth  at  the  onset  or  even  later,  nor,  if  possible,  as  long 
as  inflammatory  s3^mptoms  continue;  if  these  retard,  or  the  condition  of 
the  patient  show^s  that  the  strength  must  be  increased  at  any  cost,  the 
same  dietary  mentioned  upon  page  561  should  be  employed.  The  intake 
of  water  by  mouth  must  be  moderate,  always  small  quantities  only  at  a 
time,  and  perhaps  only  ice.  At  the  onset  food  should  never  be  given 
by  rectum ;  nor  should  enemata  then  be  given  to  empty  the  rectum ;  never- 
theless, in  protracted  cases  it  may  be  necessary  to  risk  nutritive  enemata 
when  that  mentioned  upon  page  562  may  be  used.  In  such  cases  the 
subcutaneous  injection  of  water  may  also  be  necessary. 

The  application  of  ice  or  cool  or  lukewarm  Priessnitz  compresses  may 
depend  upon  the  wishes  of  the  patient.  At  the  onset  hot  cataplasms  must 
be  strenuously  forbidden. 


570       ACUTE   PERITONITIS,   APPENDICITIS,   AND   PERITYPHLITIS 

Here  also  opium  is  the  sovereign  remedy;  it  must  be  employed  in  all 
cases  of  appendicitis  and  perityphlitis,  provided  it  does  not  induce  vomit- 
ing; in  this  case  suppositories  are  to  be  resorted  to,  and  only  when  these 
are  not  well  borne  should  morphin,  which  does  not  act  so  favorably,  be 
used  as  advised  upon  page  563. 

In  the  old  so-called  typhlitis  stercoralis  it  was  found  necessary  to  vindi- 
cate the  position  of  opium,  and  this  is  the  case  even  to-day.  The  same 
deleterious  effects  are  alleged  as  in  the  case  of  acute  peritonitis,  and  it 
i.s  maintained  that  by  increasing  the  stagnation  of  feces  it  induces  a 
relapse  in  appendicitis  (Eiedel).  Particularly  is  this  true  in  perityphlitis, 
which  frequently  shows  a  retardation  of  all  the  symptoms  after  the  first 
fecal  evacuation,  and  invariably  leads  to  the  assumption,  similarly  as  in 
stercoral  typhlitis,  that  any  evacuation  of  the  intestine  as  such  acts  favor- 
ably, and  that  stagnation  of  the  feces  therefore  acts  unfavorably,  so  thiat 
we  dare  not  increase  the  latter  condition. 

It  must  be  admitted  that  those  who,  in  milder  cases  of  acute  peri- 
typhlitic  tumor  (therefore,  those  in  whom  a  cecal  stasis  of  feces  was 
previously  looked  upon  as  the  cause  of  the  disease),  risk  a  decided  dose 
of  castor  oil  occasionally  see  all  the  symptoms  disappear  when  the  oil 
has  had  its  full  effect;  in  such  cases  it  is  questionable  whether  we  are 
not  dealing  with  a  relapse  of  a  chronic  appendicitis  (without  periappen- 
dicitis!) and  secondary  fecal  tumor  from  intestinal  paralysis,  or  whether 
the  appendicitis  was  not  favorably  influenced  by  the  evacuation  of  the 
large  intestine.  I  can  readily  imagine  that  the  future  will  see  a  purgative 
treatment  of  chronic  appendicitis  and  an  energetic  purgative  treatment 
for  acute  relapses,  provided  that,  in  the  individual  case,  the  presence  of 
a  fecal  calculus  in  the  appendix  and  the  presence  of  inflammatory  products, 
etc.,  of  the  appendix  may  he  excluded  with  absolute  certainty,  and  also 
til  at  we  may  exclude  a  beginning  invasion  of  the  serosa;  to-day  we  have 
not  advanced  so  far! 

In  every  case,  however,  of  fecal  calculus,  or  when,  without  fecal  calculus, 
])roducts  of  inflammation  appear  upon  the  surface  of  the  serosa,  or  when 
they  are  extending  to  this  tissue,  or  have  already  formed  adhesions,  the 
stimulation  of  peristalsis  is  a  grave  danger,  and  absolute  rest  of  the  intes- 
tine is  the  principal  indication. 

And,  since  it  is  as  yet  impossible  to  exclude  these  cases  with  certainty 
in  acute  disease  accompanied  by  pain  in  the  right  iliac  fossa,  purgative 
treatment  in  cases  of  this  kind  should  not  be  resorted  to.  According  to 
the  present  status  of  diagnosis,  we  must  reject  this  form  of  treatment, 
not  only  by  the  mouth  but,  with  very  recent  inflammation,  for  even  a 
longer  time  by  rectum. 

Opium,  on  the  other  hand,  is  even  more  valuable  here  than  in  diffuse 
])('ri(o]iitis:  for  the  salutary  intestinal  paralysis  due  to  inflammation  in 
circuiiiscribod  perityphlitis  implicates  only  the  nearest  and  most  adjacent 


CIRCUMSCRIBED  PERITONITIS,  PARTICULARLY   PERITYPHLITIS    571 

parts:  The  cecum,  a  portion  of  the  colon,  perhaps  the  lowest  portion  of 
the  ileum;  it  is,  however,  necessary  to  prevent  peristalsis  in  wide  areas, 
to  increase  the  localization  of  the  poison,  and  to  moderate  the  propulsion 
of  the  contents  of  the  small  intestine  toward  the  lowest  portion  of  the 
ileum  and  cecum.  This  latter  point  appears  to  me  to  call  for  a  little 
reflection. 

Therefore,  in  every  acute  case,  as  in  the  case  of  acute  peritonitis,  the 
treatment  should  be  opium  by  the  mouth  in  large  doses,  abstention  from 
food,  and  absolute  bodily  rest  in  so  far  as  this  admits  of  the  transportation 
of  the  patient;  with  repeated  vomiting,  suppositories,  possibly  morphin 
subcutaneously. 

WTien  there  is  stubborn  and  violent  vomiting,  particularly,  however, 
when  there  are  symptoms  of  intestinal  obstruction,  subcutaneous  injec- 
tions of  morphin  are  indicated,  •  as  well  as  when  very  severe  pains  are 
present  which  necessitate  speedy  relief;  here  this  remedy  may  also  be 
combined  with  opium. 

In  the  opium  treatment,  however,  it  must  be  borne  in  mind  that  pro- 
longed, continued  doses  of  opium  rapidly  lose  their  effect  upon  intestinal 
peristalsis,  as  is  usually  evident  in  the  treatment  of  chronic  diarrhea; 
therefore,  it  is  advisable  that  after  the  administration  of  two  doses,  smaller 
doses  should  rapidly  follow  or  the  treatment  be  interrupted  if  the  circum- 
stances at  all  warrant  this  (fever,  vomiting,  pain,  meteorism,  decrease  in 
the  size  of  the  tumor) ;  with  the  slightest  aggravation  the  dose  should 
be  immediately  increased.  In  severe  cases  in  which  operation  is  declined, 
or  in  which  it  is  impossible,  this  drug  under  some  circumstances  may  also 
be  given  for  weeks  with  remissions  and  intermissions,  and  in  these  patient? 
we  will  have  an  opportunity  of  observing  the  highly  ameliorating  and 
localizing  effect  of  the  remedy. 

In  severe  cases,  the  periodic  administration  of  mild  narcotics,  even 
when  the  pupils  are  moderately  contracted,  is  permissible,  and  is  recom- 
mended; naturally,  in  such  cases  there  must  be  careful  and  experienced 
watching  continuously.  Where  this  is  impossible  the  doses  must  be 
smaller. 

The  most  serious  misuse  of  this  remedy  should,  however,  be  strenu- 
ously avoided;  it  consists  in  this,  that  physician  and  patient  are  content 
with  the  amelioration  of  pain  instead  of  deciding  upon  an  absolutely 
necessary  operation! 

In  regard  to  local  derivatives  in  the  acute  stage,  leeches  alone  can  be 
considered,  as  is  also  stated  by  Nothnagel;  I  have  seen  amelioration  from 
their  use  (which,  however,  may  also  be  induced  by  opium  or  morphin), 
and  perhaps  lessening  of  the  vomiting,  but  scarcely  more  than  this.  With 
the  previously  mentioned  indications  they  may  occasionally  be  applied  in 
very  robust  individuals,  at  least  four  at  a  time. 

If  the  perityphlitis  ameliorates,  the  local  application  of  cold  should 


572      ACUTE  PERITONITIS,  APPENDICITIS,  AND  PERITYPHLITIS 

be  followed  by  moist  heat,  and  this,  if  possible,  should  be  continuously 
used  until  the  resistance  disappears;  food  may  be  very  cautiously  admin- 
istered according  to  the  indications  upon  page  561,  Drugs  had  better 
be  avoided.  It  is  important  in  this  stage  that  patient  and  physician  wait 
for  the  first  fecal  movement,  in  case  this  has  not  yet  appeared. 

I  saw  two  serious  relapses  which  occurred  after  the  disappearance 
of  fever  for  several  days  and  with  an  almost  painless  limited  tumor  and 
otherwise  entirely  normal  abdomen,  after  the  cautious  injection  of  a  small, 
lukewarm  enema,  and  since  then  I  leave  the  rectum  alone  as  long  as 
possible,  all  the  more  so  as  I  cannot  remember  having  seen  a  relapse 
which  was  due  to  constipation.  Now  and  then  accumulations  of  feces 
in  the  colon  are  uncomfortable  for  the  patient,  although  here  a  psychical 
factor,  i.  e.,  the  knowledge  that  the  feces  have  not  been  voided  for  such 
and  such  a  length  of  time,  is  cooperative;  but  this,  too,  is  exceptional; 
constipation  of  eight  days  and  longer  is  usually  well  borne.  In  the  case 
of  tenesmus  it  is  self-evident  that  the  patient  must  be  cautioned  against 
employing  the  abdominal  press,  but  this  caution  is  often  neglected.  Fol- 
lowing the  first  spontaneous  and  very  copious  fecal  evacuation  I  have 
observed  renewed  sensitiveness  upon  pressure  and  fever.  Not  a  few  pa- 
tients report  a  "  wound  "  sensation  upon  the  right  side  low  down.  This 
indicates  the  need  of  care.  In  case  of  necessity,  after  the  first  evacuations 
have  occurred,  emulsions  of  oil  or  castor  oil  may  later  be  given  by  rectum. 

With  a  tumor  still  decreasing  in  size,  with  continued  fomentations, 
the  diet  must  be  strict  (gruels,  eggs,  meat  juice,  beef  tea,  cooked  cereals)  ; 
the  patient  must  be  kept  in  bed  until  all  symptoms  have  disappeared.  If 
absorption  of  the  tumor  is  delayed,  if,  moreover,  there  is  not  the  slightest 
indication  of  pus  after  two,  three  or  four  weeks,  the  time  comes  when 
the  patient  can  no  longer  be  kept  in  bed,  and  more  solid  food  cannot  be 
denied  him.  At  all  events,  he  must  not  leave  his  bed  until  spontaneous 
pains  have  disappeared,  until  the  freest  movement  of  the  right  leg  is 
painless,  and  the  pain  upon  pressure,  except  an  indistinct,  dull  sensation, 
has  disappeared;  then  an  abdominal  bandage  (which  should  also  be  worn 
while  in  bed  between  the  fomentations)  must  be  worn;  it  should  firmly 
support  the  parts  and  protect  them;  the  patient  should  remain  in  the 
recumbent  posture  as  much  as  possible,  particularly  after  meals.  The 
bowels  must  be  carefully  regulated,  above  all,  by  the  unsurpassed  enemata 
of  oil.  There  should  be  no  sudden  movements,  no  bending,  etc.,  for  the 
first  period. 

Subsequently  and  for  a  long  time  the  physician  should  watch  the 
abdomen  and  the  fecal  movements.  If  the  latter  are  disturbed  he  must 
ascertain  whether  intestinal  torpidity,  mechanical  obstructions  by  indura- 
tion and  adhesions,  or  new  inflammatory  irritation  is  the  reason.  In 
the  latter  case  absolute  rest,  abstention  from  food,  and,  perhaps,  according 
to  the  intensity  and  duration  of  the  symptoms,  opium,  are  indicated,  but 


CIRCUMSCRIBED  PERITONITIS,   PARTICULARLY  PERITYPHLITIS    573 

by  no  means  a  purgative.  If  intestinal  torpidity  or  obstructions  due  to 
induration,  etc.,  are  present,  mild  purgative  treatment  is  advisable,  but 
in  the  latter  case  we  must  be  careful,  above  all,  when  infectious  peri- 
typhlitic  residues  cannot  be  excluded  with  certainty.  Under  these  cir- 
cumstances it  is  obvious  that  purgative  enemata  are  often  to  be  preferred 
to  drugs  by  the  mouth. 

The  treatment  of  persistent  indurations  with  various  baths,  above  all, 
with  mud  baths,  fango,  poultices,  etc.,  is,  as  is  well  known,  often  effective. 
Satisfactory  results  are  doubtless  now  and  then  seen  from  massage,  but 
usually  it  is  productive  only  of  harm,  and  as,  up  to  the  present  time,  it 
is  impossible  to  foreknow  the  cases  in  which  it  will  be  useful  and  cer- 
tainly do  no  harm,  the  method  is  too  risky  and  should  be  rejected;  still 
more  is  this  the  case  with  horseback  riding,  bicycling,  etc.,  which  are 
now  and  then  advised. 

For  the  rest,  many  conditions  which  are  here  considered  will  also  be 
discussed  in  the  description  of  chronic  peritonitis. 


11.     CHRONIC   PERITYPHLITIS 
By  J.  BOAS,  Berlin 

As  is  the  case  with  acute  perityphlitis,  chronic  inflammations  of  the 
vermiform  process  have  multiplied  with  the  changes  produced  in  this 
realm  of  disease  by  surgical  intervention.  By  its  agency  our  formerly 
vague  conceptions  of  the  nature  and  the  course  of  inflammatory  processes 
have  assumed  definite  shape,  and  are  based  upon  exact  knowledge.  Lapa- 
rotomy has  solved  numerous  problems  which,  up  to  very  recent  times, 
still  clouded  the  teaching  of  perityphlitis,  and  solved  them  much  more 
completely  than  did  necropsy. 

Internal  medicine  with  its  greater  conservatism  followed  the  paths 
marked  out  by  laparotomy  only  slowly  and  cautiously.  But  the  impres- 
sion produced  by  surgical  successes  was  soon  profoundly  felt.  Gradually 
it  was  conceded  that  in  chronic  inflammations  of  the  cecum,  even  more 
than  in  the  acute  form,  internal  remedies  were  ineffectual.  Convinced 
by  surgical  achievements,  although  at  first  incredulous,  internal  medicine 
retreated  from  its  original  position. 

But  this  complete  change  of  view  furnished  to  internal  medicine  new 
problems  to  be  solved.  If  perityphlitis  is  not  to  become  a  mere  byplay 
in  the  operative  technic  of  many  surgical  enthusiasts,  as  to-day  appears 
to  be  the  case,  although  only  in  isolated  instances,  internal  medicine 
must  closely  unite  with  surgery  in  weighing  the  indications  and  contra- 
indications of  operative  and  internal  treatment,  and  thus  satisfactorily 
explain  their  many  contrasts.     Moreover,  it  is  the  duty  of  internal  clini- 


574      ACUTE  PERITONITIS,  APPENDICITIS,  AND  PERITYPHLITIS 

cians  to  fill  out  the  numerous  gaps  which  still  appear  in  the  teaching 
of  acute  and  of  chronic  perityphlitis. 

In  the  treatment  of  neither  form  has  the  final  word  been  spoken.  In 
acute  perityphlitis  especially,  the  revision  of  our  present  therapeutic  method 
is  all  the  more  necessary  because  here  surgical  measures  do  not  always 
avert  the  dangers  which  threaten  life. 

From  this  it  is  evident  that  in  the  teaching  of  perityphlitis  there  is 
not,  as  is  often  stated,  a  boundary  dispute  between  internal  medicine  and 
surgery  but,  on  the  contrary,  an  honorable  contest,  worthy  of  the  zeal 
of  the  most  noble  in  both  branches  of  medicine,  to  attain  the  same  end: 
To  preserve  by  the  best  possible  means  the  life  of  the  patient  who  is  in 
danger. 

From  this  point  of  view  I  shall  enter  upon  the  discussion  of  chronic 
perityphlitis,  which  with  its  frequency  and  obduracy  so  often  falls  within 
the  domain  of  the  practising  physician. 

Before  describing  the  clinical  picture  of  chronic  perityphlitis,  a  few 
remarks  may  be  in  order  regarding  the  nomenclature  of  the  disease,  par- 
ticularly since,  by  an  improper  designation,  two  fundamentally  different 
f<^rius  of  the  disease  are  \)ften  confounded  with  each  other. 

The  Americans  and  the  English  have  long  differentiated  between  two 
forms  of  chronic  appendicitis:  Relapsing  and  recurrent  appendicitis.  The 
latter  term  they  apply  to  a  recurrence  of  an  acute  attack,  while  by  re- 
lapsing appendicitis  they  mean  a  chronic  form  developing  insidiously. 
In  French  literature  these  forms  are  divided  into  appendicite  a  rechutes 
and  appendicite  a  recidives  (Talamon). 

I  recently  proposed  ^  the  designation  residiial  perityphlitis  for  that 
form  which  continues  after  an  acute  attack,  that  is,  the  recurring  form, 
and  for  the  second  form  which  runs  a  chronic  course  the  term  chronic 
recurrent  perityphlitis. 

How  important  is  the  differentiation  of  these  forms  of  perityphlitis 
will  be  seen  from  the  following: 

ETIOLOGY   OF   CHRONIC   PERITYPHLITIS 

What  is  the  origin  of  chronic  perityphlitis? 

Residual  perityphlitis  develops,  as  remarked  above,  upon  the  basis  of 
an  acute  attack.  It  may  be  stated,  as  a  law,  that  anatomically  every  acute 
attack  leaves  residua.  But  these  need  not  result  in  functional  disturb- 
ance. In  some  cases,  however,  residua  may  be  permanent,  and  continu- 
ously produce  more  or  less  severe  symptoms. 

In  the  chronic  relapsing  form  of  perityphlitis  the  conditions  are  re- 

1  Boas,  "  Ueber  die  Diagnose  und  Therapie  der  chronischen  Perityphlitis." 
Deutsohe  med.  Wochenschr.,  1905,  Nr.  27. 


CHANGES  IN  CHRONIC  INFLAMMATION  OF  THE   APPENDIX    575 

versed.  Here  the  preceding  chronic  intestinal  catarrh  forms  the  chief 
and  most  frequent  etiologic  factor. 

These  intestinal  catarrhs  may  vary  in  character.  They  may  appear  as 
an  ordinary  colitis  mucosa  or  colitis  membranacea,  or  they  may  be  ushered 
in  with  the  symptoms  of  chronic  catarrhal  diarrhea. 

Habitual  constipation,  spastic  as  well  as  atonic,  may  occasionally  be 
the  precursor  of  chronic  perityphlitis.  But  in  my  experience  actual  colitis 
is  by  far  its  most  frequent  cause. 

It  is  well  known  that,  in  a  small  number  of  cases,  the  intestinal  canal 
may  function  in  a  perfectly  normal  manner  prior  to  the  development 
of  chronic  inflammation  of  the  appendix. 

Besides  chronic  intestinal  catarrh,  in  the  female  the  uterine  adnexa 
upon  the  right  side  play  an  extraordinarily  important  role ;  ^  disease  of 
these  adnexa  may  be  communicated  to  the  vermiform  process,  or,  vice 
versa,  the  appendicular  process  may  gradually  spread  to  the  right  tube 
and  the  right  ovary.  How  often  disease  of  the  appendix  and  a  gynecologi- 
cal affection  may  simultaneously  occur  is  shown  by  the  fact  that  among 
75  gynecological  cases  Hermes  found  in  no  less  than  40,  therefore  in  53.3 
per  cent,,  demonstrable  changes  in  the  appendix. 

Furthermore,  as  has  long  been  known  of  acute  perityphlitis,  in  the 
chronic  forms  traumatic  influences  may  be  of  etiologic  significance,  and 
cause  so-called  latent  inflammation  to  become  manifest  or  irritative  con- 
ditions suddenly  to  exacerbate  into  acute  attacks.  In  the  chronic  re- 
lapsing form  not  only  acute  and  powerful  but  continuous  and  weaker 
mechanical  irritation  may  be  a  factor, 

ANATOMICAL   AND    HISTOLOGICAL   CHANGES   IN   CHRONIC 
INFLAMMATION   OF   THE   APPENDIX 

Laparotomy  has  permitted  us  a  deep  insight  into  the  changes  which 
the  diseased  appendix  and  its  surroundings  undergo  in  acute  and  chronic 
inflammation. 

According  to  the  most  recent  investigations  of  Aschoff,  the  inflamma- 
tory process  in  acute  cases  begins  in  the  crypts  of  the  mucous  membrane. 
The  pathogenic  microorganisms  which  here  collect  in  consequence  of  toxic 
action  first  damage  the  epithelium  of  the  mucous  membrane.  By  this 
effect  of  the  toxin,  or  by  the  subsequent  entrance  of  bacteria,  a  circum- 
scribed softening  of  the  muscularis  takes  place  while  macroscopically  no 
changes  are  visible  in  the  serosa  or  in  the  mucosa.     Either  these  altera- 

1  Compare  0.  Hermes,  "  Ueber  einige  Beziehungen  der  Appendicitis  zu  Erkrankun- 
gen  der  weiblichen  Genitalorgane."  Deutsche  Zeitschr.  f.  Chir.,  Bd.  L.  Also,  "  Er- 
fahrungen  liber  VerJinderungen  des  Wurmfortsatzes  bei  gyniikologisehen  Erkrankun- 
gen."  Ibid.,  Bd.  LVIII;  further,  Th.  Landau,  "  Wurmfortsatzentziindung  und  Frauen- 
leiden."  Berlin,  1904,  Aug.  Hirschwald. 
38 


576      ACUTE   PERITONITIS,   APPENDICITIS,   AND  PERITYPHLITIS 

tions  disappear  or  a  small  intramuscular  abscess  forms  which  ruptures 
into  the  peritoneum. 

During  this  perforation  the  mucosa  is  still  intact.  If  a  fecal  calculus 
is  accidentally  present  in  this  area,  it  occasionally  vaults  the  still  intact 
mucous  membrane  below  it.  The  inflammation  extends  more  deeply  into 
the  mucosa.  Diphtheritic  coating  and  softening  of  the  mucosa  appear. 
Through  the  ruptured  mucosa  the  fecal  calculus  finds  its  way.  These 
fecal  calculi  in  themselves  are  benign.  Only  when  the  vermiform  appen- 
dix is  simultaneously  affected  does  the  stone  assist  the  process  by  local- 
izing the  inflammation,  thus  promoting  a  severe  course  and  retarding  the 
process  of  healing. 

The  estimation  of  anatomical  and  histological  changes  in  chronic  re- 
lapsing inflammation  of  the  appendix  is  much  more  difficult. 

Long  ago  v.  Renvers  and  Finkelstein  pointed  out  that  anatomical  and 
liistological  changes  in  the  appendix  are  found  at  the  necropsy  of  indi- 
viduals who,  intra  vitam,  never  showed  any  disturbance  of  this  organ. 
Tn  a  remarkably  thorough  study  Tuffier  and  Jeanne  ^  lately  determined  the 
numerous  abnormalities  of  the  vermiform  process  under  normal  conditions 
in  regard  to  size,  position,  and  form.  I  think  it  advisable  to  enumerate 
some  of  the  most  important  findings  of  this  investigation. 

The  position  of  the  normal  vermiform  process  varies  from  2^  to  20 
cm.  and  more;  it  is  usually  from  7  to  11  cm.  in  length.  From  its  inser- 
tion at  the  apex  the  diameter  is  generally  uniform.  If  the  vermiform 
process  is  incised  longitudinally,  and  the  breadth  of  the  organ  is  meas- 
ured, the  width  is  found  to  be  from  4  to  17  mm. ;  upon  the  average  it  is 
from  10  to  13  mm.  Yet  there  are  many  normal  cases  in  which  the 
organ  is  club-shaped,  i.  e.,  the  diameter  increases  from  its  insertion  to  its 
free  end  so  that  the  breadth  may  be  from  3  to  6  mm. ;  more  frequently 
the  inverse  is  found,  and  the  caliber  then  gradually  decreases  toward  the 
free  end,  perhaps  to  such  an  extent  that  the  last  2  or  3  cm.  of  the  organ 
are  thready  and  resemble  thin  silk,  the  passage  finally  being  reduced  to 
ahnost  nothing. 

The  opening  of  the  vermiform  process  into  the  cecum  varies  in  differ- 
ent individuals;  it  is  circular  and  funnel-shaped. 

The  position  of  the  vermiform  appendix  is  sometimes 

below  and  parallel  to  the  ileum  =  sub-ileal ; 

anterior  to  the  ileum  =  pre-ileal ; 

posterior  to  the  ileum  =  retro-ileal ; 

below  the  cecum  =  sub-cecal ; 

posterior  to  the  cecum  =  retro-cecal ; 

1  Tuffier  and  Jeanne,  "  Etude  anatomique  sur  I'Appendice  et  la  region  il^ocoecale, 
bas^e  sur  ISO  neerojjsiees."  Revve  de  gynecologies  1899,  p.  235,  quoted  from  Th. 
Landau,  "  Wurnifortsatzentziindung  und  Frauenleiden."     Berlin,  1904,  p.  4  u.  f. 


CHANGES   IN   CHRONIC   INFLAMMATION  OF  THE  APPENDIX     577 

at  the  anterior  surface  covered  by  the  cecum  =  internal  retro-cecal ; 
anterior  to  the  cecum  z=  pre-cecal  • 

posterior  to  the  ascending  colon  =  retro-cecal  • 

beside  the  colon  =  para-cecal. 

Sometimes  the  vermiform  process  is  found  in  the  pelvis,  sometimes 
above  it. 

As  to  the  form  of  the  vermiform  process  it  is  usually  rectilinear; 
often,  however,  it  is  slightly  curved  or  bent,  sometimes  sharply  kinked 
to  form  a  right  angle,  or  it  may  be  hook-shaped  or  semilunar. 

Its  relation  to  neighboring  organs  also  varies  greatly,  and  naturally 
depends  upon  the  manner  of  insertion  but  also  to  some  extent  upon  the 
movable  cecum  and  the  position  of  the  vermiform  process  itself.  It  may 
extend  to  the  liver,  or  may  be  anterior  to  a  displaced  kidney;  sometimes 
it  may  reach  to  the  rectum  or  the  sigmoid  flexure,  at  other  times  nearly 
to  the  bladder. 

The  contents  of  the  normal  appendix  differ  both  in  quantity  and  qual- 
ity; often  a  fluid  or  soft,  doughy  mass  is  found,  sometimes  small,  hard, 
fecal  particles,  or  it  may  be  empty. 

In  regard  to  the  so-called  Gerlach  valve,  the  recent  interesting  inves- 
tigations of  V.  Hansemann  ^  show  that  its  power  of  closure  bears  an  inti- 
mate relation  to  the  presence  or  absence  of  fecal  concrements.  The  same 
is  to  a  certain  extent  true  of  regurgitation  into  the  cecum. 

The  anatomical  changes  in  chronic  relapsing  perityphlitis  are  mani- 
fold, and,  corresponding  to  the  nature  of  the  case,  they  are  relatively 
slight.  According  to  Federmann,^  whose  description  we  shall  follow,  the 
mucous  membrane  is  more  or  less  thickened.  In  the  mucosa  we  find  a 
plentiful  accumulation  of  round  cells  or  connective  tissue  proliferation 
with  swelling,  bulging  and  polypoid  excrescences  (appendicitis  polyposa). 
In  other  cases  the  decrease  of  the  glandular  tissue  leads  to  atrophy  or 
may  cause  partial  or  total  obliteration  of  the  lumen. 

In  other  instances  the  appendix  is  more  or  less  thickened,  rigid,  or 
erect,  as  Talamon  expresses  it,  often  abnormally  adherent  or  firmly  agglu- 
tinated to  its  surroundings.  Frequently,  however,  it  is  absolutely  free. 
The  lumen  of  the  rigid  structure  gapes,  and  is  filled  with  a  smeary,  mu- 
coid, or  hemorrhagico-purulent  mass  admixed  with  portions  of  feces  or  fecal 
concrements  of  disagreeable  odor.  The  mucous  membrane  is  thickened, 
moderately  tumid,  injected,  and  in  many  eases  is  covered  with  ulcers. 
The  muscular  layer  is  distributed  partly  by  inflammatory  infiltration, 
partly  by  true  labor  hypertrophy.     The  surroundings  of  the  process  are 

1  V.  Hansemann,  Mittheilungen  aus  den  Grenzgebieten  der  inneren  Medicin  und 
Chirurgie,  XI T,  p.  514,  u.  f. 

2  Federmnnn,  in  Sonnenburg,  "  Pathologie  und  Therapie  der  Perityphlitis." 
5.  Aufl.,  Leipzig,  1905,  p.  48. 


578      ACUTE  PERITONITIS,  APPENDICITIS,  AND  PERITYPHLITIS 

also  implicated.  The  appendix  is  more  or  less  adherent  to  the  cecum, 
to  the  neighboring  intestinal  coils,  and  to  the  parietal  portion  of  the 
peritoneum,  and  this  leads  to  stasis  of  secretion,  and  the  accumulation 
of  mucus  and  fecal  constituents. 

If  obstruction  occurs  during  a  time  in  which  the  cavity  of  the  vermi- 
form process  is  empty,  and  if  no  virulent  microbes  are  present  in  the 
obstructed  area,  inflammatory  processes  do  not  arise  but  the  cavity  becomes 
more  or  less  distended,  and  so-called  dropsy  of  the  vermiform  process 
sets  in.  The  glandular  apparatus  undergoes  a  gradual  retrogressive 
change,  the  epithelium  is  desquamated,  the  mucous  membrane  loses  its 
original  character,  and  all  of  its  constituents  undergo  hypertrophy.  The 
extent  of  the  dropsy  may  attain  the  size  of  a  fist.  If  during  the  time  in 
which  adhesions  are  forming  many  virulent  bacteria  are  present,  empyema 
of  tlie  vermiform  process  results,  or  a  dropsy  empyema  may  subsequently 
arise  from  secondary  infection. 

THE   CLINICAL   PICTURE   OF   CHRONIC   PERITYPHLITIS 

I.  RESIDUAL  PERITYPHLITIS 

We  have  already  stated  that  every  acute  attack  of  perityphlitis  leaves 
traces  in  the  vermiform  appendix  or  in  its  surroundings.  Nevertheless 
in  a  clinical  sense  the  affection  may  be  regarded  as  having  run  its  course 
provided  there  are  no  subsequent  attacks  or  other  sequelae.  Such  a  cure, 
however,  does  not  occur  in  the  majority  of  cases,  and  we  must  always 
count  upon  the  possibility  and  even  likelihood  of  a  relapse  soon  or  late. 
Daily  experience  teaches  us  that  the  greater  the  lapse  of  time  after  the 
first  attack  the  less  the  danger  of  a  relapse.  This,  however,  is  by  no 
means  absolutely  true,  for  under  some  circumstances  relapses  more  or  less 
severe  may  develop  years  after  the  first  attack.  Some  authors  incline 
to  the  opinion  that  this  is  not  a  true  relapse  but  a  new  attack;  yet  from 
the  fact  that  small  pus  foci  may  remain  for  years  encapsulated  in  the 
surroundings  of  the  appendix  as  well  as  that  numerous  mechanical  changes 
in  the  appendix  (obliteration,  inflammatory  thickening,  adhesion,  exu- 
dates, dropsy,  empyema)  follow  an  acute  attack,  the  view  of  an  acute 
]'t'lapse  seems  more  likely. 

A  relapse  following  an  acute  attack  may  develop  in  three  different 
ways,  as  follows : 

1.  Acute  attacks  occur  after  certain  intervals  and  these  may  differ 
entirely  from  the  first  in  severity  and  intensity.  It  must  here  be  empha- 
sized that  a  mild,  primary  attack  may  be  followed  by  very  severe  and 
rapidly  fatal,  secondary  relapses.  To  this  category  belongs  the  following 
case  wliicli  I  observed  a  few  years  ago: 

S.  B.,  a  merchant,  aged  24,  was  attacked  in  the  spring  of  1902  with  mild  peri- 
typhlitis and  moderate  fever.    Against  my  advice  the  patient  made  a  long  foot  tour 


THE  CLINICAL  PICTURE   OF  CHRONIC  PERITYPHLITIS  5?9 

of  Switzerland  in  the  following  summer.  Upon  the  3rd  of  September,  following  an 
angina  follicularis,  possibly  also  after  an  error  in  diet,  severe  pain  appeared  in  the 
abdomen,  especially  in  the  ileo-cecal  region.     The  temperature  rose  to  101.3°  F. 

When  I  saw  the  patient  the  next  day  with  the  family  physician  the  general  con- 
dition was  good.  The  temperature  was  101.1°  F.,  the  pulse  92  and  of  good  tension; 
he  had  slept  well  during  the  night.  Above  Poupart's  ligament  on  the  right  there  was 
a  moderately  dull,  tympanitic  zone  which  was  sensitive  to  pressure. 

Upon  the  5th  of  September,  1902,  there  was  jaundice  and  repeated  vomiting 
occurred,  the  vomitus  being  distinctly  hemorrhagic  (guaiac  test  positive).  Slight 
meteorism  was  present.  The  pulse  was  96,  the  temperature  102°  F.;  the  hepatic 
region  was  insensitive  to  pressure,  and  the  same  condition  was  present  in  the  ileo- 
cecal region  as  on  the  previous  day.  Considering  the  severity  of  the  case  operation 
upon  the  same  day  was  advised.  The  surgeon  was  E.  Hahn.  Finding:  Gangrenous 
appendix  with  suppuration  into  the  surroundings.  Collapse  and  death  upon  the  7th 
of  September,  1902. 

Here  we  were  dealing  with  one  of  those  quite  rare  cases  designated  by 
Dieulafoy  ^  as  vomito  negro. 

On  the  other  hand,  after  an  exceedingly  severe  case,  one  or  several 
mild  relapses  may  follow. 

The  assumption  is  obvious  that  relapses  are  the  immediate  result  of 
mechanical  conditions  (trauma,  too  great  bodily  exertion,  acute  indiges- 
tion, etc.),  but  there  are  also  cases  in  which  the  most  scrupulous  care 
in  questioning  Mall  elicit  no  clue  to  the  cause. 

2.  The  sequelae  of  an  acute  attack  are  of  exceedingly  chronic  character. 
Among  them  are  chronic  exudates  or  indurations,  adhesions  about  the 
vermiform  process,  empyema  or  dropsy,  thickening  or  kinking  of  the 
appendix,  and  other  similar  affections  of  the  appendix  or  in  its  sur- 
roundings. 

The  clinical  course  in  this  group  of  cases  is,  as  a  rule,  the  same  as 
that  of  chronic  relapsing  perityphlitis  (see  below), 

3.  The  clinical  picture  of  chronic  relapsing  perityphlitis  may  already 
exist  but  suddenly  more  or  less  severe  acute  symptoms  develop.  These 
are  probably  to  be  attributed  to  purulent  residues  or  ulcers  upon  the 
mucous  membrane  of  the  appendix,  but  even  sudden  perforation  may  be 
the  cause.  The  case  now  to  be  described,  which  at  the  same  time  proves 
that  even  after  repeated  rupture  through  the  intestine  with  discharge  of 
pus  recovery  may  occur,  is  an  illustration  of  this  form. 

Miss  L.,  from  W.,  aged  22,  whose  parents  are  living  and  well,  and  who  states  that 
she  has  always  been  healthy. 

Toward  the  end  of  February,  1903,  she  was  attacked  by  pain  in  the  region  of 
the  cecum  with  vomiting,  constipation,  and  a  temperature  of  102.2°  F.  An  abscess 
formed,  and  after  ten  days  an  incision  was  made  from  the  rectimi  and  a  tampon 
introduced.  On  incision  a  large  amount  of  pus  was  discharged.  Following  this  the 
patient  remained  in  bed  for  three  weeks  but  did  not  recuperate;  she  emaciated  so 
greatly  that  in   the   spring  she  was  sent  to  Pyrmont.      Here,  eight  days  later,  she 

1  Dieulafoy,  Bullet,  de  Vacademie  de  medec,  1901,  No,  6. 


580       ACUTE   PERITOxNITIS,   APPENDICITIS,   AND  PERITYPHLITIS 

was  again  attacked  by  symptoms  of  perityphlitis,  and  for  the  second  time  pus  was 
discharged  through  the  rectum.  Notwithstanding  this  the  pain  persisted  for  some 
time,  and  the  patient  was  confined  to  bed  for  eight  weeks.  She  gradually  recovered, 
but  continued  very  weak.     Upon  September  7th,  1903,  she  entered  a  sanatorium. 

Tlic  patient  did  not  complain  of  pain,  her  bowels  moved  regularly,  and  she  was 
clinically  treated  merely  to  improve  her  nutrition;  she  was  carefully  watched. 

Status  Prannis:  The  patient  is  small,  undeveloped,  and  emaciated,  with  scanty 
nmseuhiture  and  a  delicate  frame.  No  edema,  no  eruption,  no  enlargement  of  glands. 
Patella  reflex  increased,  pupillary  reflex  normal.     Lungs  normal. 

Heart:   Uulness  normal;  the  second  sound  markedly  accentuated  but  pure. 

Abdomen :  Only  a  small  circumscribed  area  midway  between  the  navel  and  the 
spinous  process  of  the  right  ilium  shows  slight  sensitiveness  to  pressure.  No  abnor- 
mal dulness. 

Urine  contains  neither  albumin  nor  sugar. 

Bowel  movement  well  formed  with  no  admixture  of  pus  or  mucus. 

Weight  43.5  kilograms. 

Treatment:  Alcohol  compresses  over  the  region  of  the  appendix,  rest  in  bed, 
stimulating  diet. 

Under  this  treatment  there  was  decided  improvement  and  a  marked  increase  in 
weight.  The  patient  left  her  bed  for  the  first  time  on  the  3rd  of  October,  1903.  Her 
weight  was  then  47  kilograms. 

Al)out  half-past  seven  in  the  evening  the  patient  suddenly  complained  of  severe 
pain  in  the  region  of  the  cecum.  The  temperature  was  98.2°  F.  Cold  compresses 
were  applied,  and  suppositories  of  codein  and  belladonna  were  given;  at  midnight, 
on  account  of  increasing  pain,  0.01  of  morphin  hypodermically.  The  temperature 
was   normal. 

October  4th,  1903.  The  pains  had  been  less  severe  after  the  use  of  morphin,  but 
in  the  morning  they  increased.  Treatment:  Morphin  0.01  subcutaneously  and  ice- 
bags.  In  the  ileo-cecal  region  there  was  an  area  of  resistance  about  the  size  of  a 
plate  and  markedly  sensitive  to  pressure.  The  note  upon  percussion  was  very  dull. 
The  temperature  in  'the  morning  was  99.1°  F.,  in  the  evening  100.6°  F.  An  ice-bag 
was  ordered,  also  fluid  diet,  and  15  drops  of  tincture  of  opium  every  three  hours. 

A  consultation  with  Prof.  Korte  was  held  on  the  evening  of  the  same  day.  On 
considering  the  danger  of  an  immediate  operation  and  the  fact  that  the  temperature 
was  but  slightly  elevated,  the  pulse  90  and  strong,  the  decrease  of  the  pain  and  the 
absence  of  peritoneal  symptoms,  it  was  decided  to  postpone  operation  and  to  wait 
until  the  acute  symptoms  disappeared. 

October  5th,  1903.  In  the  morning  the  condition  was  somewhat  better;  the  tem- 
perature was  98.8°  F.,  the  pulse  108.  There  was  still  sensitiveness  upon  pressure, 
especially  in  the  region  of  McBurney's  point,  and,  although  to  a  lesser  extent,  to  the 
left  of  the  navel.  The  resistance  in  the  region  of  the  cecum  was  apparently  some- 
wliat  less,  the  percussion  note  rather  dull,  but  normal  in  other  areas.  There  was  no 
singultus,  no  vomiting.     The  treatment  was  continued. 

Afternoon:  Condition  less  good;  pulse  120,  temperature  100.2°  F.  Toward  evening 
file  general  condition  worse,  pulse  128,  temperature  100.6°  F.  The  pains  in  the 
r('!,nnn  of  the  cecum  and  also  upon  the  left  side  had  become  very  severe.  Flatus  was 
]tassr(l  twice;  there  was  no  eructation,  no  vomiting.  On  account  of  the  danger  of 
jHTforation  Prof.  Korte  operated  at  10  o'clock  at  night,  the  patient  being  imder 
I'll loro form  anesthesia. 

The  posterior  surface  of  the  colon  was  covered  with  purulent  coating,  the  remain- 
ing serosa  of  the  intestine  being  smooth  and  glistening.  The  vermiform  process  was 
found  deep  down  below  the  colon  and  was  elevated,    A  point  from  which  pus  was 


THE  CLINICAL  PICTURE   OF  CHRONIC  PERITYPHLITIS  581 

discharged  could  be  recognized.  The  appendix  was  about  6  cm.  in  length,  and  greatly 
swollen ;   it  was  extirpated  in  the  usual  manner. 

Course:   Without  complications. 

The  patient  was  discharged  cured  upon  the  14th  of  November,  1903,  weighing  50.5 
kilograms. 

n.  CHRONIC   RELAPSING  PERITYPHLITIS 

>  In  contrast  with  residual  perityphlitis,  chronic  relapsing  perityphlitis 
is  of  much  milder  and  more  benign  type.  Yet  it  is  often  characterized 
by  such  an  enormous  number  of  individual  points,  variations  and  com- 
plications as  to  make  it  an  extraordinarily  interesting  affection. 

In  the  chronic  relapsing  form  of  perityphlitis  two  distinctly  different 
varieties  may  be  diagnosticated:  First,  that  running  its  course  without  an 
acute  attack,  or,  more  correctly,  acute  exacerbation,  and  secondly,  that 
in  which  the  chronic  process  is  interrupted  by  mild  attacks  now  and  then 
occurring.  In  very  rare  cases  (Rosenheim^)  of  these  forms  perforation 
is  said  to  occur  suddenly. 

However,  it  is  doubtful  whether  in  these  instances  we  are  not  dealing 
with  abortive  cases  of  residual  perityphlitis.  At  all  events  a  favorable 
and  benign  course  in  chronic  relapsing  perityphlitis  is  so  much  the  more 
frequent  that  practically  we  need  not  consider  the  previously  mentioned 
serious  eventualities. 

In  a  study  of  chronic  relapsing  perityphlitis  we  meet  with  a  number 
of  forms  w^hose  clinical  symptoms  are  so  well  characterized  that  their 
recognition  is  of  great  practical  importance. 

We  shall  begin  with  latent  perityphlitis. 

(a)  Latent  Perityphlitis. — Although  this  form  is  not  technically  the 
subject  of  professional  treatment,  we  particularly  desire  to  discuss  it, 
primarily  because  it  plays  an  important  role  in  the  prophylaxis  of  peri- 
typhlitis. These  cases  may  occur  either  in  persons  who  years  before  passed 
through  a  positive  attack  of  perityphlitis  or  in  those  who  have  never  shown 
any  of  its  symptoms.  The  patients  w^ho  consult  us  for  other  disturbances 
present  absolutely  no  symptoms  referable  to  the  ileo-cecal  region,  but 
caj-eful  and  repeated  examinations  reveal  a  very  characteristic  sensitive- 
ness to  pressure  in  this  area.  Among  106  cases  of  chronic  perityphlitis 
that  I  observed  a  year  ago  I  noted  this  latent  perityphlitis  in  23.  It  is 
true  the  differentiation  of  such  cases  is  difficult  for,  according  to  the 
reports  of  Keith,^  McBurney's  point  is  normally  sensitive  to  pressure,  but, 
like  Lennander  (loc.  cit.),  I  emphatically  deny  this. 

It  may  be  admitted  that  McBurney's  point  is  tender  on  exaggerated 
pressure,  but  a  comparison  of  this  sensitiveness  with  that  caused  by  pres- 

1  Rosenheim,  Deutsche  med.  Wochenschr.,  1905,  Nr.  27. 

2  Keith,  quoted  from  Lennwnder,  "  Meine  Erfahrungen  iiber  Appendicitis."  Mit- 
theilungen  aus  den  Grensgebieten,  1904,  Bd.  XIII,  p.  326. 


582       ACUTE   PERITONITIS,   APPENDICITIS,   AND  PERITYPHLITIS 

sure  in  the  homologous  area  upon  the  left  side  will  at  once  indicate 
whether  we  are  dealing  with  a  physiologic  or  an  abnormal  zone  sensi- 
tiveness. 

An  interesting  question  is  involved  in  the  decision  whether  acute  or 
chronic  perityphlitis  will  in  the  course  of  time  develop  from  such  latent 
cases.  In  so  far  as  I  have  been  able  to  review  the  literature,  such  transi- 
tions have  not  been  described,  but  we  must  not  overlook  the  fact  that 
these  abdominal  diseases  have  been  recognized  only  in  the  last  few  years 
by  careful  palpation  of  the  cecal  region.  The  analogous  occurrence  of  a 
latent  cholelithiasis  or  cholecystitis,  which  I  have  not  infrequently  ob- 
served, strongly  favors  a  latent  perityphlitis.  Here  I  have  several  times 
noted  the  appearance  of  acute  inflammation  or  typical  attacks. 

It  is  highly  desirable  that  clinicians  and  physicians  should  devote  more 
attention  to  the  occurrence  and  the  significance  of  latent  perityphlitis 
llian  has  thus  far  l)ecn  the  case. 

(b)  Typical  Cases  of  Chronic  Relapsing  Perityphlitis. — Probably  most 
cases  of  chronic  relapsing  perityphlitis  set  in  very  insidiously  and  without 
]ij-odronies,  and  gradually  the  symptoms  become  more  severe.  If  the 
patients  are  asked  from  what  period  of  time  they  date  their  disease  but 
few  can  give  a  satisfactory  answer,  for  the  disease  is  of  chronic  type 
from  the  onset. 

The  symptoms  vary  greatly  in  intensity.  Sometimes  drawing  pains  in 
llie  ileo-cecal  region  are  caused  by  any  motion,  or  by  bending  or  lifting, 
or  by  prolonged  sitting;  in  other  cases  there  are  only  sensations  of  pressure 
and  weight  in  the  right  abdominal  region  which  are  annoying  to  the 
patient;  sometimes  it  is  merely  a  sense  of  fatigue  after  prolonged  walk- 
ing; sometimes  the  disturbances  are  more  or  less  dependent  upon  defe- 
cation, which  in  such  cases  is  usually  irregular;  occasionally  there  are  also 
more  or  less  typical  bladder  symptoms  (tenesmus,  painful  passage  of 
urine,  etc.). 

The  previously  mentioned  disturbances  now  show  distinct  exacerba- 
tions and  remissions  which  are  probably  to  be  attributed  to  the  factors 
of  bodily  rest  and  avoidance  of  exertion  of  any  kind.  The  occupation  of 
the  patient  of  course  here  plays  an  important  role.  Those  who  are  able 
to  take  care  of  themselves  sometimes  have  intervals  of  fair  or  even  normal 
healtli  while  the  symptoms  almost  invariably  increase  in  those  whose 
circuinstances  compel  them  to  labor.  I  have  a  patient  whose  case  is 
interesting  because  his  appendicular  symptoms  were  increased  after  each 
coitus. 

In  their  objective  signs,  there  is  a  marked  difference  between  residual 
perityphlitis  and  the  pure,  chronic  form.  This  is  shown  by  the  fact  that 
in  the  residual  form  and  during  the  interval  we  not  infrequently  find 
distinct  traces  of  inflammation  which  has  run  its  course  by  palpating 
exudates,  strands,  or  thickening  in  the  ileo-cecal  region.     It  may  be  re- 


THE  CLINICAL  PICTURE  OF  CHRONIC  PERITYPHLITIS  583 

garded  as  a  rule  with  but  few  exceptions  that  when  such  plastic  changes 
in  the  region  of  the  appendix  can  be  determined  an  acute  inflammatory 
process  has  always  preceded. 

Only  under  rare  circumstances  are  these  plastic  changes  found  in  the 
true,  chronic,  relapsing  form.  Therefore,  I  do  not  concur  in  the  views 
of  H.  Herz,^  who  has  published  an  otherwise  excellent  article  concerning 
the  condition  under  discussion  and  who  states  that  the  exudate  or  the 
tumor  is  the  unmistakable  sign  of  chronic  perityphlitis; 

Here  I  wish  to  call  attention  to  the  fact  that  the  possibility  of  demon- 
strating thickening,  adhesions,  etc.,  at  or  around  the  appendix,  is  often 
greatly  overestimated.  Such  adhesive  changes  may  be  suspected  in  the 
residual  processes  of  an  acute  perityphlitis.  Since  they  occur  with  relative 
frequency  they  are  not  rarely  met  with  at  a  laparotomy,  but  under  such 
circumstances  the  diagnosis  is  merely  an  accidental  one.  If  honest,  we 
must  admit  that  only  a  distinctly  palpable  tumor  or  resistance  permits 
conclusions  in  regard  to  residual  processes.  In  my  opinion  there  is  rarely 
a  doubt  as  to  whether  or  not  resistance  is  present,  especially  in  the  ileo- 
cecal region;  but  there  may  possibly  be  a  question  as  to  its  character 
(exudate,  malignant  tumor,  ileo-cecal  tuberculosis,  or  induration). 

In  the  overwhelming  majority  of  cases  of  the  chronic  relapsing  form, 
we  find  as  an  objective  expression  of  perityphlitis  the  presence  of  a 
painful  pressure  zone  in  the  region  of  McBurney's  point. 

This  can  be  easily  found  by  drawing  upon  the  body  two  imaginary 
lines  one  of  which  connects  the  anterior  superior  spine  of  the  ilium  upon 
the  right  side  with  the  umbilicus,  and  the  other  outlines  the  external 
margin  of  the  right  rectus  muscle.  The  point  where  these  lines  intersect 
each  other  coincides  with  McBurney's  point. 

The  importance  of  McBurney's  point  in  the  diagnosis  of  perityphlitis 
will  be  more  fully  discussed  in  the  section  devoted  to  diagnosis.  Here 
I  shall  only  add  that  the  point,  or,  more  correctly,  McBurney's  zone,  is 
nothing  more  than  a  convenient  landmark. 

There  can  be  no  doubt  that  in  chronic  perityphlitis  McBurney's  point 
is  usually  sensitive  to  pressure,  and  it  would  be  a  misrepresentation  of 
facts  if  we  were  to  ignore  this  painful  zone;  in  its  intimate  relation 
to  the  other  symptoms  it  is  naturally  a  clinical  aid. 

When  the  processes  in  typical  cases  of  chronic  relapsing  perityphlitis 
show  acute  increase,  this  is  of  limited  extent.  The  temperature  is  but 
moderately  elevated  (100.4°  to  101.3°  F.),  and  upon  the  next  or  the 
succeeding  day  falls  to  the  norm.  Corresponding  with  the  temperature 
the  pulse  remains  normal  as  to  quality,  it  shows  no  intermissions,  and 
is  only  moderately  rapid.  Except  for  the  increase  of  the  ileo-cecal  pain 
the  general  condition  is  but  slightly  disturbed.     Signs  of  peritoneal  irri- 

1  E.  Herz,  Therap.  Monatshefte,  1905,  H.  3  u.  4. 


584       ACUTE   PERirONITIS,  APPENDICITIS,   AND  PERITYPHLITIS 

tation  arc  absent  (vomiting,  meteorism,  facies  peritonealis,  singultus). 
Tlie  ileo-cecal  region  itself  is  more  sensitive  to  pressure  upon  the  first  or 
second  day  of  the  disease  than  during  the  interval,  but  under  suitable 
treatment  this  tenderness  upon  pressure  either  disappears  in  from  twenty- 
four  to  forty-eight  hours  or  ameliorates  to  the  degree  present  in  the  inter- 
vening period. 

(c)  Atypical  Cases  of  Chronic  Relapsing  Perityphlitis. — There  are 
numerous  variations  from  the  type  above  described.  To  enumerate  and 
to  describe  these  would  be  to  include  an  enormous  number  of  histories. 
Nevertheless,  among  the  irregular  forms  there  are  certain  pathologic 
grou])s  with  common  and  easily  recognizable  features,  and  these  are  the 
more  important  in  practice  because  a  failure  to  observe  them  leads  to 
erroneous  therapeutic  measures. 

Appendicular  Colic. — Among  the  atypical  cases  colica  appendicu- 
laris  (colique  appendiculaire,  Talamon)  must  primarily  be  mentioned. 
Under  this  name  Talamon  was  the  first  to  describe  in  a  publication/ 
whieli  is  even  to-day  a  masterpiece,  a  form  of  chronic  perityphlitis  distin- 
guished l)y  the  following  characteristic  symptom-complex:  The  patients, 
frequently  without  a  recognizable  cause,  or  occasionally,  as  they  report, 
in  conse(iuence  of  an  error  in  diet,  are  attacked  by  severe  colic  which 
extends  over  the  entire  abdomen  (not,  as  is  stated  in  some  text-books, 
limited  to  the  ileo-cecal  region).  This  is  extraordinarily  severe  and  lasts 
from  6  to  8  hours  or  longer.  During  the  attack  the  entire  abdomen  is 
more  or  less  sensitive  and  tense,  just  as  in  the  case  of  flatulent  colic,  but 
after  the  attack  has  passed  a  sensitiveness  in  the  ileo-cecal  region  appears 
and  lasts  for  several  days — and  this  is  the  most  important  feature  in  the 
entire  symptom-complex.  This  subjective  tenderness  which  becomes 
noticeable  on  active  movements  and  even  in  walking  and  bending  over 
corresponds  to  the  extreme  tenderness  in  the  region  of  the  appendix.  But 
the  sul)jcctivc  sensations  and  the  objective  sign  of  tenderness  on  pressure 
disappear  after  a  few  days,  until  a  renewed  attack  produces  the  same 
symptoms.  Fever  and  other  changes  referable  to  inflammation  are  absent, 
as  a  rule,  in  the  ordinary  form  of  colica  vermicularis. 

What  is  the  cause  of  these  peculiar  attacks?  Most  authors  quite  prop- 
eily  attrilnite  them  to  spasmodic  contractions  of  the  appendix  which  result 
from  the  attempt  of  the  organ  to  expel  foreign  bodies,  fecal  concrements, 
or  other  substances  which  have  found  their  way  into  the  appendix  from 
the  cecum. 

A  very  interesting  case  of  this  kind  from  Wolfler's  Clinic  was  de- 
scril)ed  by  Goldbach.^ 


1  Talamon,    "  Appendicite    et    Perityphlite."      Bibliothiqtie    m^dicale,    Cha/rcot- 
Ifchovc.  Paris,  1892. 

-  (luklhach,  Prager  med.  Wochenschr.,   1898,  Nr.  16. 


THE  CLINICAL  PICTURE   OF  CHRONIC  PERITYPHLITIS  585 

A  student,  aged  16,  had  for  a  year  following  jaundice  severe  colicky  pains  under 
the  right  arch  of  the  rihs.  During  the  attack  of  pain  there  was  never  vomiting  or 
fever,  but  obstinate  constipation  was  present.  Later  the  pains  reappeared,  particu- 
larly in  the  evening;  there  was  no  pain  in  the  morning.  At  the  time  of  examination 
the  pains  were  felt  in  the  ileo-cecal  region,  the  pain  being  definitely  localized  in 
McBurney's  point.  Calculi  were  never  found  in  the  feces.  Palpation  revealed  an 
oval,  somewhat  soft  tumor  (cecum),  upon  which  an  elongated,  cylindrical  body  was 
distinctly  palpated.  This,  as  a  whole,  appeared  to  be  movable,  and  was  sometimes 
found  in  the  hepatic  region,  at  other  times  in  the  lower  abdominal  region.  The  liver 
was  not  enlarged.  At  the  operation  two  small  stones  were  found  in  the  cecum. 
If  the  stones  were  forced  toward  the  vermiform  process  they  readily  slipped  into 
this  organ  and  just  as  readily  were  returned  to  the  cecum,  which  was  absolutely 
normal.     Extirpation  of  the  appendix.     Recovery. 

Among  the  atypical  cases,  masked  (Treves)  and  larval  perityph- 
litis (Ewald)  must  be  enumerated. 

Under  the  name  of  "  masked  perityphlitis "  Treves  ^  has  described  a 
number  of  cases  in  which  there  were  absolutely  no  signs  of  perityphlitis, 
and  in  which  the  ileo-cecal  region  was  free  from  pain.  In  one  of  these 
cases  the  symptoms  were  chiefly  those  of  pylephlebitis,  while  the  necropsy 
showed  small  hepatic  abscesses  and  (as  a  primary  infection)  a  completely 
transformed  appendix  filled  with  pus.  I  recently  observed  a  case,  in  many 
respects  similar  to  this,  which  caused  great  perplexity  in  diagnosis. 

Mr.  O.  F.,  a  merchant,  aged  22,  from  Antwerp;  his  parents  were  healthy.  As 
a  child  the  patient  had  measles,  diphtheria,  and  whooping-cough,  and  five  years  ago 
enteric  fever.  From  childhood  he  had  a  tendency  to  diarrhea  in  consequence  of 
dietetic  errors.  In  June,  1903,  while  in  New  Orleans  and  after  a  slight  alcoholic 
excess,  the  patient  had  a  mild  attack  of  fever  accompanied  by  pain  in  the  gastric 
region  and  the  back  and  also  diarrhea;  the  attack  lasted  for  a  few  days  and  then 
yielded.  In  the  beginning  of  August,  1903,  a  "  mild  attack  of  colic  "  with  pains  in 
the  abdomen  and  diarrhea  occurred  very  suddenly  (without  known  cause).  In  the 
following  months  he  frequently  had  diarrhea  without  pain. 

In  March,  1904,  the  patient  had  an  attack  of  jaundice.  Prior  to  the  outbreak 
there  was  slight  malaise  for  a  few  days  and  some  fever  ("like  an  influenza"). 
Pain  was  not  present.  After  the  jaundice  had  existed  for  three  weeks,  pains  were 
felt  in  the  anus  and  also  periodic  pains  in  the  genitalia  which  radiated  to  the  anus. 
These  attacks  always  lasted  from  fifteen  to  thirty  minutes.  During  this  time  the 
patient  could  void  his  urine  only  in  drops.  After  a  few  days  the  pain  passed  away, 
and  micturition  was  normal.  The  jaundice  also  gradually  disappeared,  and  in  the 
spring  of  1904  the  patient  completely  recovered  at  Baden-Baden.  In  July,  1904,  diar- 
rhea and  vomiting  appeared  suddenly  in  the  night ;  at  first  without  pain,  but  toward 
morning  pains  were  felt  in  the  entire  abdomen,  passing  away  in  a  few  hours.  The 
patient  is  said  to  have  had  no  fever.  Three  weeks  later  there  was  sudden  severe 
pain  in  the  "gastric  region"  (left  side  of  the  abdomen),  which  later  radiated  to 
the  riffht  lotver  side  of  the  belly;  there  was  mild  fever.  The  physician  suspected 
perityphlitis.  After  three  days  the  patient  was  able  to  resume  his  occupation.  In 
August  there  was  diarrhea  with  the  passage  of  mucus  and  tenesmus.  Early  in  Sep- 
tember, 1904,  he  was  again  suddenly  attacked  by  chills  and  fever  with  severe  pains 
— _ — ___ _ — _ — . 1 

1  Treves,  "  Perityphlitis  and  Its  Varieties,"  London,  1897,  p.  37. 


586       ACUTE   PERITONITIS.   APPENDICITIS,   AND  PERITYPHLITIS 

in  the  gastric  region  (epigastrium)  which  radiated  to  the  lower  abdominal  region, 
also  vomiting.  An  injection  of  morphin  soon  relieved  the  pain,  but  for  a  few.  days 
there  was  marked  sensitiveness  below  the  right  arch  of  the  ribs  which  to  a  slight 
extent  had  existed  since  the  attack  of  jaundice  in  the  spring.  Since  the  last  attack 
there  has  been  a  tendency  to  diarrhea  alternating  with  constipation,  occasionally 
mucus  in  the  dejecta,  and  sometimes  mild  pain  in  the  right  abdominal  region  (be- 
tween the  hip  and  the  right  border  of  the  ribs). 

The  patient,  wlio  liad  made  a  journey  from  Antwerp  to  Berlin  without  difficulty, 
was  suddenly  attacked  the  first  night  with  severe  pain  in  the  abdomen  (in  the 
middle  of  the  belly  somewhat  above  the  navel)  which  soon  radiated  to  the  right 
lower  side  and  the  region  of  the  bladder,  this  being  accompanied  by  bilious  vomiting 
and,  toward  morning,  by  chills.  The  temperature  rose  to  101.7°  F.,  the  pulse  was 
104.  but  regular,  full,  and  of  good  tension.  The  abdomen  was  retracted;  the  walls 
sliowed  only  moderate  tension.  Just  above  the  navel  the  belly  was  very  sensitive 
to  pressure.  The  ileocecal  region  and  the  other  parts  of  the  abdomen  were  moder- 
ately tender  to  ordinary  pressure. 

Tlie  liver  and  gall-bladder  were  not  palpable,  nor  painful  on  pressure.  The  splenic 
dulness  was  normal,  the  organ  could  not  be  palpated.  The  urine  was  clear  and  free 
from  albumin  and  sugar.  Digital  rectal  examination  was  very  painful,  the  prostate 
gland  slightly  enlarged;  otherwise  nothing  abnormal  could  be  palpated.  Lungs  and 
heart  normal. 

The  fever  continued  for  several  days;  the  pulse  was  always  regular  and  full, 
the  greatest  rapidity  being  108.  After  the  2nd  of  November  the  abdomen  was  mod- 
erately distended.  Above  the  navel  and  also  in  the  region  of  the  sigmoid  flexure 
there  was  extreme  tenderness  both  spontaneously  and  on  pressure,  but  pressure  in  the 
ileocecal  region  evoked  no  actual  pain,  nor  was  there  pain  upon  pressure  in  the 
region  of  the  liver  and  gall-bladder.  The  pains  above  the  navel  radiated  downward 
to  the  bladder  region.  Up  to  the  4th  of  November  neither  feces  nor  flatus  were 
passed.  After  intestinal  irrigation  there  was  a  slight  fecal  evacuation  accompanied 
by  vomiting.  Pain  was  everywhere  produced  on  pressure,  and  was  most  marked 
above  the  navel.  Upon  the  5th  of  November  the  bowels  moved  freely;  the  abdomen 
was  no  longer  distended  but  soft,  although  painful  upon  pressure  above  the  navel, 
and  somewhat  less  so  in  the  region  of  the  sigmoid  flexure;  other  areas  not  painful. 
The  temperature  returned  to  the  norm  and  remained  so  for  a  few  weeks  except  for  a 
transitory  rise  in  consequence  of  catarrhal  tonsillitis.  The  patient  constantly  had 
lleeting  pain  in  the  abdomen  which  radiated  from  the  middle  of  the  epigastrium 
down  to  the  bladder  and  the  ileo-cecal  region.  Upon  pressure  in  the  latter  area  there 
was  but  little  pain,  but  this  pressure  invariably  produced  pain  in  the  epigastrium 
and  sometimes  in  the  region  of  the  bladder.  At  the  end  of  urination  also  there  was 
frequently  slight  pain  in  the  bladder.  The  urine  was  somewhat  turbid;  the  sedi- 
ment contained  sodium  urate  and  isolated  bladder  epithelia.  The  bowels  moved 
daily,  the  dejecta  were  formed,  and  on  rare  occasions  were  admixed  with  a  little 
mucus  (immediately  after  the  attack  the  mucus  was  considerable).  The  patient 
recovered  witliin  the  next  week,  gained  5  kilograms  in  weight,  was  out  of  bed,  and 
liad  taken  two  carriage  drives  when,  upon  the  morning  of  the  12th  of  December, 
tliere  was  sudden  severe  pain  in  the  bladder  region  and  in  the  radix  penis  accom- 
])anied  by  bilious  vomiting.  The  temperature  rose  above  100.4°  F.  The  abdomen 
was  retracted,  tense,  and  everj'^vhere  painful  on  pressure,  particularly  in  the  bladder 
rt'jjion  over  the  symphysis.  Pressure  over  the  liver  and  gall-bladder  was  not  espe- 
cially painful.  At  the  termination  of  urination  there  was  intense  pain  in  the  blad- 
der whicli  radiated  to  the  epigastrium.  The  urine  showed  nothing  abnormal.  The 
pulse  was  124,  and  full  and  strong.  Rectal  examination  and  palpation  revealed 
nothing  abnormal.     After  an  injection  of  niorphin  the  pains  ceased  for  a  short  time. 


THE  CLINICAL  PICTURE  OF  CHRONIC  PERITYPHLITIS  587 

Tlie  temperature  continued  liigh  for  the  next  few  days,  the  abdomen  tense  and  pain- 
ful, especially  in  the  bladder  region,  more  so  upon  the  right  side  than  upon  the 
left,  and  very  tender  upon  pressure.  Nothing  abnormal  could  be  palpated.  The 
pulse  was  invariably  full  and  strong,  the  pulse  rate  as  high  as  132.  Up  to  Decem- 
ber loth,  notwithstanding  oil  enema ta  and  the  introduction  of  an  intestinal  tube, 
neither  feces  nor  flatus  were  passed,  and  upon  the  14th  vomiting  and  eructations 
were  frequent.  Upon  the  15th  of  December,  after  two  profuse  intestinal  irrigations 
with  soap-suds  a  large  amount  of  feces  and  flatus  was  discharged.  The  abdomen 
became  soft.  The  bladder  region  was  still  painful  upon  pressure.  The  temperature 
fell  to  normal.  Sensitiveness  in  the  epigastrium  (spontaneous  and  on  pressure)  con- 
tinued, as  well  as  severe  pain  on  pressure  immediately  over  the  symphysis,  and  more 
marked  upon  the  right  than  upon  the  left  side.  The  ileo-cecal  region  and  the  region 
of  the  liver  and  gall-bladder  showed  no  tenderness.  The  abdomen  revealed  nothing 
abnormal  upon  palpation  or  rectal  examination.  At  the  termination  of  micturition, 
as  well  as  prior  to  defecation,  there  was  still  occasional  pain  in  the  bladder  region. 
A  tentative  diagnosis  was  made  of  appendicitis,  the  appendix  being  displaced  down- 
ward and  adherent  to  the  bladder.  Operation  was  advised.  Upon  the  25th  of  De- 
cember there  was  another  slight  rise  in  temperature.  On  the  27th  the  patient  was 
admitted  to  Prof.  Korte's  Clinic,  where,  in  an  examination  under  an  anesthetic,  noth- 
ing abnormal  could  be  found.  Operation  was  performed  by  Prof.  Korte  upon  the 
2nd  of  January,  1905.  Under  chloroform  anesthesia  an  incision  was  made  in  the 
median  line  above  the  navel  and  extending  two  fingerbreadths  above  the  symphysis. 
The  omentum  was  found  to  be  adherent  to  the  pelvis,  the  cecimi  adherent  to  the 
bladder,  the  appendix  was  displaced  dowTiward  into  the  pelvis  behind  the  bladder  and 
there  adherent  to  the  bladder.  Tlie  adhesions  of  the  omentum  to  the  bladder  were 
broken  up  as  well  as  the  adhesion  of  the  omentum  to  the  sigmoid  flexure.  Upon 
loosening  the  appendix,  perforation  occurred  at  the  base  of  the  organ  and  a  fecal  cal- 
culus exuded.  Amputation  of  the  appendix.  In  the  pelvis  a  small  abscess  was 
opened  in  loosening  the  adhesions.  Coils  of  the  small  intestine  adhered  to  each  other, 
and  their  dissolution  was  impossible  on  account  of  the  extent  of  the  adhesions.  The 
serosa  of  the  intestines  was  reddened;  in  some  areas  there  were  small  whitish  nodules 
(tubercles?).  Gall-bladder:  No  adhesions;  no  stones  could  be  palpated.  In  the  liver, 
so  far  as  it  could  be  palpated,  there  was  nothing  abnormal.  The  abdominal  walls 
were  sutured  with  drainage.  Near  the  base  of  the  appendix  which  was  opened  an 
ulceration  the  size  of  a  pea  was  found,  and  this  had  perforated  when  the  organ 
was  removed.  The  appendix  contained  purulent  feces.  The  muscularis  and  sub- 
mucosa  were  thickened. 

Recovery  was  slow,  but  there  was  no  complication  except  a  suture  abscess.  The 
highest  temperature  range  was  from  98.6°  to  100.4°  F.  Upon  February  18th,  1905, 
the  patient  was  discharged  well.  The  intestinal  function  was  somewhat  torpid  but 
otherwise  normal. 

According  to  Treves,  in  numerous  other  eases  there  are  no  symptoms 
which  point  to  perityphlitis,  but  they  chiefly  indicate  general  dyspepsia 
(loss  of  appetite,  constipation,  occasional  vomiting).  The  abdomen  is 
somewhat  distended,  feels  tense,  and  is  frequently  the  seat  of  indefinite 
colicky  pains.  Fever  is  either  absent  or  is  but  slight.  Upon  deep  pressure 
in  the  right  iliac  fossa  there  may  possibly  be  some  sensitiveness.  The 
swelling  may  be  in  the  impacted  cecum,  the  intestinal  contours  being 
sharply  defined.  The  cases  run  an  indefinite  course  until  the  diagnosis 
is  confirmed  by  the  detection  of  an  abscess. 


588      ACUTE  PERITONITIS,  APPENDICITIS,  AND  PERITYPHLITIS 

As  is  obvious,  the  group  last  described  bears  a  certain  similarity  to 
the  cases  designated  by  Ewald  ^  as  pebityphlitis  larvata.  In  this  form 
also  there  are  atypical  gastric  and  intestinal  symptoms  of  varying  nature 
and  intensity  but,  in  contradistinction  to  the  masked  cases  of  Treves,  in 
perityphlitis  larvata  there  is  an  evident  sensitiveness  to  pressure  in  the 
ileo-cecal  region.  Such  atypical  cases  are  by  no  means  rare,  and  can  be 
correctly  diagnosticated  only  when,  as  already  remarked,  the  area  of  the 
appendix  is  carefully  palpated  in  every  case  of  visceral  disease. 

In  my  article  quoted  above  ^  I  have  called  attention  to  another  variety 
of  atypical  perityphlitis  distinguished  by  this  feature:  That  the  patients 
complain  little  of  distress  in  the  ileo-cecal  region  but,  on  the  contrary, 
refer  their  symptoms  to  the  hepatic  region,  while  here  objective  examina- 
tion reveals  normal  conditions,  but  extreme  sensitiveness  to  pressure  at 
McBurney's  point. 


COMPLICATIONS   OF   CHRONIC  PERITYPHLITIS 

In  the  residual  as  well  as  in  the  relapsing  forms  of  perityphlitis  com- 
plications frequently  set  in.  In  the  former  they  may  under  some  circum- 
stances so  completely  dominate  the  pathologic  picture  that  the  actual  focus 
of  the  disease  is  masked.  To  this  category  belong  the  dreaded  hepatic 
abscess  and  pyopneumothorax  subphrenicus,  secondary  pleurisy  and  pneu- 
monia, and  the  embolic  processes  in  the  lungs  which  develop  in  the  course 
of,  or  after  an  operation  for,  acute  or  residual  perityphlitis. 

This  by  no  means  exhausts  the  number  or  the  varieties  of  the  com- 
plications; were  we  to  attempt  at  this  point  to  give  a  comprehensive 
description  of  this  grave  disease  which  so  frequently  threatens  life,  it 
would  be  necessary  to  describe  the  entire  pathology  of  acute  perityphlitis. 

We  shall  lipiit  ourselves  to  mentioning  a  restricted  number  of  the 
complications  of  chronic  perityphlitis. 

Here  two  groups  are  alike  interesting:  Chronic  catarrh  of  the  colon 
and  (in  woinen)   diseases  of  the  right-sided  adnexa. 

In  regard  to  the  first,  catarrh  of  the  colon  in  its  various  forms  and 
manifestations  is  among  the  most  frequent  and,  we  may  almost  say,  daily 
accompanying  symptoms.  Here  we  must  discuss  the  question  in  how  far 
colitis  is  the  cause  or  the  effect  of  chronic  perityphlitis.  We  must  admit 
that  catarrh  of  the  colon  precedes  as  well  as  follows  perityphlitis,  and  in 
such  a  manner  that  the  bland  diet  necessitated  and  the  lack  of  sufficient 
bodily  exercise  leads  to  habitual  constipation  and  gradually  to  true  catarrh. 

The  second  group  of  complications  relates  to  diseases  of  the  female 
genital  organs,  especially  of  the  right-sided  adnexa.     It  is  not  within  my 

•  Eirnhl,  "  Die  Krankheiten  des  Darmes  und  des  Bauchfells,"  Berlin,  1902,  p.  237. 
'Boas,  Deutsche  med.  Wochenschr.,  1905,  Nr.  27. 


THE  CLINICAL  PICTURE  OF  CHRONIC  PERITYPHLITIS  589 

province  to  describe  minutely  these  serious  affections.  Those  who  desire 
detailed  information  are  referred  to  the  instructive  and  exhaustive  mono- 
graph of  Th.  Landau,  which  is  a  critical  analysis  of  extraordinary  merit. 

According  to  Th.  Landau,  besides  the  true  diseases  of  the  adnexa,  the 
ovarialgia,  the  retroflexioversio  uteri  mobilis,  and  the  dislocated  right 
kidney  may  be  combined  with  perityphlitis,  and  thus  mask  the  actual 
underlying  affection. 

Besides  these  most  common  maladies,  there  are  many  others  which 
may  accompany  perityphlitis.  First  to  be  mentioned  here  are  calcareous 
processes  of  the  right  kidney  and  of  the  gall-bladder,  which,  more  fre- 
quently than  we  are  prone  to  believe,  cause  errors  in  diagnosis.  Further- 
more, as  already  stated,  there  may  be  a  dislocated  right  kidney  as  well 
as  perityphlitis,  and  if  the  symptom-complex  be  not  typical  this  may  make 
a  differential  diagnosis  either  perplexing  or  impossible.  We  shall  discuss 
these  difficulties  more  minutely  in  the  section  devoted  to  diagnosis. 


DIAGNOSIS  AND  DIFFERENTIAL  DIAGNOSIS  OF  CHRONIC  PERITYPHLITIS 

The  diagnosis  of  chronic  perityphlitis  may  be  easy,  even  to  the  novice, 
or,  inversely,  may  present  to  the  most  experienced  great  and  occasionally 
even  insurmountable  difficulty. 

Starting  from  the  principle,  which  has  been  reiterated,  that  residual 
perityphlitis  and  chronic  relapsing  perityphlitis  are  two  clinically  different 
forms,  we  shall  enunciate  the  fundamental  laws  regarding  the  first  men- 
tioned group. 

Here,  primarily,  the  history  must  be  regarded  as  the  decisive  factor. 
The  more  clearly  this  reveals  the  occurrence  of  a  prior  typical  attack  the 
more  readily  can  we  decide  as  to  the  nature  of  the  possible  acute  relapse. 
Nevertheless,  experience  shows  that  milder  attacks  are  frequently  forgotten 
by  the  patient,  especially  if  they  have  occurred  a  long  time  previously. 
If  the  patient  is  a  very  young  person,  we  frequently  find  that  such  mild 
attacks  have  not  been  recognized  by  the  physician  owing  to  the  insignifi- 
cant symptoms,  hence  in  a  given  case  an  existing  attack  may  not  be  re- 
garded as  a  relapse  but  as  a  primary  attack. 

Aside  from  this,  in  all  essential  points  the  diagnosis  of  residual  peri- 
typhlitis in  its  acute  form  is  evolved  as  in  the  primary  attack.  Besides 
this,  however,  as  mentioned  before,  the  chronic  residua  must  be  consid- 
ered. In  the  discrimination  of  these  the  prior  history  of  the  patient 
is  the  best  guide.  The  occurrence  of  fever  and  of  the  febrile  movement, 
the  duration  and  severity  of  the  attack,  and  possible  complications  are 
especially  valuable  aids  to  the  recognition  not  only  of  the  nature  but  also 
of  the  intensity  of  the  process. 

These  are  the  cases  also  in  which,  following  the  acute  attack,  objective 
symptoms  persist  which  can  be  demonstrated  with  more  or  less  accuracy. 


590      ACUTE  PERITONITIS,   APPENDICITIS,   AND  PERITYPHLITIS 

The  region  of  McBurney's  point  is  probably  sensitive  to  pressure,  but 
in  its  surroundings  we  find  at  the  same  time  a  certain  amount  of  thick- 
ening which  may  be  demonstrated  even  on  very  slight  percussion.  In  some 
cases  an  exudate  may  be  felt.  According  to  Ewald  ^  and  Sonnenburg  * 
this  is  said  to  become  prominent  after  inflation  of  the  colon. 

Sometimes  the  differentiation  between  an  exudate  and  a  neoplasm  is 
extremely  difficult,  and  casuistry  furnishes  a  number  of  instances  in  which 
laparotomy  or  the  necropsy  has  revealed  numerous  fundamental  errors  and 
confusions. 

Among  the  most  serious  conditions  leading  to  mistakes  are  carcinoma 
of  the  cecum  and  ileo-cecal  tuberculosis. 

In  fact  these  affections,  provided  positive  symptoms  and  a  clear  history 
do  not  guide  the  physician,  run  their  course  with  manifestations  which 
closely  resemble  chronic  perityphlitis. 

In  the  following  we  will  present  a  few  principles  for  the  differentiation 
of  these  clinical  pictures  the  prognosis  of  which  varies  so  greatly,  but  in 
which,  however,  we  cannot  deny  that  no  differentiating  factors  will  invari- 
ably protect  us  from  error. 

Cecal  Tuberculosis. — Cecal  tuberculosis  usually  occurs  in  comparative 
youth  (from  the  second  to  the  fourth  decade),  runs  an  exceedingly  chronic 
course,  and  frequently,  although  by  no  means  always,  is  accompanied  by 
tul)erculous  processes  in  the  lungs.  As  Obrastzow  correctly  points  out, 
tl)o  cecum  does  not  form  an  actual  tumor,  but  has  the  appearance  of  a 
rigid,  irregular,  nodular  infiltration.  Cecal  tuberculosis  invariably  runs 
its  course  with  symptoms  of  stenosis  which  in  such  cases  are  revealed  in 
a  typical  manner  (well  developed  intestinal  peristalsis,  alternation  between 
constipation  and  diarrhea,  attacks  of  obstruction).  Blood  and  pus  are 
rarely  present  in  the  feces,  but  tubercle  bacilli  may  be  frequently  found. 
Fever  is  rare. 

Carcinoma  of  the  Cecnin. — As  a  rule,  in  carcinoma  of  the  cecum  which 
usually  occurs  late  in  life  the  tumor  is  sharply  limited.  Symptoms  of 
stenosis  may  be  absent,  or  may  be  present  in  a  greater  or  less  degree. 
Fresli  or  occult  blood  (Boas  ^)  appears  in  the  feces  in  from  10  to  15 
per  cent,  of  all  cases;  pus  is  either  not  found  or  is  exceedingly  rare. 
Fever  may  occur  in  carcinoma  of  the  cecum,  but  only  in  advanced  stages 
of  the  affection. 

Where  there  is  no  thickening,  tumor  formation,  or  even  symptom  of 
stenosis,  the  only  objective  sign  is  sensitiveness  to  pressure  in  the  ileo- 
cecal region. 

In  rare  cases,  to  find  at  the  autopsy  an  inflammatory  or  even  malignant 

1  K)cahl.  "  Die  Krankheiten  dos  Darmes  und  des  Bauchfells,"  Berlin.  1902. 
-  Sonnenhurg,  "  Pathologie  und  Therapie  der  Perityphlitis,"  5  Aufl.,  Leipzig,  1905. 
•'!  Boas,   "  Ueber  occulte  Magen-   und  Darmblutungen."      Volkmann's   Sammlung 
kiin.  \ortruge,  1905,  Nr.  387. 


THE  CLINICAL  PICTURE  OF  CHRONIC  PERITYPHLITIS  591 

tumor  instead  of  the  expected  perityphlitis  is  an  experience  from  which 
even  the  most  skilful  diagnostician  is  not  exempt. 

In  these  and  other  doubtful  cases  I  must  call  attention  to  a  factor 
that  aids  materially  in  the  diagnosis  of  residual  perityphlitis:  This  is  a 
regular  temperature  record  continued  for  weeks,  and  especially  the  com- 
parison of  temperatures  taken  simultaneously  in  the  axilla  and  in  the 
rectum.  A  copy  is  here  presented  of  a  temperature  curve  which  clearly 
portrays  these  differences. 

I  have  been  several  times  convinced  that,  under  some  circumstances, 
these  more  or  less  high  elevations  of  temperature,  and  especially  the  simul- 
taneous rectal  and  axillary  temperatures,  form  the  only  guiding  and 
determining  symptom.     The  following  case  may  serve  as  an  example: 

A  girl,  aged  4,  daughter  of  a  manufacturer  from  G.  Following  a  doubtful  acute 
perityphlitis  she  complained  of  periodic  abdominal  pains  which  lasted  but  a  few 
seconds  and  occasionally  ceased  after  vomiting.  Localization  of  the  pain  was  impos- 
sible. The  objective  finding  was  entirely  negative,  the  region  of  the  cecum  being 
painless  upon  pressure.  Regular  and  continuous  records  of  the  temperature  showed 
occasional  falls  or  elevations  of  brief  duration.  A  diagnosis  of  residual  perityphlitis 
was  accordingly  made  and  the  child  was  operated  upon  by  Prof.  Korte.  The  opera- 
tion revealed  the  following : .  In  the  mesentery  a  swollen  gland  which  was  extirpated. 
The  appendix  was  about  10  cm.  in  length,  contained  semisolid  feces,  and  in  the  center 
a  mucous  membrane  cicatrix.  The  cecum  and  ascending  colon  Were  palpated  and 
found  to  be  normal.     Course  normal;  discharged  cured. 

While  in  residual  perityphlitis  the  prior  history  will  usually  give  us 
valuable  data  for  the  diagnosis,  in  the  chronic  relapsing  form  we  must 
depend  principally  upon  the  clinical  course.  Frequently  this  ensures  a 
diagnosis;  but  there  are  also  cases  so  faintly  characterized  that  only 
repeated  and  thorough  examinations  will  enable  us  to  come  to  a  decision. 
Among  the  diagnostic  factors  which  favor  chronic  perityphlitis  the  most 
prominent  are  the  characteristic  subjective  symptoms:  The  persistent  pains 
starting  from  the  ileo-cecal  region  and  centrifugally  radiating  to  the  thigh, 
to  the  lumbar  and  the  hepatic  regions.  Among  the  objective  symptoms, 
as  already  mentioned,  there  is  frequently  nothing  but  the  sensitiveness  at 
McBurney's  point. 

In  some  cases  another  phenomenon  appears  upon  palpation,  which  at 
this  point  must  be  described  somewhat  more  explicitly  since  it  is  fre- 
quently and  variously  referred  to  in  literature:  This  is  palpation  of  the 
diseased  vermiform  process.  The  American  surgeon,  Edebohls,  deserves 
credit  for  having  called  attention  to  the  possibility  of  palpating  the  dis- 
eased vermiform  process,  and  in  1894  he  made  the  statement  that  this 
organ  could  be  recognized  in  every  case  of  perityphlitis. 

That  this  assumption  is  not  borne  out  by  the  facts  can  to-day  scarcely 

be  doubted  by  physicians  of  experience.     In  cases  of  acute  perityphlitis 

the  swelling  of  the  mesentery,  the  appearance  of  the  exudate,  etc.,  make  the 

conditions   for  palpating  the  diseased   appendix   extremely  unpropitious. 

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THE  CLINICAL  PICTURE  OF  CHRONIC  PERITYPHLITIS  593 

The  circumstances  are  somewhat  more  favorable  for  palpating  the  appen- 
dix in  chronic  perityphlitis,  a  fact  to  which  some  authors  (Ewald,  Haus- 
mann)   have  attached  a  certain  diagnostic  significance. 

In  these  instances  we  may  admit  that  now  and  then  when  the  vermi- 
form process  is  in  a  favorable  position  it  may  be  felt  as  a  round,  painful 
organ,  sometimes  with  surprising  distinctness.  Nevertheless,  dozens  of 
cases  of  chronic  perityphlitis  may  be  observed  in  which  the  result  of 
palpation  is  not  only  once  but  repeatedly  negative.  In  other  cases  in 
which  we  think  that  something  is  palpated,  the  body  that  is  felt  cannot 
be  clearly  recognized,  and  we  waver  in  opinion  between  the  assumption 
of  a  contracted  portion  of  the  colon,  of  a  coil  of  the  ileum,  of  adhesive 
intestines,  or  of  the  rolled-up  mesentery,  etc. 

At  all  events,  in  my  experience  palpation  of  the  diseased  appendix  is 
only  of  diagnostic  importance  if  we  constantly  find  in  the  ileo-cecal  region 
a  distinctly  palpable  body  which  is  sensitive  to  pressure,  and  which  is  of 
the  same  form  and  thickness  as  the  vermiform  process.  In  such  isolated 
cases,  of  course,  the  diagnosis  may  be  much  more  readily  made. 

The  actual  difficulties  in  the  diagnosis  of  chronic  perityphlitis  depend 
upon  our  distinguishing  this  from  other  chronic  forms  of  colitis,  as  well  as 
upon  the  differentiation  from  chronic  disease  of  the  uterine  adnexa. 

In  the  great  majority  of  cases  the  condition  in  the  former  is  such  that 
we  must  decide  whether  merel}'  colitis  is  present  or  whether  this  coexists 
with  chronic  perityphlitis. 

The  differentiation  is  extremely  difficult  when  the  chronic  colitis  has  its 
seat  in  the  cecum,  i.  e.,  when  a  true  chronic  typhlitis  exists.  Then  a  symp- 
tom picture  may  develop  which  nowise  differs  from  chronic  perityphlitis. 
As  a  matter  of  fact  the  diseases  may  exist  simultaneously. 

The  condition  is  somewhat  more  favorable  when  the  colitis  occurs  in 
a  more  peripheral  section  of  the  colon,  and  when  a  severe  but  circum- 
scribed pain  upon  pressure  is  produced  in  the  ileo-cecal  region.  If  the  clin- 
ical picture  of  perityphlitis  is  simultaneously  present,  we  can  hardly  doubt 
their  coexistence. 

The  diagnosis  is  facilitated  if  acute,  mild,  febrile  exacerbations  appear 
similar  to  those  which  occur  in  the  course  of  chronic  relapsing  perityph- 
litis; this  impresses  the  stamp  of  certainty  upon  the  previously  doubtful 
case. 

Nevertheless  it  cannot  be  denied  that  in  a  not  inconsiderable  percentage 
of  cases  doubts  will  arise  which  cannot  be  removed  even  by  careful  investi- 
gation and  observation. 

To  this  category  belong,  for  example,  the  apparently  not  rare  cases 
of  so-called  pseudo-perityphlitis  to  which  Nothnagel  ^  first  called  attention, 
and  which  all  experienced  physicians  have  met  with. 

^Nothnagcl.  Wien.  klin.  Wochenschrift .  1899,  Nr.  15;  compare  also  O.  Singer, 
"  Pseudoappendicitis  und  lleococalschmerz,"  Wien  und  Leipzig,  1905. 


594      ACUTE  PERITONITIS,  APPENDICITIS,  AND  PERITYPHLITIS 

We  are  not  always  in  a  position  to  verify  our  diagnosis  by  operation, 
as  was  the  case  with  Nothnagel.  Nevertheless,  there  are  some  symptoms 
which  may  be  looked  upon  as  landmarks  in  the  differential  diagnosis  be- 
tween true  and  pseudo-perityphlitis.  Paramount  among  these  is  the 
course:  At  certain  irregular  intervals  the  patients  suffer  from  pain  in  the 
ileo-cecal  region,  but  this  is  not  associated  with  rises  in  temperature  and 
is  not  increased  by  active  or  passive  movements.  The  region  of  the  appen- 
dix is  either  insensitive  to  pressure  or  the  sensitiveness  is  only  referred  to 
the  skin,  and  it  is  not  circumscribed  but  diffuse.  Occasionally  cutaneous 
hyperesthesia  alternates  with  normal  sensation  upon  pressure. 

I  recently  had  an  opportunity  of  observing  a  very  instructive  case  of 
well-developed  typhlophohia.  In  a  family  which  was  well  known  to  me 
for  years  a  fatal  case  of  severe  acute  perityphlitis  had  occurred  in  a  near 
relative.  This  case  was  for  weeks  the  subject  of  conversation  in  the  family, 
and  one  of  the  two  daughters  of  the  house,  a  girl  aged  fourteen,  became 
espt^cially  concerned  and  uneasy.  A  short  time  afterward  she  complained 
of  severe  pain  in  the  region  of  the  cecum,  lost  her  appetite,  remained 
away  from  school,  became  anxious,  and  caused  her  mother  a  great  deal  of 
worry.  The  history  showed  that  the  child  had  never  had  fever.  Exami- 
nation of  all  parts  of  the  abdomen  revealed  absolutely  no  sensitiveness  nor 
resistance,  and  the  adduction  of  the  thigh  which  was  several  times  at- 
tempted produced  no  pain.  This  proved  that  there  could  be  no  question 
of  perityphlitis.  I  quieted  the  anxious  patient,  and  advised  her  to  return 
to  school  the  next  day  and  to  consider  herself  as  well.  From  this  moment 
the  child  was  well  and  remained  so. 

Besides  organic  and  neuralgic  intestinal  affections,  in  the  female  the 
differentiation  of  diseases  of  the  adnexa  may  come  into  question  in  a  diag- 
nostic respect.  We  have  already  indicated  the  possibilities  which  exist, 
and  at  this  point  attention  must  be  called  to  the  necessity  of  considering 
these  symptomatically  with  chronic  perityphlitis,  for  these  genital  affec- 
tions may  be  quite  analogous.  In  the  diagnosis  of  inflammation  of  the 
adnexa  a  considerable  degree  of  practice  and  experience  is  a  prerequisite, 
tlierefore  in  cases  at  all  doubtful  the  opinion  of  a  gynecologist  should  be 
sought. 

Besides  these  factors  which  dominate  the  differential  diagnosis  of 
clironic  perityphlitis,  there  are  still  others  which  now  and  then  come  into 
(juestion. 

Among  these  are  cases  of  calculus  in  the  right  kidney  or  of  the  uric 
acid  diathesis.  The  regular  finding  of  abnormal  amounts  of  uric  acid 
combined  with  small  amounts  of  albumin  in  the  urine,  the  appearance  of 
typical  attacks  with  their  characteristic  urinary  changes,  the  demonstra- 
tion of  a  gouty  substratum  in  characteristic  areas  of  the  body,  and  the 
pal])ation  of  the  kidney  itself  will  in  many  cases  reveal  the  correct  diagno- 
sis.    Nevertheless,  the  ensemble  of  the  previously  mentioned  symptoms  is 


THE  CLINICAL  PICTURE   OF  CHRONIC   PERITYPHLITIS  595 

not  always  so  favorable  that  the  underlying  condition  can  be  clearly  dis- 
cerned. 

With  reference  to  the  kidney,  its  dislocation,  at  least  so  far  as  sub- 
jective factors  are  concerned,  may  produce  symptoms  which  to  a  certain 
extent  resemble  those  of  chronic  perityphlitis.  But  no  actual  attacks  are 
observed,  there  is  no  t^'pical  pressure  point  in  the  ileo-cecal  region,  and  the 
characteristic  localization  of  the  pains  is  also  lacking. 

Atypical  cases  of  cholelithiasis  and  of  cholecystitis  may  be  confounded 
with  chronic  perityphlitis,  particularly  as  they  are  not  infrequently  com- 
bined in  the  same  individual.  To  this  must  be  added  another  source 
of  error,  the  not  rare  coexistence  of  cholelithiasis  and  colitis.  An  accu- 
rate history  combined  with  cautious  and  repeated  examinations  of  the 
liver  and  the  region  of  the  gall-bladder  and  the  occasional  finding 
of  biliary  coloring  matter  in  the  urine  will  often  clear  the  complicated 
picture. 

Finally,  we  must  mention  the  not  infrequent  possibility  of  error 
from  the  presence  of  ill-defined  hernia,  particularly  of  right-sided  in- 
guinal and  crural  hernia.  I  have  several  times  seen  cases  of  supposedly 
chronic  jjerityplilitis  which  were  permanently  cured  by  wearing  a  hernial 
truss. 

This  by  no  means  exhausts  the  number  of  perplexities  which  may  arise 
in  differential  diagnosis,  but  from  what  has  been  stated  it  is  obvious  that 
in  some  cases  the  diagnosis  of  chronic  perityphlitis  requires  considerable 
acumen,  practice,  and  experience. 

One  factor  in  particular  must  not  be  omitted  from  consideration, 
namely,  that  chronic  perityphlitis  may  appear  simultaneously  with  or  inde- 
pendently of  diseases  of  other  organs.  Sometimes  we  are  inclined  to  fol- 
low an  old  rule  and  to  substitute  one  or  more  pathologic  varieties  for  each 
other.  But  nature  does  not  sanction  such  a  method,  and  we  must  there- 
fore consider  not  only  whether  one  or  the  other  affection  is  present  but — 
this  is  often  the  most  difficult  problem — whether  they  do  not  exist  inde- 
pendently of  each  other. 


PROGNOSIS  OF  CHRONIC  PERITYPHLITIS 

In  this  article  we  have  repeatedly  called  attention  to  the  fact  that  the 
prognosis  in  residual  and  in  chronic  perityphlitis  presents  fundamental 
differences.  This  is  evident  from  the  etiology  of  both  forms  of  the  dis- 
ease. While,  as  is  shown  by  the  fitting  designation  of  Sahli,  in  acute 
perityphlitis  there  is  always  "  a  purulent  nucleus,"  the  changes  in  the 
chronic  form  are  referred  more  to  the  mechanical  realm,  and  consist  of 
kinking,  thickening,  adhesions  and  obliterations. 

This  is  the  reason  why  the  process  in  acute  perityphlitis  may  heal 
functionally,  for  example,  by  self -drainage   (Sahli),  or  by  rupture  into 


.396       ACUTE   PERITONITIS,   APPENDICITIS,   AND  PERITYPHLITIS 

the  intestine  or  into  other  organs.  The  conditions  are,  however,  different 
in  the  cases  with  a  chronic  beginning  and  running  a  chronic  course. 
Here  mechanical  disturbances  when  once  developed  to  such  a  height  as  to 
produce  symptoms  rarely  or  never  heal.  From  the  fact  that  even  when 
acute  perityphlitis  terminates  in  recovery  it  leaves  residua  of  varying 
extent  and  absolutely  unlike  quality,  it  follows  that  the  prognosis  of  resid- 
ual perityphlitis  precludes  any  a  priori  judgment.  Experience  also  teaches 
us  that  the  primary  attack  may  yield  without  any  difficulties  and  compli- 
cations while  the  second  attack  may  develop  in  an  extremely  fulminant 
manner,  and  if  timely  surgical  aid  is  not  at  hand  may  cost  the  life  of 
the  patient.  And,  vice  versa,  the  first  attack  may  be  exceedingly  dangerous 
while  the  following  ones  may  run  a  smooth,  mild  course. 

In  such  cases,  any  attempt  to  lay  down  definite  rules  and  to  institute 
a  plan  of  treatment  in  accordance  with  these,  in  opposition  to  the  ex- 
prossi\o  voice  of  practical  experience,  must  be  unwise  and  even  dangerous. 
Here  and  there,  it  appears  as  if  certain  laws  in  the  course  of  residual 
perityphlitis  were  decisive,  but  this  is  nothing  more  than  an  accidentally 
iavoral)!c  sequence  in  the  individual  cases,  and  with  some  patients  it  col- 
lapses like  a  house  built  of  cards. 

The  prognosis  of  chronic  relapsing  perityphlitis  is  much  more  certain 
than  that  of  the  residual  form.  With  few  exceptions  the  prognosis  of 
the  latter,  in  so  far  as  life  is  concerned,  may  be  regarded  as  favorable. 
This  is  true  of  the  intervals  as  well  as  of  the  attacks  which  occur  period- 
ically. Although  I  am  well  aware  that  no  conclusive  significance  attaches 
to  a  single  observation,  nevertheless  the  following  clinical  history  may  be 
here  in  place  because  it  shows  how  even  extensive  and  chronic  disease 
of  the  vermiform  process  may  set  in  yet  not  decidedly  impair  the  organ. 

The  case  was  tliat  of  a  la\vyer,  aged  25,  who  in  the  year  1904  began  his  voluntary 
service  as  a  soldier  in  the  army.  In  1905  he  presented  himself  to  me  for  treat- 
ment sliowing  all  the  signs  of  chronic  relapsing  perityphlitis.  Besides  this  there  was 
an  obstinate  habitual  constipation  with  colitis.  Although  1  warned  the  patient  of 
the  incompatibility  of  military  duty  with  his  disease,  he  insisted  upon  continuing  his 
service  in  the  army.  He  passed  energetically  through  the  difficult  period  of  his 
recruit  service;  gradually,  however,  his  symptoms  increased  so  that  in  April,  1905, 
I  strenuously  advised  operative  removal  of  the  appendix.  Even  then  his  condition 
was  still  bearable,  and  only  the  fear  that  in  all  probability  he  could  not  serve  his 
time  induced  him  to  consent  to  the  operation,  which  was  successfully  performed  by 
Prof.  Korte  upon  the  21st  of  May,  1905.  The  appendix  was  long,  its  end  thickened, 
and  it  contained  fecal  concrements.     Microscopic  finding:  Appendicitis  ulcerosa. 

Xotwithstanding  the  strenuous  corporeal  exertion  to  which  the  patient 
was  o.\]i()sed  during  his  military  career,  and  although  he  punctiliously 
ixii'ormed  all  of  his  duties,  no  true  attack  supervened,  which  is  certainly 
a  foreilile  illustration  of  what  has  been  said  above  that  chronic  relapsing 
cases  show  no  tendency  to  a  severe  course. 


THE  CLINICAL   PICTURE   OF  CHRONIC  PERITYPHLITIS  597 

The  prognosis  in  regard  to  a  cure  is  quite  different.  While  in  an 
acute  attack,  even  when  most  severe,  a  cure  in  the  ordinary  sense  enSues 
and  may  be  permanent,  in  the  chronic  relapsing  form,  for  reasons  previously 
mentioned,  the  result  is  quite  different.  Since  in  this  form  the  symptoms 
at  the  onset  are  frequently  very  slight,  it  cannot  be  denied  that  by  imme- 
diate and  suitable  remedies  which  will  be  described  in  the  chapter  upon 
treatment  the  disturbances  may  be  so  lessened  as  to  constitute  a  cure; 
but  a  true  cure  which  under  observation  lasts  for  years  I  am  not  cognizant 
of,^  and  in  such  a  case  I  should  be  inclined  to  doubt  the  correctness  of 
the  diagnosis. 

The  most  characteristic  feature  of  chronic  peritjrphlitis,  not  only  in 
its  course  but  also  in  its  prognosis,  is  the  fact  that  under  favorable  ex- 
ternal conditions  (bodily  rest,  lessening  of  tension,  mineral  spring  cures, 
etc.),  distinct  remissions  occur.  But  this  somewhat  subjective  euphoria 
is  in  sharp  contrast  with  the  objective  investigation  which  shows  that  a 
distinctly  recognizable  sensitiveness  to  pressure  is  constantly  present  in 
the  ileo-cecal  region. 


TREATMENT   OF  CHRONIC   PERITYPHLITIS 

In  the  borderland  between  internal  and  operative  treatment,  the  treat- 
ment of  chronic  perityphlitis  most  frequently  lies.  It  is  everywhere  rec- 
ognized that  the  most  radical  and  relatively  the  least  dangerous  method 
of  cure  of  chronic  perityphlitis  consists  in  the  extirpation  of  the  appendix 
in  the  afebrile  stage. 

Upon  superficial  observation  any  further  discussion  as  to  the  best 
mode  of  treatment  of  chronic  perityphlitis  would  appear  to  be  superfluous. 
But  upon  accurate  weighing  of  the  conditions  they  are  found  to  be  not 
quite  so  simple,  and  it  is  therefore  necessary  most  carefully  to  investigate 
this  question. 

In  the  first  place,  in  the  therapeutic  indications  and  contra-indications 
there  is  a  fundamental  difference  between  those  of  residual  and  chronic 
perityphlitis. 

As  we  have  seen,  an  acute  attack  may  result  either  in  complete  recov- 
ery (in  a  functional  sense)  or  the  residua  may  generate  chronic  symptoms, 
or,  finally,  may  lead  to  a  subsequent  attack. 

The  more  resultless  the  investigation  of  the  anatomical  relations  the 
more  positively  is  therapeutic  treatment  indicated. 

We  must,  therefore,  decide  to  what  extent  the  changes  after  an  attack 

1  Albu,  in  an  article  recently  published,  "  Zur  Diagnose  und  Therapie  der  ehro- 
nischen  Perityphlitis"  {Deutsche  mod.  Wochenschr.,  1905,  Nr.  25  u.  26),  mentions 
two  apparently  cured  cases  of  residual  perityphlitis.  But  in  both  cases  the  period 
of  observation  was  too  brief  to  permit  a  definite  opinion. 


598       ACUTE   PERITONITIS,   APPENDICITIS,   AND  PERITYPHLmS 

are  perceptible,  and  in  how  far  we  may  prognosticate  with  probability  the 
type  of  subsequent  relapses. 

Considering  first  the  residua,  the  presence  of  an  exudate  may  be  cer- 
tainly determined  and  its  growth  or  retardation  demonstrated  by  continu- 
ous observation.  On  the  contrary,  exact  knowledge  of  the  condition  of  the 
vermiform  process  and  its  immediate  surroundings  is  much  more  diflBcult 
to  acquire.  It  may  still  contain  pus,  a  tendency  to  perforation  and  ulcera- 
tion may  still  be  present,  the  mesenteriolum  may  be  inflamed  or  gangre- 
nous, yet  there  may  be  no  marked  or  grave  symptoms  to  indicate  the  gravity 
of  the  condition.  Inversely,  a  slowly  progressive  healing  may  take  place,, 
but  whether  this  is  permanent  is  a  question  to  be  answered  only  with  the 
greatest  reserve. 

As  we  have  already  emphasized,  the  prognosis  in  a  second  or  third 
attack  is  most  perplexing.  We  have  only  to  consult  one  of  the  numerous 
clinico-surgical  reports  upon  appendicitis  to  be  convinced  that  here  every 
rule  finds  its  paradigm  in  the  inexhaustible  variations  of  the  clinical  course 
of  perityphlitis.  Only  ripe  experience,  as  has  often  been  demonstrated, 
warrants  the  following  prognosis:  The  longer  the  interval  after  the  first 
attack  the  less  the  danger  of  subsequent  and  severe  relapses.  But  even 
here,  as  every  one  who  has  followed  the  literature  of  perityphlitis  knows, 
exceptions  now  and  then  occur. 

To  find  the  proper  indication  for  our  therapeutic  procedure,  we  must 
consider  impartially  what  internal  medi(iine  has  accomplished  in  the  treat- 
ment of  residual  perityphlitis.  There  can  be  no  doubt  that  the  exudative 
form  is  a  relatively  favorable  one  for  treatment.  In  such  cases,  indeed, 
local  compresses  of  peat  or  salt  and  peat  and  salt  baths  have  actually 
caused  the  exudate  gradually  to  disappear,  and  thus  the  symptoms  were 
either  entirely  relieved  or  diminished  to  a  great  extent. 

Where  there  is  no  exudate,  the  result  of  this  or  any  similar  form  of 
treatment  is  much  less  certain.  We  must  be  careful  not  to  mistake  a  peri- 
odic amelioration  of  the  process  for  recovery.  As  a  rule,  however,  there 
is  nothing  to  cause  us  to  regard  too  optimistically  an  improvement  in 
chronic  perityphlitis — this  is  true  of  both  forms.  We  have  no  criterion 
for  deciding  whether  a  process  in  the  ileo-cecal  region  has  healed  or  whether 
it  is  only  latent. 

For  the  prevention  of  new  attacks  a  number  of  methods  have  been 
suggested.  These  consist  mainly  of  bodily  rest,  the  careful  regulation  of 
the  diet,  the  prevention  of  an  accumulation  of  feces  and  gas  in  the  intes- 
tines, the  long-continued  use  of  compresses  of  various  kinds  and  of  dif- 
ferent temperatures,  etc.  For  obvious  reasons  it  is  very  difficult  to  decide 
whether  these  measures  are  actually  of  any  use  in  preventing  relapses. 
Unquestionably  the  most  important  of  these  factors  are  bodily  rest  and 
proper  care. 

But  when  we  regard  these  and  similar  prophylactic  measures  in  their 


THE  CLINICAL  PICTURE  OF  CHRONIC  PERITYPHLITIS  599 

proper  light,  in  the  majority  of  cases  we  will  cling  to  no  illusions  concern- 
ing them,  even  if  it  were  possible  and  practicable  to  carry  them  out  ener- 
getically, whereas  in  most  cases  they  cannot  be  employed  at  all. 

It  is  evident  from  this  discussion  that  the  operative  treatment  of 
residual  perityphlitis  is  from  principle  to  he  preferred  to  any  other  mode 
of  relief.  Only  in  those  cases  in  which  we  find  an  exudate  and  in  which 
the  other  clinical  symptoms  appear  favorable  may  we  temporize.  The  same 
is  true  of  the  residua,  which  may  exist  for  many  years  and  produce"  no 
important  symptoms.  _-^ 

After  recovery  from  a  severe  attack  we  are  placed  in  a  position  of  great_J 
responsibility. 

To  temporize  here  means  to  allow  the  patient  to  run  risks  which  prog- 
nostically  cannot  be  estimated.  On  this  point  I  am  much  more  in  favor 
of  surgery  than  many  surgeons,  and  I  believe  the  future  will  show  that  I 
am  right.  Even  with  attacks  of  medium  severity,  I  advise  an  operation 
in  the  interval.  An  expectant  treatment  should  be  instituted  only  in  tbose 
mild  cases  which  show  but  slight  elevation  of  temperature  and  which 
terminate  in  recovery  in  a  few  days.  Of  course  the  individual  circum- 
stances of  the  patient  must  be  most  carefully  considered,  especially  his 
occupation,  since  prolonged  bodily  rest  is  an  absolute  necessity. 

A  decidedly  more  favorable  perspective  is  afforded  by  the  chronic 
relapsing  cases.  If  we  bear  in  mind  the  previously  stated  fact  that  the 
overwhelming  majority  of  cases  of  perityphlitis  running  a  chronic  course 
assume  no  life  threatening  aspect,  we  are  justified  in  employing  the  reme- 
dies of  internal  and  expectant  treatment  to  the  fullest  extent. 

Here  also  bodily  rest  and  careful  nursing  are  the  first  considerations. 
How  long  rest  should  be  insisted  upon  depends,  in  the  first  place,  upon 
the  intensity  of  the  process,  and,  secondly,  upon  the  extent  of  time  which 
is  possible  in  the  individual  case.  In  the  latter  respect,  as  we  have  stated, 
our  advice  is  disregarded  more  frequently  than  is  desirable.  In  such  cases 
rest  for  at  least  a  part  of  the  day  or  upon  holidays  may  be  insisted  upon. 
Distinct  remissions  are  frequently  observed  after  several  weeks  of  absolute 
rest  in  bed;  in  other  cases,  however,  these  either  do  not  occur  or  are 
only  of  brief  duration.  And  here  the  factor  previously  mentioned,  the 
special  regulation  of  the  entire  digestive  function,  comes  into  consideration. 

In  acute  attacks  there  can  be  no  doubt  that  indigestion  plays  a  decidedly 
causative  role;  chronic  indigestion  also  increases  chronic  inflammation,  and 
vice  versa.  At  this  point,  therefore,  a  few  practical  suggestions  for  the 
treatment  of  intestinal  disturbances  are  not  out  of  place.^ 

Primarily,  as  everywhere  else  in  gastrointestinal  pathology,  the  diet 
must  be  so  regulated  as  to  be  adapted  to  the  character  of  the  intestinal 
affection.     In  simple,  habitual  constipation  we  institute  a  diet  which  wiU 


1  See  also  Boas,  "  Constipation  and  Hemorrhoids,"  in  this  volume. 


I 
600      ACUTE   PERITONITIS,   APPENDICITIS,   AND  PERITYPHLITIS 

actively  siimulato  intestinal  peristalsis,  and  one  in  which  sugar  and  very 
sweet  substances  are  prominent.  The  same  result  is  accomplished  by  food 
containing  much  fat;  only  such  articles,  however,  should  be  employed 
which  at  a  low  melting  point  are  to  a  great  extent  free  from  fatty  acids 
(olive  oil,  butter,  cream,  almond  milk),  and  these  constitute  important 
aids.  Organic  acids,  used  with  discretion,  are  of  great  use  (buttermilk, 
sour  milk,  and  the  juice  of  apples,  oranges,  and  lemons). 

It  is  much  more  difficult,  however,  in  cases  of  chronic  perityphlitis  to 
decide  the  question  whether  food  which  leaves  much  residue  and  raw 
fruits  are  to  be  allowed  or  prohibited.  Traditionally  we  are  inclined  to 
prohibit  these  strictly.  Whether  this  is  necessary  to  such  an  extent  as  is 
nowadays  generally  maintained  is  doubtful  if  we  consider  that  an  actual 
residue  of  food  in  the  appendix  is  an  extremely  rare  occurrence.  In  all 
eases  the  prohibition  of  raw  fruit  should  extend  to  only  those  varieties 
wliieli  contain  small  seeds;  vegetables,  particularly  those  which  cause  fer- 
mentation, should  be  absolutely  avoided  or  given  only  when  suitably  pre- 
pared. No  decided  objection  can  be  raised  to  the  use  of  rye  bread,  provided 
it  be  well  baked. 

The  prohibition  of  highly  carbonated  drinks,  of  the  immoderate  drink- 
ing of  cold  fluids,  and,  finally,  of  the  use  of  ice  cream  and  fruit  ices  is 
(juite  justifiable.  Here  the  interdiction  of  strong  acids  (vinegar),  as  well 
as  of  mustard,  horse-radish,  etc.,  should  also  be  mentioned. 

In  case  the  previously  mentioned  diet  does  not  regulate  the  bowels  the 
most  effective  and  least  irritating  treatment  is  by  oil  enemata.  On  prin- 
ciple I  am  opposed  to  actual  purgatives,  and  only  under  exceptional  cir- 
cumstances do  I  advise  temporarily  even  the  mildest  laxatives,  such  as 
castor  oil,  rhubarb,  flowers  of  sulphur,  the  preparations  of  sagrada,  and 
Carlsbad  salt.  Powerful  purgatives  or  those  which  are  of  uncertain  action 
are  absolutely  prohibited. 

The  treatment  of  habitual  constipation  combined  with  chronic  intes- 
tinal catarrh  is  based  on  the  same  principles  as  that  of  colitis  membrana- 
cea.  On  the  other  hand,  the  cases  of  catarrh  of  the  colon  running  their 
course  with  habitual  diarrhea  must  be  treated  by  a  regime  the  opposite 
of  that  mentioned  above.  Beyond  a  certain  extent  sugar  and  milk,  perhaps 
eggs  also,  must  be  entirely  prohibited,  while,  on  the  other  hand,  meat, 
fish,  mucilaginous  soups  (rice,  sago,  barley),  red  wine  and  elderberry  wine, 
and  acorn  cocoa  are  recommended.  Fats  of  good  quality  are  permissible. 
TTere  also  carbonated  drinks  as  well  as  all  kinds  of  beer,  ice  cream  and 
fruit  ices  must  be  avoided.  In  simple  colitis  these  measures  will  usually 
l)e  sufficient;  but,  if  not,  the  well  known  astringents  and,  secondly,  intes- 
tinal irrigation  with  astringent  solutions  must  be  considered. 

Besides  rest  and  a  regulated  diet,  mineral  spring  and  bath  cures  come 
into  (juestion;  although  they  are  often  only  palliative  and  transitory,  there 
can  l)e  no  doubt  that  these  sometimes  produce  favorable  results  because 


THE  CLINICAL  PICTURE  OF  CHRONIC  PERITYPHLITIS  601 

individual  curative  factors  are  readily  combined  in  this  treatment,  which 
is  difficult  to  attain  in  treatment  at  home. 

In  the  rare  cases  in  which  the  intestinal  canal  is  absolutely  intact,  we 
may  limit  ourselves  to  baths,  salt  baths,  or  peat  baths;  in  others  it  is 
better  to  combine  these  with  spa  treatment.  For  the  latter  the  waters 
of  Carlsbad,  Marienbad,  Homburg,  Kissingen  and  Wiesbaden  are  especially 
suitable.  By  drinking  the  spring  water  at  home,  or  by  baths,  the  less 
well-to-do  classes  may  attempt  to  substitute  for  these  cures.  After  the 
cure  it  is  well  to  continue  the  local  peat  and  salt  compresses  for  a  long 
time.  The  same  effects  may  be  produced  by  hot  linseed  or  oatmeal  poul- 
tices, as  well  as  by  compresses  of  absolute  alcohol,  after  which  a  more  or 
less  distinct  remission  in  the  inflammatory  symptoms  will  be  observed. 

Although  it  is  undoubtedly  true  that  these  cures  energetically  and  per- 
sistently carried  out  exert  a  favorable  and  palliative  effect,  yet  the  ultimate 
curative  result  is  uncertain.  Now  and  then  long-continued  improvement 
takes  place  and  resembles  a  cure,  but  in  the  overwhelming  majority  of 
instances  we  merely  attain  a  certain  condition  of  latency.  For  some 
individuals  this  is  very  desirable,  particularly  for  those  who  from  the 
onset  show  less  serious  disturbances  or  who  are  in  comfortable  circum- 
stances. For  the  remainder,  however,  even  after  the  most  thorough  trial 
of  this  or  similar  cures,  the  result  is  merely  armed  neutrality.  After 
long  or  short  intervals  of  rest,  disturbances  appear,  at  first  mild  and  of 
brief  duration,  but  gradually  becoming  severe  and  continuous. 

After  considering  all  of  the  questions  which  here  arise,  we  cannot  re- 
frain from  expressing  the  opinion  that  the  operative  removal  of  the  diseased 
appendix  is,  on  principle,  not  only  the  most  radical  but  also  the  most 
effective  measure  to  bring  final  relief;  of  course,  with  certain  limitations 
which  must  be  carefully  discussed. 

First,  I  must  reiterate  that  the  indication  for  the  operative  removal 
of  the  appendix  in  chronic  processes  is  never  urgent.  We  may  quietly 
await  the  results  of  thorough  palliative  treatment.  Although,  as  has  been 
stated,  absolute  recovery  is  rare,  yet  remissions  are  often  very  decided. 
Frequently  we  find  we  are  dealing  with  appendiceal  neurasthenics  who 
torment  themselves  and  their  friends  with  groundless  fears.  Unfortu- 
nately these  fears  are  at  times  augmented  by  some  surgeons  who  grossly 
exaggerate  the  dangers  of  chronic  perit3rphlitis.  I  have  met  a  large  number 
of  these  appendiceal  hypochondriacs,  and  it  proved  no  easy  task  to  con- 
vince them  of  the  mildness  of  their  affection. 

But  even  with  more  serious  symptoms  the  indication  for  operative  treat- 
ment is  not  always  pressing.  This  is  especially  true  in  the  case  of  aged 
and  debilitated  persons  in  whom  any  laparotomy  is  fraught  with  more  or 
less  danger.  Here  may  be  enumerated  the  cases  with  complications  on  the 
part  of  the  heart,  the  kidneys,  the  lungs,  or  with  diabetes  and  the  like. 

On  the  other  hand,  there  are  cases  in  which  operation  is  undoubtedly 

i_i  c  »\ 

COLLlieiE   OF   .c  ii_ 


602       ACUTE   PERITONITIS,  APPENDICITIS,   AND  PERITYPHLITIS 

indicated;  for  example,  in  chronic  perityphlitis  at  the  age  of  puberty. 
Even  with  relatively  slight  symptoms  it  is  our  duty  in  such  cases  to 
advise  operation,  as  here  the  bodily  rest  insisted  upon  is  directly  opposed 
to  the  no  less  important  bodily  development. 

The  same  is  also  true  of  those  whose  symptoms  preclude  their  following 
their  occupations.  Here  also  the  intensity  of  the  symptoms  must  be  sub- 
ordinated to  the  fact  that  such  persons  are  permanently  unable  to  earn 
a  living.  Naturally  the  indication  is  more  urgent  if  the  symptoms  become 
extremely  aggravated  and  are  but  little  or  not  at  all  ameliorated  by  pallia- 
tive measures. 

With  every  indication  for  operation  it  is  presupposed  that  the  diagnosis 
is  positive  or  at  least  extremely  likely.  Errors  on  account  of  existing 
complications,  such  as  intestinal  catarrh  or  disease  of  the  right-sided 
adnexa,  will  frequently  be  unavoidable;  nevertheless  it  is  invariably  our 
duty  to  exhaust  all  of  the  diagnostic  aids  and  methods  at  command  before 
coming  to  a  definite  decision. 

Before  concluding  we  must  discuss  the  dangers  and  results  as  well  as 
the  possible  sequelae  of  an  operation.  In  regard  to  the  first,  statistics 
quite  uniformly  show  a  mortality  of  from  one  to  2  per  cent.  Many  sur- 
geons, however,  perform  hundreds  of  operations  without  a  fatal  case. 
Taken  all  in  all  we  may  therefore  designate  an  operation  for  uncom- 
plicated chronic  perityphlitis  as  one  relatively  free  from  danger. 

It  is  different  with  the  results.  In  the  first  place,  the  influence  of  the 
operation  upon  the  appendix  and  upon  the  remaining  intestine  which,  as 
already  mentioned,  is  frequently  implicated,  must  be  considered  separately. 
While  in  the  great  majority  of  cases  the  effect  upon  the  appendix  is  salu- 
tary, this  cannot  be  maintained  for  the  remaining  intestinal  canal.  Yet 
we  must  reiterate  that  after  removal  of  the  appendix  the  cure  of  an  intes- 
tinal affection  is  much  more  rapid  because  the  physician  need  no  longer 
take  into  consideration  the  restrictions  which  were  previously  necessary 
(rest,  gymnastics,  massage,  etc.). 

Nevertheless,  in  a  few  (but,  as  we  must  admit,  the  minority)  of  the 
cases  of  chronic  perityphlitis,  increasing  experience  proves  that  the  actual 
curative  results  are  by  no  means  satisfactory. 

But  that  I  may  not  be  suspected  of  disparaging  the  great  successes  of 
surgeons  in  this  realm,  I  must  call  attention  to  a  recent  communication 
from  one  of  the  most  distinguished  operators  for  perityphlitis,  namely, 
the  English  surgeon,  Treves.^ 

Among  231  cases  operated  upon  in  the  stage  of  latency,  in  45  recovery 
was  incomplete.  In  these  45  cases  ventral  hernia  and  all  of  the  disturb- 
ances due  to  healinff  of  the  wound  are  excluded. 


1  Treves,    "  The    Prospects   and   Vicissitudes   of   Appendicitis   After   Operation." 
British  Medical  Journ.,  1905,  March  4. 


THE  CLINICAL  PICTURE   OF  CHRONIC  PERITYPHLITIS  603 

Among  the  causes  of  failure  were  incomplete  removal  of  the  appendix 
(2  cases),  disturbances  on  the  part  of  the  ovaries  (9  cases),  chronic  or 
relapsing  colitis  (8  cases),  continuance  of  local  pain  (7  cases),  neuras- 
thenia or  hypochondria  (5  cases),  persistent  pain  from  gall-stones  (3 
cases),  from  colic  (2  cases),  wandering  kidney  (2  cases),  renal  calculi 
(one  case),  soft  masses  in  the  right  iliac  fossa  (5  cases),  unknown  cause 
(one  case). 

In  the  two  eases  in  which  the  removal  of  the  appendix  was  incom- 
plete, this  was  removed  at  a  second  operation. 

The  recent  reports  of  Haberer  ^  from  von  Eiselberg's  Clinic  in  Vienna 
are  similar.  Among  96  cases  of  operation  during  the  interval,  all  of  whom 
survived,  in  only  50  were  the  symptoms  relieved  by  the  operation.  "  Forty 
patients,  lioivever,  continued  to  have  more  or  less  marked  disturbances,  in 
some  stuhhorn  constipation,  in  some  severe  pain,  even  attacks  of  colic, 
such  as  they  had  suffered  from  prior  to  the  operation." 

Keports  of  relapses  after  operation  for  perityphlitis  are  increasing  in 
literature.-  One  of  the  first  authors  to  report  these  occurrences  was  Ger- 
hardt.^* 

I,  too,  have  observed  5  cases  of  post-operative  typhlitis,  some  of  which 
were  very  obstinate.     I  shall  quote  one  case,  that  of  a  colleague : 

Dr.  H.,  of  F.,  aged  38,  suffered  for  many  years  from  constipation.  In  1901  he 
had  an  acute  attack  of  perityphlitis  with  fever  and  subsequently,  at  intervals  of 
four  weeks,  five  attacks,  all  running  their  course  with  slight  fever.  He  was  oper- 
ated upon  in  March,  1902    (Professor  v.  Czerny,  Heidelberg). 

The  conditions  found  were  as  follows:  The  appendix  was  bent,  twisted  in  the 
form  of  a  spiral,  adherent  posteriorly  and  laterally,  but  there  was  no  suppuration. 
Following  this  he  continued  well  until  October,  1902.  At  that  time  there  was  again 
an  acute  attack  of  typhlitis  with  no  rise  of  temperature  but  with  great  pain  over 
McBurney's  point.  He  was  in  bed  for  three  months.  Subsequently,  in  March,  1903, 
another  operation  was  performed  and  the  ascending  colon  was  found  to  be  adherent 
to  the  peritoneum.  Since  that  time  there  have  been  no  attacks,  but  there  is  still  pain 
over  McBurney's  point  even  upon  moderate  movement.  Moreover  the  patient  still 
suffers  from  constipation.  During  an  evacuation,  and  even  for  hours  afterward,  he 
invariably  has  great  pain  in  the  region  of  the  cecum.  The  patient  reports  that  since 
the  two  operations  he  is  decidedly  worse  than  before. 

Examination  of  the  cecal  region  reveals  decided  sensitiveness  to  pressure,  particu- 
larly in  the  center  of  the  cicatrix,  from  the  operation;  but  even  the  remaining  cecal 
region  is  distinctly  painful  upon  pressure. 


1  Baberer,   "  Beitrag   zur   Appendixfrage,   mit   besonderer   Beriicksichtigung  von 
Dauerresultaten."    Arch.  f.  klin.  Chirurgie,  Bd.  LXXVI,  H.  1  u.  2. 

2  Leop.  Fischl,  "  Typhlitis  nach  Amputation  des  Wurmfortsatzes."    Prager  med. 
Wochenschr.,  1904,  Nr.  7. 

^Gerhardt,   "Perityphlitis   mit   Ruckfallen."     Mittheilungen  aus  den   Grenzge- 
bieten,  1896,  I,  p.  354. 


604      ACUTE  PERITONITIS,  APPENDICITIS,  AND  PERITYPHLITIS 

Probably  in  these  and  similar  cases  extensive  adhesions  form  which 
result  in  .a  more  or  less  decided  kinking  or  stenosis  of  the  cecum  or 
ascending  colon.  As  is  well  known,  the  prognosis  in  these  cases  of  adhe- 
sions is  by  no  means  favorable,  and  there  is  no  known  remedy  which 
will  positively  prevent  their  recurrence. 

Although  the  number  of  such  unfavorable  results  is  relatively  small 
in  proportion  to  the  fortunate  successes,  nevertheless  they  demand  our 
scientific  and  serious  consideration. 

From  this  description  it  is  evident  that  the  treatment  of  chronic  peri- 
typhlitis must  be  adjusted  to  the  character  and  the  nature  of  its  develop- 
ment. In  genuine  chronic  perityphlitis  it  may  be  expectant  and  without 
risk.  In  the  residual  forms,  with  few  exceptions,  it  must  be  operative. 
Even  in  the  iirst  group  operative  treatment  is  the  most  hopeful.  But 
the  indication  for  this  necessitates  most  careful  consideration  which  de- 
volves chiefly  upon  the  physician. 


EXAMINATION    OF    THE    FECES 
By  J.  STRASBURGER,  Bonn 

Until  recently  but  slight  interest  was  manifested  in  professional  cir- 
cles in  the  semeiology  of  the  feces  and  in  the  question  of  their  diagnostic 
value.  Of  course,  in  the  investigation  of  metabolism,  and  especially  of 
absorption,  the  chemical  examination  of  the  feces  has  for  more  than  half 
a  century  held  its  place  among  the  methods  of  the  physiologist.  But  the 
objects  in  view  had  little  in  common  with  clinical  diagnosis. 

Omitting  from  consideration  those  clinicians  who  made  a  specialty 
of  the  study  of  the  digestive  organs,  the  pediatricians  were  the  first  to 
attach  importance  to  the  examination  of  the  feces  in  the  differentiation  and 
recognition  of  pathological  alterations.  The  conditions  in  nurslings  are  in 
every  respect  much  more  simple  and  more  favorable  than  in  the  adult. 
The  dejecta  are  shown  to  the  physician  in  the  diaper,  they  have  no  dis- 
agreeable odor,  and,  on  account  of  their  simple  composition,  they  necessi- 
tate much  less  diagnostic  experience  than  those  of  later  life.  But  this 
does  not  alter  the  fact  that  also  in  many  diseases  of  the  adult  a  thorough 
investigation  of  the  feces  is  absolutely  necessary  in  order  to  arrive  at 
an  exact,  anatomical,  functional,  or  etiologic  diagnosis.  I  must  refer 
here  to  Jfothnagel's  oft  quoted  statement  that  in  the  pathology  and  diag- 
nosis of  intestinal  diseases  the  examination  of  the  dejecta  is  of  even 
greater  importance  than  is  the  examination  of  the  sputum  in  diseases  of  the 
respiratory  tract.  The  foundation  for  a  rational  examination  of  the  feces 
was  established  by  Nothnagel  more  than  twenty  years  ago  iu  his  "  Bei- 
tragen  zur  Physiologic  und  Pathologic  des  Darmes."  But  the  last  few 
years  only  have  intensified  our  interest  in  this  subject,  and,  fortunately 
for  the  patients  with  intestinal  disease,  this  is  still  increasing,  a  fact 
which  is  unquestionably  due  to  the  labors  of  Ad.  Schmidt. 

To  investigate  the  feces  successfully  and  thus  to  recognize  the  finer 
disturbances  of  intestinal  activity  we  must  avoid  the  difficulties  with  which 
earlier  investigators  were  commonly  confronted.  What  these  were  will 
appear  when  we  ask  ourselves  why  an  examination  of  the  excrements  of 
the  nursling  is  so  much  easier  and  is  so  much  oftener  carried  out  than 
that  of  the  adult. 

"We  have  already  stated  that  the  infantile  feces  are  always  at  the 
disposal  of  the  investigator.  If  not  found  in  the  diaper,  we  may  intro- 
duce into  the  rectum  a  small  instrument  something  like  the  bulb  of  a 

605 


606  EXAMINATION  OF  THE  FECES      ' 

syringe,  or,  still  better,  an  instrument  invented  by  P.  Cohnheim — a  medium 
thick  glass  tube  which  is  inserted  within  the  anus  and  which,  at  the  end 
that  is  introduced,  is  closed  in  front;  this  may  readily  be  inflated  ovally. 
Laterally,  at  the  distended  portion,  it  has  an  oval  opening.  If  rotated 
a  few  times  in  the  ampulla  of  the  rectum  we  can  almost  always  secure 
witli  this  small  instrument  as  much  material  as  is  necessary  for  an  ex- 
amination. 

We  find  on  estimating  the  feces  of  nurslings  that  the  simple  and  uni- 
form composition  of  the  food,  as  compared  with  that  of  adults,  greatly 
facilitates  the  process. 

Tlie  conclusion  drawn  from  this  is  that  we  must  first  make  it  easy 
for  adults  to  furnish  a  specimen  of  their  feces  for  examination;  secondly, 
in  all  cases  where  the  change  in  the  dejecta  is  not  so  great  but  that  it 
can  be  recognized  with  every  kind  of  nourishment,  we  must  order  the 
patient  a  definite  diet  of  uniform  material.  It  is  evident  that  deviations 
from  the  normal  will  thus  be  more  readily  recognized.  With  a  mixed  and 
constantly  varying  diet,  fecal  examination  to  a  certain  extent  resembles 
a  comparison  of  two  alternating  factors  which  simultaneously  influence 
each  other;  for  the  composition  of  the  feces  is  the  result  on  the  one  hand 
of  the  nature  of  the  food,  and  on  the  other  hand  of  the  digestive  power 
of  the  intestine.  If  we  remove  from  this  comparison  the  one  changeable 
factor,  the  influence  of  varying  food,  and  replace  it  by  a  constant  one,  the 
condition  of  affairs  becomes  simpler.  In  gastric  pathology  this  has  been 
for  some  time  recognized  in  the  form  of  the  Ewald-Boas  test-breakfast 
as  well  as  in  the  Leube-Eiegel  test-meal. 

But  to  return  to  the  primary  point:  In  a  hospital,  naturally,  there 
is  no  difficulty  in  procuring  the  necessary  specimen  for  an  examination. 
But  the  majority  of  those  who  suffer  from  intestinal  diseases  do  not  go 
to  a  hospital  but  to  the  clinic  for  treatment.  In  office  practice,  however, 
we  must  reckon  upon  the  patient's  delicacy  in  regard  to  everything  con- 
cerning the  dejecta.  Here  we  ask  the  patients  to  bring  on  their  next  visit 
a  portion  of  their  dejecta,  naturally  that  which  appears  to  them  to  be 
pathologic,  enclosed  in  a  bottle  with  a  wide  mouth,  perhaps  in  a  preserv- 
ing jar  with  patent  lid.  Some  patients  will  refuse,  for  this  appears  to 
them  to  be  worse  than  the  disease,  and  only  when  they  are  accustomed 
to  examinations  of  the  kind,  or  when  the  physician  has  the  necessary 
appliances  and  can  furnish  them  with  a  glass  jar  with  a  proper  stopper, 
will  they  comply.  This  proposition,  if  I  am  not  mistaken,  emanated  from 
Raudnitz,  and,  like  many  suggestions  in  practical  medicine,  is  valuable. 
Pasteboard  may  be  used  to  place  the  feces  in  the  glass  jar  or  other  con- 
tainer. 

The  point  just  discussed  is  a  question  of  external  nature.  Much  more 
important  and  vital  is  the  formulation  of  a  test  diet.  Based  on  the  pre- 
viously mentioned  considerations,  this  was  introduced  into  intestinal  pathol- 


TEST  DIET  607 

ogy  by  Schmidt  and  myself.  At  first  somewhat  complicated,  it  was  grad- 
ually so  simplified  by  considerations  of  a  secondary  nature  that  the 
difficulties  connected  with  it  seemed  to  disappear.  We  have  successfully 
employed  this  method  for  a  number  of  years,  and  have  reported  the  results 
obtained  by  it  in  our  monograph  upon  human  feces.^ 

By  numerous  researches  we  have,  in  the  main,  determined  the  limits 
of  what  may  be  regarded  as  normal  in  a  test  diet  and  what  belongs  to  the 
realm  of  pathology,  and  we  possess  a  criterion  for  the  microscopic  and 
macroscopic  investigation  of  the  feces.  Our  test  diet  in  the  form  last 
advised  by  Schmidt  ^  is  composed  of  the  following : 

TEST  DIET 

Morning:  0.5  of  a  liter  of  milk  (or,  if  milk  is  badly  borne,  0.5  of  a 
liter  of  cocoa  [made  of  20  grams  of  powdered  cocoa,  10  grams  of  sugar, 
400  grams  of  water  and  100  grams  of  milk]). 

With  this  50  grams  of  zwieback. 

Midday:  0.5  of  a  liter  of  oatmeal  gruel  (made  with  40  grams  of  oat 
grits,  10  grams  of  butter,  200  grams  of  milk,  300  grams  of  water  and 
one  egg)  ;  this  mixture  should  be  strained. 

Dinner:  125  grams  of  scraped  beef  (weighed  raw),  broiled  only 
slightly  so  that  it  is  raw  in  the  center,  and  prepared  with  20  grams  of 
butter.  With  this  250  grams  of  mashed  potatoes  (190  grams  of  potatoes, 
100  grams  of  milk,  and  10  grams  of  butter). 

Afternoon:  The  same  as  in  the  morning. 

Evening:  The  same  as  at  midday. 

This  test  diet  contains  120  grams  of  albumin,  111  grams  of  fat,  and 
191  grams  of  carbohydrates;  it  corresponds  to  2,234  large  calories,  and 
almost  furnishes  the  food  requirement  of  a  person  not  doing  corporeal 
labor.  For  the  majority  of  patients  with  intestinal  disease,  and  with 
these  we  are  dealing,  it  is  sufficient.  Individual  caprices  of  appetite  may 
perhaps  be  indulged  by  modifying  the  quantity  of  milk  without  specially 
influencing  the  result  of  the  fecal  investigation.  The  objection  has  been 
made  that  the  test  diet,  on  account  of  the  unsuitability  of  milk  for  intes- 
tinal patients,  is  frequently  not  effective,  and  this  is  undoubtedly  true  in 
some  cases;  but,  as  Schmidt  and  I  have  ascertained  by  numerous  inves- 
tigations, it  applies  to  only  a  very  small  percentage  of  patients.  We  should 
not  at  once  yield  the  point  if  the  patient  states  that  he  cannot  digest  milk, 
but  should  resort  to  a  few  well  known  artifices.  As  one  such,  I  must  men- 
tion the  avoidance  of  raw  milk.  It  should  be  given  in  the  food,  and 
perhaps  with  various  additions.     According  to  Schmidt,  0.3  of  a  gram 

1  Schmidt  und  Strashurger,  "  Die  Fiices  des  Menachen  im  normalen  und  krank- 
haften  Zustande."     2.  Aufl.,  Berlin,  1905. 

2  "  Die  Functionsprufung  des  Darmes  mittelst  der  Probekost."     Wiesbaden,  1904. 

40 


608  EXAMINATION   OF  THE   FECES 

ot  pure  salicylic  acid  may  be  well  mixed  with  some  cold  milk  and  added 
to  the  entire  daily  portion  of  the  milk  (one  and  a  half  liters)  and  allowed 
to  come  to  a  boil;  this  is  especially  beneficial.  If  it  should  be  necessary, 
cocoa  may  be  used  as  a  partial  substitute  for  milk  in  the  trial  diet. 

The  test  diet  might  be  made  up  differently,  but  we  prefer  to  adhere 
to  this  form,  since,  aside  from  the  fact  that  we  have  tested  its  applica- 
bility, its  modification  and  further  testing  would  deprive  it  of  its  prin- 
cipal advantage  which  is  that  after  many  careful  investigations  of  cases 
it  has  furnished  us  a  common  basis.  Even  with  patients  walking  about  this 
test  diet  may  be  well  employed.  I  usually  give  the  patient  a  printed  slip 
with  the  necessary  instructions,  and  by  subsequent  microscopic  investiga- 
tion of  the  fecal  specimen  he  brings  with  him  I  am  convinced  that  the 
directions  have  been,  as  a  rule,  correctly  followed.  This  diet  is  enforced 
for  about  three  days,  and  the  dejecta  of  the  last  day  are  investigated. 
If  we  desire  to  be  quite  certain  that  the  feces  are  the  result  of  the  test 
diet,  or,  if  it  is  desirable  (and  this  is  important)  to  ascertain  the  rapidity 
of  the  intestinal  passage,  the  feces  may  be  made  distinctive  by  adminis- 
tering a  capsule  containing  0.3  of  a  gram  of  finely  powdered  carmine 
at  the  beginning  of  the  test  diet.  This  will  give  to  the  evacuations  a 
bright  red  color  and  the  powder  irritates  the  intestine  but  slightly.  If, 
as  sometimes  happens,  the  dejecta  in  consequence  of  their  own  peculiar 
color  do  not  show  this  red  tint  distinctly,  the  fine  carmine  granules  may 
be  readily  recognized  under  the  microscope. 

As  in  all  other  investigations,  fecal  examinations  for  diagnostic  pur- 
poses should  follow  a  definite  plan,  and  in  every  case  a  number  of  main 
])oints  be  noted.  At  first  we  naturally  elicit  a  history  of  the  frequency,  the 
form,  and  the  consistence,  of  the  dejecta,  their  probable  admixture,  and 
any  abnormal  sensations  during  defecation.  I  shall  not  here  further  dis- 
cuss the  individual  points. 

Under  some  circumstances  it  is  desirable  to  obtain  an  idea  of  the 
duration  of  the  ingesta  in  the  gastrointestinal  tract,  and  this  may  be 
readily  determined  by  the  administration  of  carmine  at  the  beginning  of 
the  test  diet,  the  results  of  which  the  patient  may  observe  for  himself. 

The  order  of  the  actual  examinations  should  be  as  follows:  1.  Macro- 
scopic; 2.  Microscopic;  3.  Chemical;  4.  Bacteriologic. 

The  macroscopic  examination,  as  must  be  at  once  premised,  is  the  most 
important  in  practice,  but  it  should  be  made  in  a  different  manner,  and 
much  more  thoroughly,  than  is  usually  the  case.  As  a  rule  this  is  fol- 
lowed by  the  microscopic  examination;  but,  according  to  the  circum- 
stances of  the  case,  or  as  a  matter  of  choice,  the  chemical  test  may  be  first 
made,  and  this  should  be  very  simple.  The  bacteriologic  investigation,  if 
not  included  with  the  microscopic,  is  usually  unnecessary;  it  consumes 
time,  and  except  in  certain  tj-pical  infectious  diseases  the  labor  expended 
upon  it  is,  as  a  rule,  not  commensurate  with  the  diagnostic  results. 


TEST  DIET  609 

With  a  flat  spatula  of  wood  a  portion  of  the  dejecta  is  taken  from  the 
vessel  and  placed  in  a  large  flat  glass  bowl;  we  observe  the  form  of  the 
feces  (in  so  far  as  this  is  still  retained),  the  consistence,  as  well  as 
the  difference  in  consistence  of  the  various  parts,  the  color,  the  odor,  and  the 
reaction.  The  latter  is  tested  with  moistened  litmus  paper,  and  we  may 
note  that  the  reaction  of  the  surface  of  the  fecal  mass  may  be  different 
from  that  of  its  interior.  Naturally  no  opinion  can  be  formed  as  to  the 
total  quantity  of  the  feces  except  by  observation  in  a  hospital  of  the  total 
amount  discharged  in  at  least  three  days,  and  passed  in  a  period  between 
the  administration  of  two  carmine  capsules. 

Water  is  added  to  the  feces  in  the  glass  bowl,  the  masses  are  disin- 
tegrated by  the  spatula,  and  if  coarser  particles  are  admixed  these  may 
be  extracted  with  a  forceps  and  placed  in  a  small  glass  bowl  containing 
some  water.  For  this  purpose  it  is  best  to  use  two  bowls,  one  with  a  black, 
and  the  other  with  a  white  lining,  and  to  work  in  a  clear  light;  Kroenig's 
table  is  very  convenient  (when  it  is  necessary  to  search  for  gall-stones, 
foreign  bodies  or  the  like  that  have  been  swallowed,  all  the  feces  must  of 
course  be  broken  up,  and  for  this  purpose  a  fecal  sieve  which  has  several 
times  been  mentioned  should  be  employed). 

A  mass  of  about  the  size  of  a  hazelnut  is  placed  in  the  mortar,  diluted 
by  the  gradual  addition  of  water  until  it  has  become  of  a  thin  fluid  con- 
sistence, when  this  is  poured  into  a  flat  glass  dish  for  further  examination. 

We  now  consider  the  following  points,  which  not  only  apply  to  the 
macroscopic,  but  to  the  microscopic  and  chemical  investigations: 

1.  The  remains  of  food: 

A.  Residue  of  food,  i.  e.,  portions  of  food  which  even  a  healthy 

intestine  cannot  absorb: 

(a)  The  bulk  of  this  is  naturally  formed  by  vegetable  con- 
stituents or  more  or  less  encrusted  cellulose.  In 
the  unopened  cells  we  not  infrequently  find  prod- 
ucts which  might  be  serviceable  in  nutrition,  but 
these  are  unabsorbed  and  discharged  in  the  feces 
because  the  husks  have  made  it  impossible  for  the 
digestive  juices  to  reach  them. 

(/3)  Animal  remains:  Firm  connective  tissue,  elastic  tis- 
sue, bone,  cartilage,  scales  of  fish,  fish  bones,  hairs, 
pieces  of  egg-shell,  scales  of  Crustacea  and  the  like. 

B.  True  remains  of  food  which  are  capable  of  being  digested  and 

may  be  acted  upon  by  the  digestive  juices,  but  for  one  reason 
or  another  have  not  been  absorbed : 

(a)  Remains  of  albumin,  chiefly  meat; 

(fi)  Carbohydrates,  particularly  starch; 

(y)  Fat  in  different  forms. 


610  EXAMINATION  OF  THE  FECES 

2.  The  kinds  and  the  amount  of  the  products  of  decomposition. 

3.  Pathologic  admixtures  from  the  intestinal  wall: 

A.  Mucus; 

B.  Blood; 

C.  Pus; 

D.  Remains  of  tissue. 

4.  Admixtures  of  other  kinds: 

A.  Such  as  have  formed  in  the  body  itself  (stones,  parasites)  ; 

B.  Such   as   have  entered  the   intestine   from   without    (foreign 

bodies). 

Between  1  A  and  1  B  of  this  group  there  is  of  course  no  sharply  de- 
fined line,  which  is  particularly  true  of  a  mixed  alternating  diet  with 
a  varying  preparation  of  the  individual  foods,  and  this  cannot  be  too 
strongly  emphasized.  In  our  test  diet  the  limitation  is  much  more  dis- 
tinctly drawn. 

It  is  worthy  of  note  that  upon  macroscopic  investigation  of  normal 
dejecta  no  undigested  constituents  are  found  which  exceed  in  size  the  head 
of  a  pin.  All  larger  particles,  therefore,  are  of  semeiotic  significance, 
and  this  increases  with  their  size.  The  conditions  are  different  with  a 
mixed  diet.  The  dejecta  of  perfectly  healthy  persons  may  be  well  formed 
and  of  normal  appearance,  yet  they  almost  invariably  contain  the  macro- 
scopically  visible  residue  of  vegetables,  especially  fragments  of  potatoes  and 
turnips,  leaves  of  lettuce,  long  shreds  of  asparagus,  perhaps  even  entire 
lentils,  the  skins  of  different  berries,  as  well  as  their  seed.  This  list  might 
be  enlarged  at  will,  and  only  the  dilution  of  normal  feces  with  water  and 
a  cursory  examination  are  necessary  in  order  to  find  these  substances. 
Diagnostic  conclusions  as  to  the  function  of  the  digestive  apparatus  should 
be  arrived  at  only  after  careful  consideration.  It  is  true  we  may  deter- 
mine from  the  presence  of  such  remains  that  mastication  was  insufficient 
and  that  the  food  was  too  rapidly  eaten;  if  these  are  absent,  the  digestive 
organs  must,  at  all  events,  be  in  a  healthy  condition. 

Of  course,  we  do  not  include  here  the  extreme  cases  in  which  numerous 
coarse  particles  are  excreted,  especially  when  the  feces  have  lost  their  nor- 
mal consistence,  and  it  is  evident  at  the  first  glance  that  these  remains  of 
food  are  but  slightly  altered,  nor  do  we  include  cases  of  lientery.  There 
can  be  no  doubt  as  to  the  significance  of  these  signs.  Animal  food  in 
general,  even  with  a  mixed  diet,  is  most  easily  absorbed.  Nevertheless  it 
IS  not  unusual  to  find  shreds  of  tendons  or  of  arteries,  imder  some  circum- 
stances also  fibers  of  meat,  and,  with  a  plentiful  ingestion,  portions  of 
tough  or  hard  unchanged  meat. 

It  is  important  for  the  physician  to  have  a  clear  conception  of  these 
facts,  since  patients,  who  for  any  reason  begin  to  observe  themselves  closely, 
frequently  bring  to  him  for  examination  some  portion  of  the  feces  which 


TEST   DIET 


611 


causes  them  anxiety,  and  the  physician  should  have  a  thorough  understand- 
ing of  such  appearances,  particularly  if  of  a  vegetable  nature.  This 
enhances  the  wisdom  of  the  physician  in  the  eyes  of  his  patient,  who  is 
not  only  relieved  in  mind  by  a  negative  diagnosis,  but  desires  to  know 
exactly  what  conditions  are  present.  In  such  cases  it  is  necessary  to  re<yu- 
late  the  diet  of  unreliable  patients,  and  the  impression  is  never  effaced  if 


Fig.  22. — A  fragment  of  grain  from  bread. 

a,  portions  of  the  pericarp;  b,  portion  of  the  pericarp  with  the  hair;  c,  fragment  of  a  hair; 
d,  cells  of  the  gluten  layer.     (Magnified  250  times.) 

the  error  in  diet  is  revealed  to  the  patient  from  the  examination  of  the 
feces. 

I  shall  first  enumerate  the  food  remains  which  most  commonly  appear: 
^\Tiile  the  residua  of  many  vegetables  so  closely  resemble  each  other 
after  digestion  that  even  the  most  skilful  botanist  cannot  differentiate 
them,  there  are,  on  the  other  hand,  a  number  of  other  food  products,  par- 
.ticularly  from  the  daily  diet,  which  can  be  recognized  at  the  first  glance. 
As  a  rule  the  aid  of  a  microscope  is  necessary.  A  number  of  illustrations 
are  given  which  are  taken  from  various  dejecta.  They  have  been  obtained 
by  centrifugation  of  the  feces  rubbed  up  with  water,  and  by  subsequent 
washing  of  the  sediment,  and  are  much  more  distinct  than  the  prepara- 
tions made  immediately  from  the  feces. 


612 


EXAMINATION   OF  THE   FECES 


We  seldom  fail  to  find  in  the  feces  the  remains  of  grain  from  bread 
(Fig.  22).  They  are  the  more  numerous  and  the  larger,  the  coarser  the 
bread  which  was   eaten.     But   these   characteristic  constituents    are   also 


Fig.  23. — Potato  cells. 

a,  emptj',  partly  contracted  and   folded;   b,  filled  with  starchy  material.     Besides  these,  a 
starch  granule  retaining  its  external  form  (stained  by  iodin).     (Magnified  250  times.) 

found  when  only  gruel  has  been  eaten :  portions  of  the  chaff  and  the  hulls 
of  the  seed,  hairs  from  the  epidermis,  and  fragments  of  the  gluten  cell 
layer. 

Almost  as  frequently  as  remains  of  grain  we  find  large  transparent 
cells    from   the  parenchyma  of  potatoes,    and  these   become  conspicuous 

on  even  slight  enlargement    (Fig. 
23). 

These  shreds  are  very  distinct, 
and  upon  the  addition  of  Congo  red 
to  the  preparation,  other  delicate 
vegetable  tissues  are  also  revealed. 
As  a  rule  they  are  empty  and  pressed 
flat;  but  some  of  them  contain  ag- 
glutinated starch,  that  is,  dextrin, 
and  in  this  case,  if  a  sufficient  quan- 
tity of  LugoFs  solution  is  employed, 
they  change  from  blue  to  red. 

The  ingestion  of  beans,  peas  and 
c  lentils  may  be  demonstrated  very 

Fig.  24. — Fragment  of  peas.  easily    (Fig.    24). 

a,  palisade  cells  of  the  seed  hull;  6,  a  Every    preparation    will    reveal 

carrier  cell  of  the   seed   hull;    c,  a  cell  from  t  x      •  ji       ji  •   i  i 

the  parenchyma  of  the  germ  leaf  filled  with  "^^^^  glisteumg,  greatly  thickened 
gluten  and  starch.      (Magnified  250  times.)  structures    in    columnar    form,    the 


TEST   DIET 


613 


so-called  palisade  cells.  Resembling  these,  but  broader  and  much  shorter, 
are  the  carrier  cells.  In  peas  these  are  detached  from  one  another,  and 
in  the  microscopic  preparation 
the}'  are  always  isolated.  The 
carrier  cells  of  beans,  however, 
form  a  continuous  layer  of 
polygonal  cells  which,  viewed 
from  the  surface,  resemble  a 
carpet.  Each  of  these  cells 
contains  a  crystal  of  calcium 
oxalate.  The  previously  men- 
tioned parts  belong  to  the  hull 
enclosing  the  seed.  The  large 
round  cells  resembling  potatoes 
filled  with  gluten  and  starch 
granules  form  the  parenchyma 
of  the  germ  leaves. 

In  the  preparation  (Fig. 
25)  we  note  very  pale,  large 
cells  which  contain  small,  isolated  structures,  orange  to  fiery  red  in  color 
(carrotin),  partly  crystalline,  partly  of  more  irregular  form ;  a  finding  which 
is  very  conspicuous  and  denotes  the  presence  of  particles  of  carrot. 

The  ingestion  of  various  leaf-like  vegetables  is  recognized  chiefly  from 
the  delicate  epidermis  with  wavy  cell  outlines  showing  intermediate  spaces. 


Fig.    25. — Carrot  cells     with    crystals    of    carrotin. 
(Magnified  250  times.) 


Fig.  26. — A  portion  of  the  leaf  of  a  head  of  lettuce. 

Above,  the  epidermis  with  wavy  limited  cells  and  with 
spaces ;  below,  the  chlorophyl  granules  in  round  cells  and 
a  branching  bundle  of  vessels.     (Magnified  250  times.) 


Fig.  27.  —  Two  stippled 
vessels  in  juxtaposition. 
(Magnified  250  times.) 


the  chlorophyl  granules  and  vessels  running  in  the  ribs  of  the  leaf  serving 
for  the  conduction  of  water,  and  adorned  with  thickened  rings  and  with 
spirals  (Fig.  26). 


614 


EXAMINATION   OF  THE   FECES 


Fig.  28. 


-Elongated  cells  from  the  stalks  of  aspara- 
gus.    (Magnified  250  times.) 


These  spirals  (see  Fig.  2T)  are  found  less  abundantly  in  other  edible 
parts  of  vegetables,  such  as  the  stems  and  roots,  and  are  less  developed  in 

the  delicate  leaves  of  flowers 
and  fleshy  fruits.  They  be- 
come tough  and  consequently 
so  indigestible  that  after  the 
consumption  of  even  small 
quantities  of  these  vegetables 
they  invariably  appear  in  the 
preparations.  Often  the  spi- 
rals are  drawn  apart,  or  are 
irregularly  layered  among 
each  other,  or  are  mixed  with 
animal  fibers  into  a  mass 
which  cannot  be  separated. 
In  the  next  preparation 
(Fig.  28)  we  see  elongated,  thin-walled  cells  originating  from  a  fiber  of 
asparagus.  These  long  threads  may  be  observed  even  macroscopieally  in  the 
feces;  they  are  usually  attached  to  shreds  of 
Tissue  or  the  hulls  of  peas  and  beans  with 
which  they  may  be  confounded.  The  micro- 
scopic picture  is  shown  because  upon  super- 
ficial view  there  is  a  decided  resemblance  to 
the  mucus  of  the  feces,  as  may  readily  be  seen 
later.  Still,  the  more  clearly  outlined  circum- 
ference is  conspicuous.  If  we  find  the 
so-called  raphides,  parallel  bundles  of  fine 
needles  consisting  of  calcium  oxalate,  this  is 
additional  proof  of  the  vegetable  nature  of 
the  preparation.     The  characteristic  cellular 

inclusions  which  are  noted  in  intestinal  mucus  are, 
of  course,  lacking. 

The  dark  truffle  spores  which  appear  in  the  feces 
after  partaking  of  this  food  are  found  in  several  com- 
bined transparent  colorless  tubes;  they  have  fine  thorns 
(Fig.  29)  and  are  easily  recognized.    The  same  is  true 
of  the  spores  of  ustilagineae  of  grain  (tilletia-caries) 
(Fig.  30)  which  not  infrequently  are  foimd  in  flour. 
A  knowledge  of  these  is  of  importance,  since  they 
may  appear  to  the  novice  to  be  the  ova  of  intestinal 
parasites ;  for  instance,  of  ascaris  lumbricoides. 
Above  all.  they  are  decidedly  smaller.     The  same  error  may  be  made 
with  lycopodium  seeds  (Fig.  31)  which,  as  is  well  known,  are  often  used 
as  a  coating  for  pills.     They  appear  to  be  partially  consumed  in  digestion. 


Fig.  29. 


Fig.  30. 


Fig.  29. — Spores  of  truffles  in  an 
ascus.     (Magnified  250  times.) 

Fig.  30. — Mildew  sjiores  of  wheat 
(tilletia-caries),  producing  stone 
or  stinking  rust.  (Magnified 
250  times.) 


Fig.  31. — Spores  of  ly- 
copodium clavatvun 
(semen  lycopodii). 
(Magnified  250  times.) 


TEST   DIET 


615 


As  the  remains  of  fruit,  I  shall  mention  only  the  very  characteristic 
core  (stone  cells)  of  pears  which  gives  to  the  pulp  its  toughness,  and  which 
is  present  even  in  the  finer  varieties   (Fig.  32). 

The  possibility  of  confounding  the  tubules  of  oranges  with  intestinal 
parasites  must  be  pointed  out  to  the  investigator,  especially  if  he  limits 
himself  to  a  macroscopic  inspection. 
Virchow  was  the  first  to  describe  a  case 
of  this  kind. 

I  must  devote  a  few  words  to  the  elas- 
tic fibers  in  the  remains  of  animal  food. 
These  belong  to  the  parts  which  are  diffi- 
cult to  digest  but  not  wholly,  indigestible ; 
their  dissolution  may  occur  in  the  gastric 
juice  as  well  as  in  the  pancreatic  juice. 
With  a  mixed  diet  we  frequently  find 
elastic  tissue,  and  attach  no  especial  diag- 
nostic importance  to  its  appearance.  Sometimes  we  observe  its  well  known 
double  contours,  beautifully  wound  fibers  in  an  unchanged  condition,  but 
their  continuity  somewhat  broken  by  the  digestion  of  the  intermediary  tissue 


Fig.  32. — Stone  cells  (core)  from  the 
pulp  of  pears.  (Magnified  250 
times.) 


Fig.  33. — Elastic  fibers.      (Magnified  250  times.) 


(Fig.  33) ;  sometimes  we  see  them  in  a  half  digested  condition,  traversed 
horizontally  by  numerous  lines  so  that  they  may  be  confounded  with  fibers 
of  wool. 


616  EXAMINATION   OF  THE   FECES 

A  middle  position  between  the  residua  of  food  and  the  true  food  stuffs 
may  be  assigned  to  connective  tissue  (Fig.  34).  The  form  in  which  it  is 
ingested,  more  than  the  absolute  quantity,  accounts  to  a  great  extent  for 
its  reappearance  in  the  feces.  According  to  Schmidt  the  greatest  bulk 
of  connective  tissue  is  left  by  smoked  meat,  next  by  raw  meat,  still  less 
by  fried  meat,  and  least  by  tender  boiled  meat.  Consequently,  especially 
after  the  ingestion  of  raw  ham,  we  not  infrequently  find  enormous  amounts 

of  connective  tissue  convolutions 
which  permeate  the  feces  like  a  fine 
film,  and  which  appear  only  upon 
breaking  up  and  washing  the  dejecta 
with  watey. 

The  knowledge  of  this  fact  warns 
us  to  be  less  liberal  in  allowing  pa- 
„,     ^         ^.       ^.  ,-,      .c  J     tients  raw  ham  than  is  the  case  at 

Pig.    34. ^Connective    tissue.      (Magnined 

250  times.)  present. 

We  see  that  with  a  freely  chosen 
diet  the  presence  of  connective  tissue  in  the  feces  as  a  rule  permits  no  con- 
clusion as  to  the  function  of  the  digestive  apparatus,  provided  large  quan- 
tities have  not  been  passed.  The  circumstances  are  different  with  our  test 
diet,  and  upon  this  foundation  Schmidt  formulated  a  very  valuable  clinical 
test.  Raw  connective  tissue,  for  instance,  is  digested  only  by  the  gastric 
juice,  not  by  the  pancreatic  juice.  Now  the  test  diet  contains  125  grams 
of  raw  scraped  beef  which,  in  order  to  make  it  palatable  for  those  patients 
who  refuse  to  eat  raw  meat,  is  broiled  very  lightly  on  the  outside.  Expe- 
rience proves  that  the  connective  tissue  in  this  so-called  "  German  beef- 
steak "  is  under  normal  circumstances  so  completely  digested  that  macro- 
scopically  no  residue  can  be  found  in  the  feces. 

Even  the  smallest  portions  visible  to  the  naked  eye  point  to  a  disturb- 
ance of  digestion  which,  as  is  obvious  from  the  preceding,  has  its  seat  in 
the  stomach,  since  only  this  organ  has  the  power  to  digest  raw  connective 
tissue.  As  a  rule,  in  such  cases  there  is  a  decrease  in  the  secretion 
of  hydrochloric  acid.  Under  some  circumstances,  however,  other  dis- 
turbances of  the  gastric  function  are  at  fault.  Thus  the  investigation 
of  the  dejecta  may  in  certain  cases  point  to  an  unsuspected  gastric 
ail'ection,  and  under  others  may  give  us  a  clue  to  the  malady  even  when 
the  patients  refuse  the  introduction  of  the  gastric  tube  for  diagnostic 
purposes. 

We  shall  now  consider  the  manner  in  which  the  true  remains  of  food 
a])pear  in  the  feces,  these  being  chiefly  represented  by  muscle  fiber,  starch 
and  fat,  the  latter  in  varying  chemical  combinations.  From  the  shape  and 
quantity  we  endeavor  to  form  an  opinion  as  to  the  function  of  the  digestive 
api^aratus,  especially  of  the  intestines  and  the  large  contiguous  glands,  the 
])anLreas  and  the  liver.     We  can  then  decide  in  how  far  a  freely  chosen 


TEST   DIET 


617 


diet  is  permissible,  and  in  how  far  we  may  succeed  with  the  test  diet 
proposed  by  Schmidt  and  myself. 

As  a  rule  remains  of  meat,  even  with  a  mixed  diet,  cannot  be  found 
by  microsco|)ic  inspection  of  the  feces.  Therefore,  the  presence  of  large 
portions  must  be  regarded  as  pathologic.  But  in  the  test  diet  the- limits 
are  more  sharply  drawn.  Here  the  presence  of  the  smallest  portion  of 
muscle,  detected  without  magnifying,  denotes  disturbance  either  on  the 
part  of  the  small  intestine  or  of  the  pancreas,  while  an  affection  which 
implicates  only  the  stomach  or  the  colon  does  not  cause  the  excretion  of 
macroscopically  recognizable  remains  of  meat.  We  may  therefore  to  some 
extent  form  an  opinion  as  to  the  seat  of  the  disturbance  of  function.  It 
is  true  this  gives  us  no  deep  insight  into  the  nature  of  the  affection.  The 
small  intestine  and  the  pancreas  have  in  common,  as  is  well  known,  three 
important  functions,  secretion,  absorption,  and  motility.  It  would  be  a 
great  advantage  if  we  could  recognize  in  the  individual  case  which  of  these 
factors  has  suffered.  As  a  rule,  however,  it  is  impossible  to  form  any 
opinion  in  regard  to  this.  A  decrease  in  the  digestion  of  meat,  taken  by 
itself,  is  no  certain  guide. 

If  the  excreted  fragments  of  muscle  are  found  permeated  by  connective 
tissue  it  is  obvious,  from  what  has  been  previously  stated,  that  a  faulty 
function  of  the  stomach  is  present  besides  the  intestinal  disturbance. 

In  the  microscopic  discrimination  of  muscle  fibers  we  must  be  much 
more  cautious  than  in  the  macroscopic  recognition  of  residue  of  meat  in 
the  excretion.  In  man,  after  the 
ingestion  of  meat,  we  invariably 
find  small  fragments  of  muscular 
fiber  in  the  feces,  and  according  to 
the  stage  of  digestion  in  which 
they  are  found  three  varieties  may 
be  differentiated:  1.  Large,  dis- 
tinctly transverse,  striated  shreds 
with  sharp,  angular  contours; 
2.  Medium  sized  particles  with 
rounded  edges,  their  transverse 
striae  less  distinct ;  therefore  a  well- 
developed  longitudinal  striation  is  usually  visible;  3.  Small  polygonal  or 
round  cells  whose  striation  has  been  somewhat  obliterated  or  is  entirely 
lacking  (Fig.  35). 

Between  these  three  forms  there  are,  of  course,  many  transitional  stages. 
After  administering  a  test  diet  we  may  assume  an  intestinal  disturbance 
if  many  remains  of  muscle  of  the  first  mentioned  category  are  conspicuous 
in  the  preparation.  In  such  instances,  as  a  rule,  fibers  of  meat  may  be 
recognized  macroscopically. 

From  the  foregoing  it  is  obvious  that  a  more  accurate  method  of  esti- 


FiQ.  35. — Muscle    fibers    in    various    stages   of 
digestion.     (Magnified  250  times.) 


618  EXAMINATION   OF  THE   FECES 

mating  the  amount  of  meat  digested  is  a  practical  necessity  to  enable  us 
to  form  a  definite  opinion  regarding  this  function  of  the  intestine.  The 
first  improvement  in  this  direction  we  owe  to  Kermauner.  But  his  method, 
based  upon  counting  the  number  of  muscle  fibers  in  a  microscopic  prepara- 
tion, is  laborious  and  does  not  always  ensure  accuracy.  The  method 
cla])oratcd  by  Schmidt  is  better.  In  this  the  amount  of  the  cleansed  sedi- 
ment of  the  feces  is  determined  volumetrically,  after  which  it  is  again 
subjected  to  digestion.  By  this  process  all  the  residue  of  meat  which  is 
at  all  digestible  is  acted  upon  by  the  digestive  juices  and  dissolved.  If 
the  remaining  volume  of  sediment  is  then  deducted  from  that  first  found, 
we  have  the  actual  amount  of  proteids  which  are  insusceptible  to  intestinal 
digestion.  In  employing  the  test  diet,  as  Schorlemmer  ascertained  under 
Schmidt's  direction,  the  difference  between  the  normal  and  pathologic  in- 
testinal functions  may  very  easily  be  determined.  This  may  be  utilized 
in  scientific  researches,  but  for  clinical  practice  it  is  much  too  laborious 
to  find  wide  application. 

Until  very  recently,  the  question  has  been  much  discussed  whether,  and 
in  what  form,  starch  normally  appears  in  the  feces.  In  order  to  form  an 
oi)ini()n,  Ave  must  first  of  all  separate  the  starch  granules  or  agglutinated 
shreds  which  are  enclosed  in  cells  from  the  free  starch.  With  a  mixed  diet 
the  first  forms  are  invariably  found  in  the  sediment  of  the  feces.  Never- 
theless Nothnagel's  opinion  that  perfectly  retained  free  starch  granules 
are  normally  absent  is  correct.  Naifurally  we  must  be  careful  to  see  that 
starch  is  not  liberated  during  the  preparation  by  pressure  upon  the  cells; 
for  this  reason,  in  the  question  under  discussion,  weight  is  attached  only 
to  the  opinions  of  those  authors  whose  researches  into  the  dejecta  have 
been  characterized  by  great  precision  and  the  consideration  of  this  point. 
The  reports  of  Ledden-Hulsebosch,  whose  investigations  were  marked  by 
extraordinary  attention  to  detail,  are  especially  reliable.  Ledden-Hulse- 
bosch found  that  even  if  well  retained  granules  do  not  appear  with  a 
mixed  diet,  nevertheless  agglutinated  starch  in  the  form  of  layers  and 
shreds  lying  free  is  detected.  Naturally  this  can  only  be  determined  by 
the  careful  investigation  of  the  cleansed  sediment  of  the  feces.  The  addi- 
tion of  iodin  to  the  simple  microscopic  preparation,  even  if  a  large  amount 
i;<  iidded.  frequently  produces  no  result,  although  it  can  be  certainly  proven 
by  other  methods  that  starch  is  present.  This  certainty  is  attained  if  we 
subject  the  feces  to  a  "  fermentation  test,"  or,  as  Schmidt  generally  ex- 
presses it,  to  an  "incubation  oven  test";  i.  e.,  the  feces  diluted  with  water 
ill  a  suitalile  vessel  are  subjected  to  the  heat  of  an  incubation  oven  after 
which  we  note  whether  processes  of  decomposition  appear  and  also  their 
action.  If  the  absorption  of  food  has  been  so  complete  that  the  feces  show 
in  the  main  only  a  residue,  no  decided  change  takes  place  after  about 
twenty-four  hours  in  the  incubation  oven.  If,  however,  constituents  of 
the  food  which  may  be  readily  acted  upon  are  admixed  (and  this  is  par- 


TEST  DIET  619 

ticularly  true  of  albumin,  starch,  and  to  a  less  degree  of  fat),  these 
are  broken  up  by  the  microorganisms  of  the  feces  on  the  formation 
of  the  characteristic  products  of  decomposition.  According  to  the  char- 
acter of  this  process,  we  differentiate  between  fermentation  and  decom- 
position. 

Fermentation,  as  a  rule,  runs  a  more  rapid  course  than  decomposition, 
and  is  attended  by  the  production  of  odorless  gas  and  an  increase  in  the 
acidity  of  the  feces,  the  color  of  the  dejecta  becoming  lighter.  The 
process  of  fermentation  depends  upon  the  decomposition  of  carbohydrates, 
particularly  of  starch,  which  is  changed  into  sugar  by  the  diastatic  ferment 
always  present  in  the  feces,  and  is  further  disintegrated  by  the  bacteria 
present  in  large  amounts.  Decomposition  is  slower;  gas,  as  a  rule,  is 
developed  in  less  amount  but  is  characterized  by  its  disagreeable  odor. 
In  this  process  the  feces  become  alkaline,  their  color  darker.  This  is  the 
consequence  of  decomposition  of  albumin,  and  less  of  the  remains  of  food 
which  do  not  so  readily  undergo  decomposition,  as,  for  instance,  the 
pathologic  products  which  are  excreted  from  the  intestinal  wall,  such  as 
mucus,  pus  and  blood. 

A  positive  reaction  of  the  fermentation  test,  therefore,  shows  us  tlfie 
presence  of  carbohydrates  in  the  feces.  A  point  to  be  observed  is  whether 
they  are  of  such  nature  that  they  may  be  readily  acted  upon  by  the 
bacteria,  and  are  therefore  susceptible  to  intestinal  digestion  and,  with 
sufficient  power  of  the  intestine,  would  have  been  digested.  We  are  dealing 
with  actual  food  residue,  not  the  remains  of  food.  In  accordance  with  the 
fact  previously  mentioned  that  we  frequently  find  free  remains  of  starch, 
the  fermentation  test  with  a  mixed  diet  is  often  positive.  It  is  a  fine 
reagent,  and  gives  results  even  in  cases  in  which  the  ordinary  examination, 
the  usual  microscopic  investigation  of  starch,  is  unsatisfactory.  If  the 
amount  of  carbohydrates  in  the  food  is  limited  to  a  certain  extent,  as  in 
our  test  diet,  fermentation  will  normally  not  be  present,  as  the  intestine 
is  fully  capable  of  absorbing  the  amount  of  carbohydrates  it  contains.  In 
some  cases,  however,  even  after  the  test  diet,  the  feces  contain  starch 
and  ferments ;  we  are  then  justified  in  speaking  of  the  "  insufficiency  of 
starch  digestion." 

At  the  same  time,  the  other  foods  may  be  well  absorbed.  Such  an 
occurrence  is  not  rare,  and  it  forms  a  symptom-complex  which  Schmidt 
and  I  have  described  as  "  intestinal  fermentative  dyspepsia."  In  this 
condition,  so  far  as  our  observations  extend,  the  stomach,  colon,  and 
probably  also  the  pancreas,  function  in  a  normal  manner;  since  the  labor 
of  starch  digestion  is  laid  principally  on  the  small  intestine,  we  have 
reason  to  believe  that  we  are  dealing  with  a  disturbance  of  the  small 
intestine,  probably  with  an  anomaly  in  the  secretion  of  the  intestinal 
juice,  a  secretion  which  has  normally  a  powerful  amylolytic  action.  To 
demonstrate  fermentative  dyspepsia  while  employing  the  test  diet,  we  use 


620  EXAMINATION   OF  THE   FECES 

the  fermentation  test,  a  method  which,   as  we  learn  by   experience,  is 
superior  to  searching  the  microscopic  preparation  for  starch. 

I  shall  demonstrate  from  the  feces  of  a  patient  the  relation  to  intestinal 
fermentative  dyspepsia.  These  dejecta  were  from  a  powerfully  built,  fairly 
well  nourished  man  in  middle  life,  who  for  months  had  complained  fre- 
quently of  abdominal  pain  particularly  in  the  region  of  the  navel,  also 
of  a  certain  lassitude  and  malaise.  There  were  no  gastric  symptoms. 
From  time  to  time  there  was  constipation ;  frequently,  however,  there  were 
two  or  three  thin,  pappy  stools  daily.  Actual  diarrhea  was  never  present. 
Upon  careful  questioning  the  patient  recalled  that  the  dejecta  were  some- 
times foamy,  of  a  light  color,  the  odor  sometimes  resembling  that  of  old 
cheese.  On  such  days  the  fecal  evacuations  occurred  three  or  four  times 
in  twenty-four  hours.  The  consistence,  however,  was  not  fluid  but  always 
pappy.  External  examination  of  the  chest  and  abdominal  organs  re- 
vealed only  a  moderate  distention  of  the  abdomen  and  a  diffused  sensitive 
ncss  to  pressure  around  the  navel,  particularly  to  the  left.  The  epigastrium 
Avas  not  painful  upon  pressure;  the  tongue  was  slightly  coated.  An  exam- 
ination of  the  evacuated  gastric  contents  showed  them  to  be  normal. 
The  feces  were  then  examined,  as  it  was  to  these  the  history  pointed. 

The  patient  was  instructed  to  bring  a  specimen  of  the  dejecta  for 
examination,  but  I  shall  not  relate  what  was  then  found  as  the  investi- 
gation revealed  nothing  definite.  The  man  was  then  placed  upon  our 
test  diet.  On  inspecting  the  feces  it  was  noted  that  the  consistency  was 
pappy,  somewhat  thinner  than  normal,  the  reaction  moderately  acid. 
Otherwise  both  microscopically  and  macroscopically  no  abnormal  admixture 
was  found.  Meat  and  fat  were  well  absorbed.  On  the  other  hand,  the 
number  of  potato  cells  was  conspicuous;  most  of  them  were  empty;  with 
iodin  they  occasionally  revealed  demonstrable  starch.  No  free  remains 
of  starch  were  found.  The  fermentation  test  was  then  made  in  the 
following  manner: 

About  5  grams  of  the  well  mixed  feces  were  disintegrated  by  means 
of  a  suitable  instrument  (a  wooden  spatula).  If  the  feces  are  hard  less 
sliould  be  taken,  if  thin  a  correspondingly  larger  amount,  so  that  approxi- 
mately about  the  same  amount  of  dry  substance  is  worked  up.  The  fer- 
iiH'utation  vessel  ^  (Fig.  36)  is  taken  apart  so  that  only  three  rubber  plugs 
aie  cornhined  with  one  another.  In  a,  the  lower  chamber  of  the  fermenta- 
tion tube,  the  feces  are  stirred  up  with  water,  after  which  the  rubber 
i)lug  is  placed  within  the  tube  to  prevent  the  formation  of  air  bubbles. 
The  chamber,  h,  is  filled  with  water  and  also  closed  with  a  smaller  rubber 
plug,  so  that  no  air  bubbles  can  form  in  the  tube.  Finally,  the  tube,  c, 
which  has  at  its  apex  a  small  hole  for  the  escape  of  air,  is  placed  in 
position.    The  illustration  shows  how  far  the  glass  tubes  which  are  united 

iMade  by  C.  Gerhardt  in  Bonn, 


TEST  DIET 


621 


project  into  the  lumen  of  the  larger  tube.  After  the  parts  of  the  appara- 
tus are  attached,  it  is  placed  for  twenty-four  hours  in  an  incubation  oven 
heated  to  37°  C,  or  into  a  water  bath  of  the  same  temperature.  If  gas 
develops  from  the  feces,  a  corresponding  amount  of  water  is  forced  into 
the  ascending  tube,  c,  where  the  height  of  the  water  may  be  read  off. 
The  reaction  of  the  feces  should  be  tested  with  litmus  paper  before. and 
after  fermentation.  The  diagnostic  employment  of  fermentation  is  only 
indicated  after  the  test  diet  recommended  by  Schmidt  and  Strasburger.^ 

Of  course,  any  other  fermentation  apparatus  may  be  employed;  for  in- 
stance, those  used  in  the'  examination  of  urine.  Our  fermentation  tubes, 
however,  permit  a  more  accurate  opinion  as  to  the 
amount  of  gas  formation  since  nothing  is  lost  in  fer- 
mentation, and  the  amount  of  displaced  water  may 
be  more  easily  read  than  that  of  the  gas  which  has 
been  formed,  since  this  in  part  permeates  the  feces  in 
the  form  of  bubbles. 

The  test  is  to  be  looked  upon  as  positive  when  at 
least  a  third  of  the  tube,  c,  is  filled  with  displaced 
water.  This  ha])pened  in  our  case.  The  examination 
with  litmus  paper  showed  a  positive  acid  reaction  of 
the  fermenting  feces,  and  we  then  determined  that  the 
gases  formed  were  odorless.  In  the  patient  in  question 
we  could  scarcely  have  formed  an  opinion  as  to  the 
malady  present  except  by  this  test.  It  is  true  our 
diagnosis  is  a  purely  functional  one,  the  anatomical 
disturbance  causing  it  being  still  unrecognizable.  But 
in  the  great  majority  of  cases  it  is  probably  due  to 
catarrh  of  the  mucous  membrane  of  the  small 
intestine. 

By  the  aid  of  the  fermentation  test  we  have  come 
to  a  conclusion  as  to  the  nature  and  the  degree  of  the 
processes  of  decomposition  to  which  the  feces,  if  we 
may  be  permitted  the  expression,  are  predisposed.  In 
well  developed  eases  this  decomposition  attains  its  full 

development  in  the  intestine  itself,  and  the  dejecta  when  discharged  are 
either  light,  foamy,  and  acid,  the  odor  reminding  us  of  butyric  acid,  or 
they  are  dark,  have  an  alkaline  reaction  and  a  fetid  odor,  which,  under 
some  circumstances,  may  be  even  putrid.  In  comparison  with  the  preceding, 
the  disturbances  last  enumerated  are  always  more  serious,  and  correspond 
with  what  we  learn  from  the  subjective  examination  of  the  patient. 

I  have  included  in  my  discussion  of  the  absorption  of  albumin  and 


Fig.  36. — Fermentation 
tubes  with  contents. 

Positive  reaction  of  the 
fermentation  test.  The 
quantity  displaced  in 
tube,  c,  is  greater  than 
that  of  the  gas  in  the 
upper  part  of  tube,  b, 
as  a  portion  of  the  gas 
has  been  retained  in 
the  feces  in  the  ves- 
sel, a.  (One-fifth  of 
natural  size.) 


1  Compare  S!chmi(lt  and  Stranhurger,  "  Die  Faces  des  Mensehen."     Berlin,  Hirach- 
wald,  2.  Aufl.,   1905;  or,  Deutsches  Archiv  fiir  klin.  Medicin,  LXIX,  p.  570. 


622  EXAMINATION  OF  THE  FECES 

carbohydrates  the  description  of  the  processes  of  decomposition,  but  I  have 
not  yet  touched  upon  the  question  of  the  digestion  of  fat,  which  naturally 
must  be  included  with  that  of  albumin  and  starch,  and  which  we  shall 
now  consider. 

Fat  is  found  in  the  feces  in  different  forms;  in  the  adult  chiefly  as 
soaps  of  earthy  alkalies,  in  short  colorless  crystals  and  needles,  or  as 
flakes.  The  latter  are  either  colorless  or  tinged  yellow  to  brown  by 
biliary  coloring  matter  when  they  form  the  yellow  calcium  salts,  so  called 
by  Xothnagel.  More  rarely  we  observe  free  fatty  acids,  long  curved 
needles  such  as  are  also  observed  in  the  sputum  in  putrid  bronchitis. 
Neutral  fat,  according  to  its  melting  condition,  occurs  either  in  the  shape 
of  granules  or  drops.  The  latter  are  normally  absent  in  adults  on  ac- 
count of  the  ready  absorption  of  fats  that  are  melted.  On  the  other  hand 
they  may  be  found  in  healthy  nurslings.  In  the  microscopic  preparation 
they  form  structures  with  borders,  like  the  lakes  upon  a  map,  and  are 
stained  an  intense  yellow  by  bilirubin. 

What  form  of  fat  is  present  is  generally  very  easy  to  decide:  Upon 
heating  of  the  preparation  neutral  fats  and  fatty  acid  needles  coalesce, 
and  may  be  separated  by  solution  in  ether.  In  the  soaps  this  is  possible 
only  after  splitting  the  preparation  with  heat  and  adding  acid.  This 
reaction  will  also  give  us  some  idea  of  the  number  and  size  of  the  fatty 
acid  drops  in  the  quantity  of  fat  present  in  the  preparation.  In  Fig.  37 
we  see,  highly  magnified,  the  many  soap  needles  of  a  fatty  stool,  while 
Fig.  38  shows  the  same  preparation  after  heating  and  the  addition  of 
dilute  sulphuric  acid.  I  chose  this  acid  chiefly  because  the  calcium  crys- 
tals so  numerously  present  in  the  preparation  furnish  proof  that  the  base 
of  the  soaps  with  which  we  are  here  dealing  is  principally  calcium.  This 
metal  combines  with  sulphuric  acid  and  forms  calcium  sulphate.  Such 
calcium  soaps,  when  mixed  with  fibers  of  vegetables,  particularly  after  the 
ingestion  of  olive  oil  or  after  oil  enemata,  may  be  found  in  the  feces, 
often  as  concrements  which  are  erroneously  considered  to  be  gall-stones. 
A  quack  in  this  neighborhood  utilizes  this  fact  in  the  treatment  of  many 
patients  who  come  to  him  with  various  symptoms;  he  institutes  an  oil 
treatment  for  gall-stones,  and  at  the  conclusion  of  the  treatment  he  hands 
to  the  patient  the  "  stones "  which  have  been  passed.  It  is  true  that, 
after  a  little  time,  these  stones  crumble  in  the  hands  of  the  patient. 

Of  course  a  considerable  increase  of  fat  in  the  stool  may  be  easily 
recognized.  If,  however,  the  amount  of  fat  is  less  marked  it  is  often 
difficult  to  define  the  limits  of  what  may  be  regarded  as  normal.  Only 
exact  chemical  analyses,  too  intricate  for  ordinary  practice,  will  enable 
us  to  arrive  at  conclusions.  Upon  microscopic  investigation,  however, 
we  may  assume  an  increase  when  in  nurslings  (except  very  young  breast- 
fed children)  flakes  of  fat  are  found  profusely  permeating  the  entire 
{)reparalion,  and  especially  if  free  fatty  acids  and  soaps  are  also  found 


TEST   DIET 


623 


in  large  amounts.  Drops  of  neutral  fat  are  not  normally  present  in  the 
feces  of  adults  except  after  the  administration  of  castor  oil.  They  are, 
however,  observed  after  severe  diarrhea,  and  then  are  stained  an  intense 
yellow  by  bilirubin.  The  appearance  of  numerous  fatty  needles,  too,  is 
pathologic.  In  jaundice,  for  example,  the  feces  consist  almost  wholly  of 
soap  needles.  On  employing  our  test  diet  we  find,  as  Schmidt  determined, 
that  only  soaps  in  the  form  of  unstained  flakes  or  as  yellow  calcium  salts 
are  normally  present;  there  are  neither  fatty  acids,  nor  soap  needles,  nor 
neutral  fat  drops. 

The  presence  of  abnormal  quantities  of  fat  in  the  feces  may  be  attrib- 
uted to  very  different  causes :  To  the  absence  of  bile,  to  disturbance  of  the 
pancreatic  secretion,  or  to  disturbance  of  intestinal  digestion.  In  the  given 
case  it  is  by  no  means  easy  to  apprehend  clearly  which  of  these  factors 
is  present.  In  the  examination  of  the  feces,  more  than  in  any  other  way, 
we  are  impressed  with  the 
absolute  necessity,  for  purely 
diagnostic  reasons,  of  insti- 
tuting various  chemical  tests 
which  are  sometimes  not  at 
all  simple. 

I  shall  illustrate  this  by 
a  concrete  case.  The  feces, 
which  were  of  a  salve-like  and 
uniform  consistence,  and  of 
silver  gray  or  whitish  color, 
had  but  slight  odor,  and  were 
of  moderately  acid  reaction. 
They  appeared  to  show  the 
characteristics  of  the  feces  in 
occlusion  of  bile.  The  fact  was  therefore  surprising  that  the  patient  who 
evacuated  these  feces  showed  no  sign  of  jaundice,  and  passed  clear  urine 
which  was  free  from  biliary  coloring  matter.  An  occlusion  of  bile,  there- 
fore, was  not  present,  and  the  following  possibilities  were  suggested  and  an 
attempt  made  to  clear  up  the  diagnosis  by  further  investigation.  The  lead 
color  of  the  feces  might  be  due:  1.  To  a  cessation  of  the  secretion  of  bile; 
3.  To  a  too  great  reduction  of  hydrobilirubin,  thus  forming  leukohydro- 
bilirubin;  3.  To  an  immoderate  amount  of  fat  which,  under  some  circum- 
stances, is  alone  sufficient  to  cause  the  ashy  color  of  the  feces. 

From  the  salve-like  consistence  and  the  peculiar  luster  of  the  feces 
in  our  case  we  decided  upon  an  increase  of  fat.  The  microscopic  prepara- 
tion showed  numerous  soap  needles,  and  upon  heating  and  adding  acid, 
large  numbers  of  acid  fat  globules  were  formed.  The  preparations  (Fig. 
37  and  Fig.  38)  which  have  been  already  described  were  obtained  from 
these  feces.     The  marked  increase  of  fat  in  the  dejecta  was  therefore 


Fig.  37. — Soap  crystals  and  soap  granules. 
(Magnified  500  times.) 


624 


EXAMINATION   OF  THE   FECES 


positive,  and  it  is  quite  likely  that  this  accounted  for  the  peculiar  color 
of  the  feces.  We  then  instituted  another  test,  an  attempt  to  prove  the 
presence  of  biliary  coloring  matter.  For  this  purpose  I  mixed  a  large 
portion  of  the  feces  with  dilute  acid,  heated  it  to  split  the  soaps,  and  after 
cooling  I  added  ether.  Thus  it  was  possible  to  remove  a  portion  of  the 
fat,  after  which  the  color  of  the  remaining  feces  became  a  distinct  brown. 
I  subsequently  attempted  to  prove  the  presence  of  biliary  coloring  matter, 
and  for  this  purpose  added  to  the  fresh  feces  some  hydrochloric  acid- 
alcohol.  When  hydrobilirubin  or 
leukourobilin  (bilirubin  is  not  found 
in  the  normal  feces  of  the  adult)  is 
present,  the  coloring  matter  may  be 
obtained  from  the  feces  in  the  fol- 
lowing manner :  To  the  clear  filtrate 
of  the  extract,  I  add  a  few  drops  of 
ammonia  and  a  solution  of  zinc 
chlorid,  whereupon,  after  some  time, 
and  in  a  clear  light,  a  beautiful 
greenish  fluorescence  is  noted.  Leu- 
kohydrobilirubin,  which  is  demon- 
strated by  this  test,  is  changed  back 
into  hydrobilirubin.  Another  por- 
tion of  the  extract  I  subject  to  a 
spectroscopic  examination.  With  a 
suitable  dilution  the  characteristic 
absorption  bands  are  found  to  be 
very  distinct  in  the  markedly  broken 
portion  of  the  spectrum,  between 
the  lines  h  F,  which  move  somewhat 
to  the  left  when  the  fluid  is  rendered  alkaline.  This,  therefore,  furnishes 
prooi'  that  the  biliary  coloring  matter  has  been  excreted  and  has  reached 
tlie  feces.  That  a  too  great  reduction  of  coloring  matter  was  the  cause  of 
tlie  white  color  of  the  feces  as  well  as  their  richness  in  fat  is  improbable 
on  account  of  the  great  amount  of  fat  present  in  the  stool,  for  the  pres- 
ence of  leukourobilin  does  not  normally  cause  a  disturbance  in  the  diges- 
tion of  fat. 

The  whitish  appearance  of  the  stool  is  therefore  due  to  the  immoderate 
amount  of  fat  present,  and  the  question  now  arises  to  what  the  insufficient 
absorption  of  fat  is  to  be  attributed.  As  the  absence  of  bile  cannot  be 
considered  the  cause,  the  possibility  remains  of  a  disturbance  in  the  secre- 
tion of  the  pancreatic  juice,  or  a  disturbance  of  intestinal  digestion. 
The  examination  of  the  feces  also  gives  us  many  points  which  aid  in  the 
elucidaiion  of  this  question. 

Absence  of  the  pancreatic  secretion  often  leads  to  a  deficient  splitting 


Fig.    38. — The  same  preparation  as  Fig.  37, 
but  after  heating  with  dilute  sulphuric  acid. 

The  fatty  acid  is  seen  in  drops.  In  the  in- 
terior and  at  the  periphery  of  a  large  drop, 
fatty  acid  needles  are  beginning  to  crystal- 
lize. Tlie  large  crystalline  needles  are  cal- 
cium crystals  and  prove  that  the  base  of  the 
soap  is  calcium.     (Magnified  500  times.) 


TEST  DIET  625 

of  fat,  which  is  excreted  in  the  feces  chiefly  as  neutral  fat.  Only  the  most 
minute  quantitative  chemical  analysis  will  positively  demonstrate  this. 
Nevertheless  if  numerous  soap  crystals  are  present  when  we  examine  the 
microscopic  preparation,  or,  on  the  other  hand,'  neutral  fat  appears  in 
the  form  of  drops,  we  may  form  a  definite  opinion.  Notwithstanding 
decreased  fat  splitting,  the  total  quantity  of  fat  excreted  is  not  necessarily 
increased;  but,  besides  a  sufficient  splitting  of  fats,  a  large  amount  of 
fat  may  be  observed  in  the  feces  in  disease  of  the  pancreas.  The  picture 
therefore  varies  greatly. 

The  absence  of  the  pancreatic  secretion  also  causes,  as  a  rule,  a  decided 
decrease  in  the  absorption  of  albumin  which  may  be  recognized  in  the 
microscopic  preparation  by  the  presence  of  numerous  fragments  of  muscle 
with  sharp  edges. 

Ad.  Schmidt  has  called  attention  to  another  significant  feature.  It 
depends  upon  the  fact  that  cell  nuclei  are  digested  only  by  the  pancreatic 
juice.  If  this  secretion  is  absent  the  cell  nuclei  are  found,  for  example, 
in  the  muscle  fibers.  Schmidt  considers  it  advisable  to  give  small  pieces 
of  meat  which  have  been  hardened  in  alcohol,  and  subsequently  placed 
within  very  thin  gauze  coverings.  These  are  easily  detected  in  the  feces, 
and  if  in  natural  condition,  otherwise  after  staining,  they  are  examined 
for  the  presence  of  cell  nuclei.  This  test  can  be  utilized  only  if  the  result 
is  positive,  since  under  some  circumstances  intestinal  decomposition  alone 
is  sufficient  to  destroy  the  cell  nuclei. 

In  doubtful  cases  the  investigation  of  the  feces  after  the  administration 
of  pankreon  may  give  us  light. 

Other  tests  for  the  diagnosis  of  disease  of  the  pancreas  must  be  omitted 
since  they  do  not  pertain  to  our  theme.  But  a  point  to  be  specially 
emphasized  is  that  the  symptoms  of  disease  of  the  pancreas  appear,  as 
a  rule,  only  when  the  gland  is  nearly  or  entirely  destroyed.  They  may 
he  absent  even  with  complete  occlusion  of  the  excretory  ducts,  and  this 
leads  us  to  think  that  the  secretion  may  find  its  way  into  the  intestine 
by  some  other  channel.  Hence  mild  disturbances  of  the  pancreatic  func- 
tion invariably  escape  recognition. 

If,  in  diseases  of  the  pancreas,  the  increase  of  fat  in  the  dejecta  is 
due  to  intestinal  disturbances,  we  often  find  an  increase  also  of  the  remains 
of  meat,  but  in  this  case  it  appears  to  be  less  marked.  As  the  excretion 
of  fat  in  intestinal  diseases  is  chiefly  caused  by  deficient  absorption, 
eventually  other  signs  of  a  lack  of  absorption  appear,  and  confirm  the 
diagnosis. 

The  presence  of  dissolved  albumin  is  especially  important  because  this 
is  not  found  in  normal  feces.  Great  care  is  necessitated  in  its  demon- 
stration, as  we  have  learned  by  the  experiences  of  the  last  few  years.  It 
is  especially  important  not  to  confound  it  with  the  nucleo-proteid  of  the 
feces  which  is  invariably  present.  The  easiest  and  most  reliable  method 
41 


626  EXAMINATION   OF  THE   FECES 

appears  to  be  that  of  0,  Simon  ^ :  Water  is  poured  over  the  fresh  feces 
and  the  mixture  is  allowed  to  stand  for  some  time,  after  which  the  liquid 
is  carefull}'  drained  off  and  filtered.  To  make  it  perfectly  clear  diatomace- 
ous  earth  is  added,  the  mixture  is  shaken,  and  again  filtered.  Dilute  acetic 
acid  is  then  cautiously  added  to  precipitate  the  nucleo-proteid,  and  the  mix- 
ture is  again  filtered.  It  is  difficult  correctly  to  estimate  the  amount  of  acid 
necessary,  for  if  the  acetic  acid  is  in  excess  it  will  again  dissolve  the  nucleo- 
proteid.  If,  after  the  addition  of  acetic  acid,  a  slight  turbidity  appears 
which  is  very  difficult  to  filter,  another  acetic  acid  test  may  be  made  with 
larger  amounts,  and  subsequently  a  test  for  albumin  with  dilute  potassium 
fenocyanid  solution.  The  precipitate  which  appears  with  this  must  be 
decidedly  more  marked  than  in  the  first  test  if  it  is  to  be  utilized  as  a  proof 
of  the  ])resence  of  albumin  (native  proteid  bodies  and  albumoses). 

We  can  also  attempt  to  demonstrate  albumin  in  a  watery  extract  of 
tlie  feces  by  tlie  aid  of  the  biuret  test  (caustic  potash  and  dilute  copper 
sulpliate).  This  is,  however,  often  difficult  because  the  coloring  matter 
of  feces  (hydrobilirubin)  reacts  with  the  biuret  test  just  as  it  does  with 
alhuiniii.  On  using  the  simple  methods  which  are  employed  to  remove  the 
coloring  matter  a  portion  of  the  dissolved  albumin  bodies  is  also  lost; 
they  arc  usually  present  in  only  very  small  amounts;  TJry's  ^  process, 
wliich  is  the  most  accurate  one,  is  much  too  difficult  for  the  general 
practitioner,  especially  as  it  necessitates  the  removal  also  of  the  nucleo- 
proteid  of  the  feces. 

Leaving  the  discussion  of  Simon's  test  for  dissolved  albumin,  I  must 
return  to  the  investigation  of  the  feces  under  consideration,  since  it  was 
demonstrated  that  they  contained  dissolved  albumin  in  considerable  amount. 
The  signs  previously  enumerated  as  favoring  pancreatic  disease  were  en- 
tirely absent. 

The  result  of  our  investigation  therefore  showed  that  the  marked  in- 
crease of  fat  in  the  feces  was  due  to  the  cessation  of  absorption  in  the 
intestine.  The  question  then  arises.  What  is  the  cause  of  this  disturbance 
in  al)sorption?  Here,  however,  I  cannot  minutely  discuss  this  question, 
for  the  investigation  detailed  gave  no  further  results,  and  it  is  my  primary 
ol)ject  to  describe  a  number  of  methods  of  investigation  and  diagnostic 
considerations  which  may  be  utilized  when  the  feces  are  difficult  to  analyze. 

When  describing  the  methods  of  demonstrating  biliary  coloring  matter 
1  omitted  to  call  attention  to  a  test  which  is  of  general  application,  and 
in  a  diagnostic  respect  leads  to  important  conclusions.  This  is  the  corro- 
sive sublimate  test  invented  by  Ad.  Schmidt,  to  which  a  few  words  will 
he  devoted.  This  test  shows  us  by  a  color  reaction  whether  the  mass  of 
feces  or  any  isolated  portion  of  the  same  is  colored  by  bilirubin  or  by  its 
reduction  product,  hydrobilirubin.    The  former  is  changed  to  green  by  the 

1  Archil-  f.  Verdauungskrankheiten,  1904,  IX,  p.  197.        2  Ibid.,  Bd.  IX,  1903,  p.  219. 


TEST   DIET 


627 


corrosive  sublimate  test,  the  latter  to  rose  red.  We  now  know  that 
the  contents  of  the  small  intestine  are  normally  stained  green  by  the 
corrosive  sublimate  test,  those  of  the  colon  red,  and  that  the  ileo-cecal 
valve  forms  a  sharp  boundary.  This  is  due  to  the  fact  that  below  this 
region  the  processes  of  decomposition  set  in  which,  hand  in  hand  with 
reduction,  transform  all  bilirubin  into  hydrobilirubin.  Only  in  the  nurs- 
ling, in  whom  intestinal  decomposition  is  normally  absent  or  very  slight, 
are  the  conditions  different,  and  here  the  coloring  matter  of  the  feces 
wholly  or  in  part  is  composed  of  bilirubin.  If  we  find  unaltered  biliary 
coloring  matter  in  feces  other  than  those  of  nurslings,  it  is  obvious  that 


--^b 


Fig.  39. — Normal  feces  from  a  test  diet. 

a,  muscle  fiber  remains;  b,  yellow  calcium-salt;  c,  soaps;  d,  chaff  remains;  e,  empty  potato  cell; 
/,  detritus ;  ^,  cacao  remains.     (Combination  picture.) 

the  coloring  matter  is  from  the  small  intestine  or  the  upper  part  of  the 
colon,  and  in  consequence  of  too  rapid  propulsion  or  other  less  obvious 
reason  it  has  permeated  the  feces  unchanged.  At  all  events  we  are  dealing 
with  a  disturbance  which,  as  a  rule,  may  be  referred  to  the  small  intestine. 
The  examination  of  the  feces  for  residue  of  meat,  the  results  of  the  fer- 
mentation test,  the  characteristic  mucus  particles,  will  then  serve  to  localize 
the  affection.  If  the  feces  contain  much  bilirubin  they  will  be  of  a  bright, 
golden-yellow  color,  like  the  feces  from  healthy,  breast-fed  children.  This 
is  found  in  the  rare  cases  designated  by  Xothnagel  as  jejunal  diarrhea. 
More  frequently  isolated  fragments,  particularly  of  muscle  fiber  and  mucus, 
show  a  greenish  discoloration  with  corrosive  sublimate. 

To  carry  out  Schmidt's  corrosive  sublimate  test  a  portion  of  recently 
evacuated  feces,  the  size  of  a  hazelnut  or  walnut,  is  carefully  diluted  with 


628 


EXAMINATION   OF  THE   FECES 


a  considerable  quantity  of  a  concentrated  bichlorid  solution.  This  mix- 
ture is  permitted  to  stand  for  several  hours  or  a  day  in  a  broad,  flat  glass 
dish  with  a  cover.  The  time  consumed  is,  of  course,  an  objection  to  this 
method.  The  green  color  of  the  familiar  Gmelin  reaction  immediately 
shows  the  presence  of  bilirubin.  Unfortunately,  however,  it  cannot  be 
used  for  the  finer  tests.  If  bilirubin  is  present  only  in  microscopic  amounts, 
Gmelin's  test  is  unreliable. 

Before  concluding  this  discussion  of  the  remains  of  food  in  the  feces, 
I  wish  to  call  attention  to  two  illustrations,  after  Schmidt,  of  the  "  test 


e-^ 


.>->Q 


Fig.  40. — Pathologic  constituents  in  feces  after  a  test  meal. 

a,  large  fragments  of  muscle ;  h,  needles  of  fatty  acids  and  soaps ;  c,  neutral  fat ;  d,  starch 
granules  in  a  potato  cell;  e,  granulosa  containifig  bacteria;  /,  yeast  cells.     (Ck)mbination 

picture.) 

of  the  function  of  the  intestine  by  means  of  the  test  diet."  In  a  com- 
bination picture  they  exhibit  the  constituents  of  the  feces  after  a  test  diet, 
the  first  illustration  showing  normal,  the  second,  pathological  conditions. 
A  large  proportion  of  the  total  fecal  mass  is  formed  by  bacteria;  this 
is  at  once  corroborated  by  the  investigation  of  a  microscopic  preparation. 
A  large  portion  of  what  is  otherwise  designated  as  detritus  proves,  upon 
close  investigation,  to  be  more  or  less  well  preserved  microorganisms.  By 
a  special  process  I  mechanically  separated  these  from  the  other  constitu- 
ents of  the  feces,  and  by  weighing  ascertained  that  with  an  easily  digested 
diet  l)acteria  formed  about  pne-third  of  the  total  amount  of  solids.  Upon 
an  average  8  grams  of  dried  bacteria  are  passed  during  twenty-four  hours. 
An  estimation  of  their  number  based  on  this  weight  and  upon  the  medium 
size  of  the  bacterium  coli  communi  gave  the  extraordinary  figure  of  about 


TEST   DIET 


629 


128  billions,  a  sum  absolutely  beyond  our  powers  of  conception.  In  this 
article  I  cannot  enter  more  minutely  upon  the  subject  of  fecal  bacteria. 
So  far  as  the  familiar  pathogenic  agents  which  find  ingress  by  way  of  the 
intestine  are  concerned,  they  have  been  referred  to  in  special  articles. 
The  question  of  the  importance  of  the  other  microorganisms  in  the  feces 
is,  however,  much  too  complicated  to  be  briefly  considered.  With  the 
exception  of  the  bacteriology  of  the  feces  of  nurslings,  the  diagnostic  con- 
clusions reached  have  been  comparatively  few. 

Nor  can  I  devote  much  attention  to  the  description  of  the  animal  para- 
sites. ( See  volume  on  "  Diseases  of  Metabolism  and  of  the  Blood,  Ani- 
mal Parasites,  and  Toxicology.") 

In  a  diagnostic  respect,  the  demonstration  in  the  feces  of  certain  patho- 
logic products  secreted  by  the  intestinal  wall  is  very  significant.  In  point 
of  frequency,  this  is  especially  true  of  mucus  and  of  blood.  The  presence 
of  pus  or  other  tissue  constituents  is  much  more  rare. 

Mucus  is  found  in  the  feces  in  varying  form  and  distribution.  Some- 
times it  is  intimately  admixed;  this  occurs  only  with  a  pappy  or  fluid 
consistence  of  the  excrement,  and,  under  some  circumstances,  the  flocculi 
are  then  so  small  that  they  cannot  be  readily  recognized;  at  other  times 
coarse  shreds  which  originate  from  the  grooves  in  the  haustra  of  the  colon, 
are  adherent  to  the  surface  of  the 
feces,  which  are  frequently  hard.  Very 
dry  dejecta  are  occasionally  coated  with 
a  thin  film  of  mucus  resembling  a  var- 
nish. Excrement  which  consists  ex- 
clusively of  large  mucus  masses,  per- 
haps in  the  form  of  tubular  casts  of 
the  intestine,  is  found  in  enteritis 
membranacea  or  in  colica  mucosa. 
Less  massive  quantities  of  hemor- 
rhagieo-purulent  mucus  are  voided  by 
patients  with  dysentery  associated  with 
marked  tenesmus.  The  mucus  in  the 
feces  is  sometimes  glassy  and  trans- 
parent, sometimes  very  turbid  or  even 
white,  according  to  its  impregnation 

with  fat  and  its  permeation  with  cells.  Its  consistency  varies  from 
that  of  extreme  fluidity  and  elasticity  to  the  toughness  of  thin  leather, 
Wlien  larger  amounts  are  evacuated  confusion  with  animal  membranes 
or  connective  tissue  convolutions  from  the  food,  or  even  with  animal  para- 
sites, is  quite  possible. 

Tlie  first  illustration  (Fig.  41)  upon  a  black  base  shows  a  coarse  shred 
of  connective  tissue  detached  from  the  feces  and  washed  clean,  and  beside 
it  a  mucus  shred  of  the  same  size  (Fig.  42).    The  latter  differs  from  the 


Fig. 


41.  —  Connective     tissue     from    the 
feces.     (Natural  size.) 


630 


EXAMINATION   OF  THE   FECES 


¥ia.  42. 


— MuciLs   from   the  feces. 
(Natural  size.) 


white  connective  tissue  by  its  dirty  color;  the  individual  processes  are  not 

so  sharply  defined;  they  are  more  rounded,  and  in  the  thin  portions  are 

somewhat  transparent.     In  doubtful  cases  a  microscopic  examination  must 

always  be  resorted  to,  and  this  will  at 
once  enable  us  to  form  definite  con- 
clusions (compare  Figs.  -43  and  44). 
The  small,  transparent,  mucus 
flocculi  which  are  most  common  are 
best  recognized  when  the  feces  are 
thoroughly  diluted  with  water  and 
spread  out  in  a  thin  layer  upon  a  glass 
plate  which  is  lighted  from  under- 
neath, or  in  a  glass  vessel  which  is  held 
toward  the  light,  the  feces  then  being 
permitted  to  trickle  down  the  sides  of 
the  vessel.  Mucus  flocculi  may  then 
be  noted  as  circumscribed  transparent 
particles.  Even  with  these  precautions 
mucus  may  be  confounded  with  swollen 

fragments  of  undigested  vegetables  or  fruit  (for  example,  potatoes,  carrots, 

]tears),  and  microscopical  proof  should  always  be  obtained  since  this  leads 

to  delinite  conclusions. 

A  feature  of  mucus  to  be  recognized  microscopically  is  the  delicate, 

often  scarcely  visible,  contour,  as  well  as  a  number  of  irregular  lines  in 

groups  and  running  almost  parallel  (Fig. 

43).     After  the  addition  of  dilute  acetic 

acid  to  the  preparation  and  a  thorough 

mixing,  the  precipitate  of  mucin  causes 

a  reaction  characteristic  of  this  tissue^         ,^ . 

namely,   dark  lines   standing  out   prom-  ""^k^K^^jl'l/l/vf'    111 

inently  (Fig.  44).     They  are  the  expres 

sion  of  the  never  absent  overlapping,  and 

the  entire  preparation  resembles  a  veil 

which  is  partially  folded.    Admixtures  of 

every  kind,  detritus,  bacteria,  remains  of 

r«)(»d,   above  all  certain  cells,  are  fotmd 

almost    invariably   in   the  mucus.     Only 

when  the  mucus  is  very  glassy  are  these 

absent ;    their   amount   is   increased    the 

more  turbid  the  mucus  and  the  whiter  its 

color.    For  the  most  part  they  consist  of 

so-called  disintegrated  intestinal  epithelia, 

i.e.,  homogeneous  cells  the  component  parts  of  which  can  no  longer  be  recog- 
nized.    This  loss  of  structure  Schmidt  proved  to  be  the  result  of  imbi- 


FiG.  43. — Mucus  with  isolated  disin- 
tegrated epitheUa.  (Magnifietl 
250  times.) 


TEST   DIET 


631 


'M^ 


bition  with  soaps,  for  if  the  preparation  is  heated  with  acetic  acid  the 
cells  become  clear  and  the  nuclei  visible.  The  demonstration  of  half 
digested  cells  in  the  mucus  is  of  significance.  In  such  cases  only  cell 
nuclei  may  be  found,  and  around  these  in  cellular  arrangement  granules 
or  crystals  of  bilirubin.  The  mucus  itself  is  stained  yellow  by  bilirubin. 
These  signs  certainly  indicate  that  the  mucus  originates  from  the  small 
intestine. 

The  fact  that  intestinal  mucus  contains  epithelia  is  noteworthy  when 
contrasted  with  the  constituents  of  the  mucus  in  sputum  in  which  leuko- 
cytes predominate  but  only  isolated  epithelium  is  found.  Under  some 
circumstances,  of  course,  pus  cells  also  may  be  found  in  intestinal  mucus. 
This  is  then  of  special  import,  a  fact  to 
which  I  shall  revert  later. 

The  diagnostic  importance  of  mucus 
is  based  on  the  fact  that  every  admixture 
of  mucus  to  the  feces,  macroscopically 
and  microscopically  evident,  denotes  a 
pathological  condition,  this  condition 
with  but  few  exceptions  being  catarrh  of 
the  intestine.  The  meconium  plug  of 
the  new-born  has  special  signifi<?ance, 
this  being  a  short  column  of  mucus 
which  is  expelled  by  the  nursling  even 
before  meconium  is  excreted.  This  meco- 
nium plug  was  discovered  only  a  few 
years  ago  by  H.  Cramer ;  that  it  escaped 
observation  is  probably  due  to  the  fact 
that  it  was  covered  in  the  diapers.  Small 
mucus  constituents  are  normally  found 
in  the  feces  of  nurslings  up  to  about  the 
second  week.  It  is  still  a  question  in  how 
far  the  large  mucus  masses  of  colica  mucosa  Avhich  are  usually  passed  with- 
out any  fecal  admixture,  and  which  are  regarded  by  Leube  and  Nothnagel 
as  the  result  of  a  neurosis  of  secretion  rather  than  an  enteritis  membranacea, 
may  be  referred  to  a  mild  catarrh. 

It  may  be  said  of  the  thin  mucus  coat  which  is  occasionally  observed 
upon  the  surface  of  hard  fecal  masses,  and  which  resembles  varnish  after 
drying,  that  it  is  quite  within  the  limits  of  physiologic  conditions. 

In  the  decision  as  to  the  seat  of  the  catarrh,  the  question  from  which 
portion  of  the  intestine  the  visible  mucus  present  in  the  feces  originates 
is  of  great  diagnostic  significance.  We  will  observe  that  the  excretion  of 
mucus  in  the  small  intestine  is  less  than  that  in  the  colon;  furthermore 
that  mucus  is  very  readily  digested,  and  when  it  is  excreted  in  the  small 
intestine  it  is  subjected  to  the  action  of  the  proteolytic  ferment,  and  that, 


Fig.  44. — The  same  after  thorough  ad- 
mixture with  dilute  acetic  acid. 
(Magnified  250  times.) 


632 


EXAMINATION   OF  THE   FECES 


therefore,  by  far  the  greatest  quantity  of  mucus  particles  admixed  with 
feces  originate  in  the  colon. 

When  there  is  highly  increased  peristalsis  of  the  small  intestine  and 
of  the  colon,  mucus  finds  its  way  from  the  small  intestine  into  the  feces, 
which  then,  under  circumstances  already  referred  to,  contain  partly  digested 
cells  stained  with  bilirubin.  This  is  chiefly  found  in  enteric  fever  and 
in  severe  intestinal  tuberculosis.  Only  the  smallest,  most  finely  distrib- 
uted mucus  flocculi  can  possibly  originate  in  the  small  intestine;  coarser 
particles  undoubtedly  come  from  the  colon.  A  more  definite  localization 
in  the  course  of  this  organ  is  only  possible  if  we  assume  that  the  seat  of 

the  catarrh  is  the  higher  the 
finer  the  mucus  flocculi,  and 
the  more  intimate  their  admix- 
ture with  feces.  We  may  ob- 
tain some  idea  of  the  intensity 
of  the  inflammation  from  the 
number  of  admixed  cells.  As 
a  rule,  a  white  appearance  of 
the  mucus  in  consequence  of 
the  presence  of  considerable 
cylinder  epithelium  of  the  in- 
testine much  more  certainly 
indicates  catarrh  than  the 
presence  of  mucus  which  is 
glassy  or  but  slightly  turbid. 
Although  the  presence  of  mu- 
cus in  the  feces  is  conclusive, 
we  dare  not  assume  from  the 
absence  of  mucus  that  catarrh 
is  not  present.  Under  some 
circumstances  mucus  may  be  found  in  the  colon  by  the  test  washing  of  the 
bowel  as  advised  by  Boas. 

Small  amounts  of  pure  blood  upon  the  surface  of  feces  are  found  espe- 
cially in  the  case  of  hemorrhoids,  perhaps  mixed  with  tough  mucus.  The 
muco-purulent  dejecta  in  intestinal  invagination  are  thin  and  profuse,  and 
the  so-called  muco-purulent  lotio  carnea  of  dysentery  also  are  often  very 
profuse.  The  erythrocytes  are  readily  d^troyed  in  the  intestinal  mucus, 
hence  they  cannot  be  demonstrated  by  the  microscope.  In  Fig.  45  we  see 
red  blood-corpuscles  of  a  rusty  appearance  and  embedded  in  the  mucus 
in  the  process  of  destruction. 

Altered  blood  coming  from  higher  portions  of  the  digestive  tract  is 
significant,  but  its  demonstration  is  often  difficult.  Diagnoses  based  upon 
the  macroscopic  appearance  alone  are  often  erroneous,  particularly  when 
the  feces  are  not  of  the  typical  tarry  consistence  but  are  compact. 


Fig 


Mucus    with    numerous    red   blood-cor- 


puscles in  the  process  of  destruction;  with  these 
are  crystals  of  triple  phosphates.      (Magnified 

250  times.) 


""TEST   FOR  OCCULT   BLOOD  633 

Confusion  with  feces  containing  bismuth  is  precluded  by  the  great 
number  of  crystals  of  bismuth  suboxid  revealed  in  every  microscopical 
preparation.  As  a  rule,  only  chemical  or  spectroscopic  analysis  will  demon- 
strate the  presence  of  hemoglobin. 

In  the  recognition  of  ulcers  or  of  malignant  neoplasms  of  the  stomach 
and  intestine,  paramount  diagnostic  importance  has  in  the  last  few  years 
been  attached  to  the  demonstration  of  minimal  amounts  of  blood  in  the 
feces,  the  so-called  occult  hemorrhages.  To  obtain  a  positive  result  from 
blood  tests,  and  this  is  especially  true  of  the  very  sensitive  Weber-van  Deen 
test,  it  is  necessary  to  exclude  blood  originating  from  food,  therefore  for 
several  days  prior  to  the  investigation  meat  should  not  be  taken  by  the 
patient:  and  we  should  also  positively  ascertain  that  small  hemorrhages 
from  the  mouth  or  the  pharynx  are  not  the  source  of  the  bleeding. 


TEST   FOR   OCCULT   BLOOD 

To  carry  out  the  Weber-van  Deen  test  which  is  now  popular,  a  large 
mass  of  feces  (if  the  amount  of  fat  is  excessive  perhaps  after  preceding 
treatment  with  ether)  is  mixed  with  water  which  contains  about  one-third 
its  volume  of  glacial  acetic  acid  until  the  mixture  is  of  fluid  consistence, 
and  the  hemoglobin  is  extracted  in  a  test-tube  by  shaking  with  ether.  To 
the  ether  which  has  been  poured  off  ten  drops  of  a  freshly  prepared  guaiac 
tincture  are  added  (one  part  of  resin  to  25  parts  of  absolute  alcohol)  and 
then  (shaking  after  the  addition  of  each  drop)  20  to  30  drops  are  added 
of  old  turpentine  oil  which  has  been  standing  for  several  weeks  in  a  flat 
bowl  exposed  to  the  air.  A  blue  tint  to  the  ether  proves  the  presence  of 
hematin.  In  shaking  the  ether  with  turpentine  we  should  avoid  covering 
the  top  of  the  test-tube  with  the  thumb  as  the  perspiration  on  the  skin 
may  affect  the  accuracy  of  the  test.  On  account  of  the  same  fallacy  in  the 
test  the  presence  of  pus  also  must  be  excluded. 

As  to  the  well  known  hemin  test  of  Teichmann,  I  think  that,  as  a 
rule,  too  much  table  salt  is  used,  a  very  small  granule  being  sufficient ;  after 
heating  we  should  wait  a  long  time  before  examining  the  preparation  so 
that  the  crystals  may  have  time  to  form;  finally,  for  unknown  reasons 
the  test  is  occasionally  negative  notwithstanding  the  positive  presence  of 
hemoglobin. 

Pus  cells  in  large  quantities,  partly  with  and  partly  without  a  mucu3 
intermediary  substance,  are  rarely  found  in  the  feces.  Their  appearance 
is,  however,  of  great  diagnostic  importance  and  proves  the  presence  of 
ulcers  or  a  ruptured  abscess.  If  merely  isolated  round  cells  permeate 
the  fecal  mucus  this  view  is  not  permissible,  and  we  can  at  most  diag- 
nosticate only  an  extreme  irritation  of  the  intestinal  mucous  membrane. 
The  impossibility  of  demonstrating  pus  cells  in  the  individual  case  by  no 
means  excludes  the  existence  of  ulceration,  since  small  clumps  in  the  diar- 


634  EXAMINATION   OF  THE   FECES 

rheic  feces  may  escape  recognition  or  they  may  have  been  dissolved  by 
decomposition  or  the  digestive  ferments. 

In  exceptional  cases  shreds  of  tissue  from  the  intestine,  of  ulcers, 
of  hemorrhoidal  nodules,  or  necrotic  portions  of  the  intestinal  wall,  espe- 
cially in  the  case  of  invagination  and  of  dysentery,  may  be  desquamated 
and  discovered  in  the  feces.  Their  origin  can  be  decided  only  by  micro- 
scopic examination.  They  must  not  be  confounded  with  tough  mucus 
and  animal  membranes  which  are  the  residue  of  food. 

This  description  of  the  investigation  of  the  feces  is  by  no  means  com- 
plete. Bacteriologic  methods  and  the  detection  of  animal  parasites  have 
not  been  touched  upon.  In  the  chemical  aspect  of  the  subject,  clinical 
reasons  constrained  me  to  be  brief;  here  much  might  be  added.  But  it 
was  my  primary  object  to  describe  fully  and  especially  emphasize  the 
points  most  important  to  us  as  practising  physicians,  and  clearly  to  por- 
tray the  method  of  analysis  of  the  feces  which  at  the  bedside  will  give  us  the 
most  accurate  information. 


DIARRHEA,   INTESTINAL  CATARRH,  AND 
INTESTINAL  TUBERCULOSIS 

By  W.  FLEINER,  Heidelberg 

I.   DIARRHEA 

The  designation  diarrhea  for  those  disturbances  of  intestinal  diges- 
tion in  which  the  discharges  become  more  or  less  soft  or  fluid,  and  also 
are  evacuated  more  than  once  during  the  day,  originates  from  the  view 
that  food  and  drink  are  propelled  very  rapidly  or  almost  rush  through 
the  intestine.  This  rapid  propulsion  through  the  intestine  indicates  in- 
creased intestinal  activity;  the  appearance  in  the  dejecta  of  constituents 
of  the  food  points  to  insufficient  digestion  and  absorption',  the  softer, 
more  fluid  composition  of  the  discharges  to  insufficient  absorption  of  fluid, 
and  to  increased  secretion  of  the  intestinal  mucous  membrane  and  the 
glands  connected  therewith.  At  all  events,  in  diarrhea  intestinal  digestion 
is  disturbed;  therefore,  all  diarrhea  is  a  symptom  of  intestinal  dyspepsia. 

As  in  gastric  pathology  we  differentiate  dyspepsias  from  organic  gastric 
disease  as  purely  functional  disturbances,  so  we  must  discriminate  between 
functional  intestinal  dyspepsias  and  organic  diseases  of  the  intestine.  It 
would,  however,  be  a  great  error  invariably  to  characterize  gastric  or  in- 
testinal functional  disturbances  as  nervous.  Dyspepsia  may,  here  and 
there,  be  of  purely  nervous  origin;  it  is,  however,  the  natural  consequence 
of  the  condition  that  we  do  not  sharply  differentiate  between  intestinal 
dyspepsia  and  intestinal  diseases,  for  sometimes  intestinal  dyspepsia  is 
the  precursor,  sometimes  an  accompaniment,  of  an  organic  intestinal  dis- 
ease. Sometimes  it  exists  independently,  or  the  disease  upon  which  intes- 
tinal dyspepsia  is  dependent  has  its  seat  in  some  other  organ  than  the 
intestine. 

formally,  the  processes  of  digestion  in  the  gastrointestinal  canal  are 
adapted  to  the  ingested  food.  The  function  of  the  digestive  glands  is 
set  in  motion  by  chemoreflexes  generated  by  the  quantity  and  quality  of 
the  food  and  drink,  and  exactly  regulated  (Pawlow).  The  epithelia  of  the 
intestines  facilitate  the  propulsion  of  the  products  of  digestion,  and  their 
villi  dip  into  the  chyle,  just  as  the  roots  of  plants  dip  into  the  earth 
which  furnishes  their  food,  taking  from  it  water,  salts  and  other  nutri- 
tive products  which  digestion  has  made  fit  for  absorption,  and  which  the 
organism  requires  for  the  structure  of  its  tissues,  for  its  growth,  its  devel- 
opment of  force,  the  rehabilitation  of  what  has  been  used,  and  for  the 

635 


636        DIARRHEA.  CATARRH,   AND   INTESTINAL  TUBERCULOSIS 

formation  of  heat.  The  unused  remains  of  chyle,  the  residue  of  food, 
tlie  products  of  excretion  from  the  liver  and  the  intestine  itself,  permeated 
by  an  enormous  number  of  bacteria,  are  excreted  by  the  intestine  as  feces. 

The  property  by  which  the  secreting  and  absorbing  organs  accommodate 
themselves  to  the  nature  and  amount  of  the  ingested  food  is,  however, 
not  absolute,  but  shows  individual  limitation.  Therefore,  a  disproportion 
between  force  and  amount  may  readily  be  brought  about,  and  the  juices 
of  digestion  and  the  power  of  absorption  in  the  intestinal  canal  prove 
insufficient  for  the  demands  made  upon  them.  The  excess  of  chyle  not 
iakcn  up  into  the  fluids  of  the  body  by  digestion  and  absorption  then 
abnormally  irritates  the  small  intestine,  which  attempts  to  rid  itself  of 
its  irritating  contents  by  increased  peristalsis — diarrhea  from  the  small 
intestine.  In  the  less  sensitive  colon  there  may  be  compensation,  and 
hy})ermotility,  or  diarrhea  of  the  small  intestine,  may  even  be  checked. 
True  diarrhea,  i.  e.,  fecal  discharges  of  soft  or  thin  consistence,  only 
occurs  after  decided  irritation  of  the  colon. 

Tlie  stimulus  for  normal  movements  of  the  stomach  and  intestines 
originates  from  the  contents,  but  in  the  intestines  also  from  the  chemical 
irritation  of  products  of  fermentation  and   decomposition. 

To  show  the  intensity  of  their  effect  upon  intestinal  movement,  Bokai 
arranged  the  organic  (fermentative)  acids  of  the  intestinal  canal  in  the 
following  order:  Lactic  acid,  succinic  acid,  valerianic  acid,  butyric  acid, 
formic  acid,  propionic  acid,  acetic  acid,  caproic  acid  and  caprylic  acid. 
The  mildest  irritation  was  produced  by  lactic  acid,  the  severest  by  caprylic 
acid.  These,  as  well  as  caproic  acid,  even  in  small  doses  produced  in 
animals  tonic  intestinal  spasm  and  decided  hyperemia.  Moreover,  the 
foregoing  acids  not  only  caused  diarrhea  but,  even  in  small  amounts, 
produced  catarrh;  given  in  larger  doses,  decided  inflammation  of  the 
intestinal  tract.  In  contrast  with  these  the  salts  of  organic  acids,  even  in 
much  larger  doses,  produced  no  intestinal  movements. 

Of  the  intestinal  gases  hydrogen  and  nitrogen  proved  to  be  indifferent, 
while  carbonic  acid,  marsh  gas,  and  sulphureted  hydrogen  caused  severe 
intestinal  movements. 

Among  the  products  of  proteid  decomposition,  Bokai  found  that  indol 
had  but  slight  action  and  phenol  none  at  all,  upon  intestinal  movements. 
On  the  other  hand,  even  small  doses  of  sJcatol  produced  severe  peristalsis 
in  the  small  intestine  and  rectum,  and  also  gave  rise  to  tonic  spasm  in 
those  areas.  Skatol  at  first  causes  the  blood-vessels  to  contract,  but  in  a 
few  minutes  this  contraction  is  succeeded  by  a  dilatation  of  the  vessels. 
Skatol  did  not  produce  catarrh. 

Tlieso  reports  indicate  the  great  importance  of  intestinal  bacteria  upon 
normal  and  pathologic  processes  in  the  intestinal  canal.  It  may,  therefore, 
b(>  interesting  to  discuss  somewhat  more  minutely  the  reldtiQn  of  hacteria 
to  the  intestine. 


DIARRHEA  637 

mTESTINAL  BACTERIA 

At  birth  the  intestinal  canal  contains  no  bacteria  (Billjoth),  but  each 
hour  of  extra-uterine  life  increases  the  number  of  bacteria  conveyed  into 
the  intestinal  canal  of  the  nursling  from  its  surroundings.  As  a  rule, 
no  harm  is  done  the  infantile  organism  by  this  bacterial  invasion  so  long 
as  the  child  is  nourished  by  its  mother's  milk  or  that  of  a  wet-nurse. 
The  extraordinary  sensitiveness  of  the  intestine  of  the  nursling  to  any 
other  food,  to  cow's  milk  and  to  substitutes  for  milk,  is,  however,  well 
known,  and  the  marked  tendency  of  infants  to  diarrhea,  and  the  great 
mortality  of  children  in  the  first  years  of  life  from  gastric  and  intestinal 
disturbances,  are  usually  attributed  to  the  abnormal  invasion  of  bacteria. 
Very  interesting  facts  were  communicated  to  us  by  v.  Behring  in  his 
article  "Diarrhea  among  Calves"  (Kalbersterbe),  and  also  concerning 
the  mortality  of  nurslings  in  his  well  known  publication  "  Sauglingsmilch 
und  Sauglingssterblichkeit "  (Therapie  dcr  Gegenwart,  Heft  I,  1904). 
In  the  dysentery  of  calves  which  is  due  to  infection  with  the  bacterium 
coli,  and  which  may  also  develop  in  newborn  calves  by  nourishing  them 
with  hailed  cow's  milk,  according  to  Joest,  tlie  best  prophylaxis  has  proven 
to  be  fresh  milk  from  the  mother  cow  immediately  after  the  birth  of  the 
calf.  Infant  mortality  can  also  be  reduced  from  upwards  of  30  to  3.55 
per  cent,  by  providing  the  child  with  a  wet-nurse:  Therefore,  in  breast 
milk,  and  in  the  milk  of  the  mother  animal_,  there  exists  a  certain  in- 
herent property  which  protects  the  nursling  and  the  sucking  animal. 

In  the  blood  of  cattle,  v.  Behring  found  isopathically  developed  anti- 
bodies for  the  most  important  intestinal  bacteria,  that  is,  for  the  bacterium 
lactis  and  bacterium  coli.  These  protective  bodies,  as  also  the  albumins 
and  globulins  of  the  blood  and  milk,  enter  the  milk  from  the  blood,  and 
V.  Behring,  in  fact,  demonstrated  that  fresh  cow's  milk  has  a  very  active 
antibody  antagonistic  to  the  bacterium  coli,  and  a  weaker  one  to  protect 
it  from  the  bacterium  lactis.  The  bactericidal  property  of  milk  is  less 
than  that  of  the  serum,  corresponding  to  the  smaller  percentage  in  blood 
albumin.  These  antibodies  are  destroyed  by  boiling  the  milk,  but  not 
by  digestion;  they  may  therefore  pass  through  the  intestinal  wall  of  the 
nursling  into  its  fluids  in  an  unchanged  condition.  Upon  the  basis  of 
these  experiences  v.  Behring  constructed  his  new  process  for  the  preserva- 
tion of  milk.  The  addition  of  formalin,  1  to  5,000  or  1  to  10,000,  to 
the  milk,  as  proposed  by  him,  is  said  to  increase  the  power  of  the  anti- 
bodies. 

With  the  advance  of  extra-uterine  life,  the  organism  itself  produces 
certain  protective  products,  the  power  of  resistance  in  the  intestinal  wall 
increases,  and,  in  consequence,  the  intestine  of  the  nursling  no  longer  acts 
like  a  filter  with  large  pores,  to  which  it  has  been  compared.  Verworn 
ascribes  exclusively  to  the  absorbent  intestinal  epithelia   (which  act  like 


()3S        DIARRHEA,  CATARRH,  AND  INTESTINAL  TUBERCULOSIS 

ameboid  cells)  their  discriminating  faculty  in  the  choice  of  food,  inas- 
much as,  among  all  the  constituents  of  the  chyle,  they  take  up  only  the 
fat  globules,  not  bacteria,  pigment  granules,  or  other  corporeal  elements. 
As  a  matter  of  fact,  intestinal  bacteria  cannot  effect  an  entrance  into  the 
interior  of  the  body  so  long  as  the  intestinal  mucous  membrane  remains 
normal  and  unimpaired. 

The  number  and  distribution  of  bacteria  in  the  intestinal  canal  is  not 
uniform.  Billroth  found  the  bacteria  to  be  most  scanty  in  the  upper  por- 
tions of  the  intestine;  they  constantly  increase  in  number  lower  down,  and 
are  most  nimierous  in  the  feces.  With  the  rapid  propulsion  of  the  con- 
tents of  the  small  intestine,  the  microbes  from  the  stomach  are  compara- 
tively soon  carried  into  the  colon;  many  of  them  fail  to  find  favorable 
conditions  for  their  development.  For  this  reason  the  bacteria  of  the 
small  intestine  capable  of  sustaining  life  differ  very  markedly  from  those 
in  the  colon.  The  former  are  almost  wJiolly  generators  of  fermentation, 
and,  while  forming  lactic  acid,  acetic  acid,  succinic  acid  and  ethyl  alcohol, 
produce  decomposition,  particularly  in  the  carbohydrates  of  the  food,  while, 
under  normal  conditions,  albumin  in  the  small  intestine  is  decomposed 
only  in  very  small  quantities  by  microbes. 

On  the  other  hand,  proteid  decomposition  is  paramount  in  the  colon, 
hence,  in  this  region,  products  of  decomposition  develop,  such  as  indol, 
phenol,  skatol,  volatile  fatty  acids,  aromatic  acids,  ammonia,  carbonic 
acid,  methane,  sulphureted  hydrogen  and  methyl  mercaptan. 

jMacfadyen,  ISTencki  and  Sieber  illustrate  these  facts  by  their  report 
that  in  the  cadaver  of  patients  who  were  treated  with  bismuth  the  mucous 
membrane  of  the  entire  small  intestine  was  only  reddened,  while  the 
mucous  membrane  of  the  colon,  from  the  ileo-cecal  valve  downward,  had 
a  black,  velvety  appearance  in  consequence  of  the  reduction  of  bismuth 
l)v  products  of  decomposition  and  the  action  of  sulphureted  hydrogen. 
A.  Schmidt  found  the  human  small  intestine,  excised  shortly  after  death 
and  placed  in  a  concentrated  corrosive  sublimate  solution,  to  be  of  a 
greenish  color;  the  mucous  membrane  of  the  colon,  however,  was  red. 
The  green  color  shows  the  reaction  of  corrosive  sublimate  upon  bilirubin, 
the  rose-red  that  upon  hydrobilirubin,  the  product  of  reduction  by  the 
decomposition  of  bilirubin. 

Fermentation  and  decomposition  in  the  intestine  do  not  exclude  each 
other,  although,  under  normal  circumstances,  their  localization  is  different. 
If,  under  pathologic  conditions,  there  is  stasis  of  chyle  in  the  small  intes- 
tine, decomposition  of  proteids  occurs  there  and  leads  to  an  increase  of 
indican,  to  the  presence  of  ethyl  sulphuric  acid  (C2H5HSO4)  in  the  urine, 
and,  in  severe  cases  of  occlusion  of  the  small  intestine  (miserere),  by 
regurgitation  of  the  decomposed  contents  of  the  small  intestine  into  the 
stomach,  to  fecal  eructation  and  fecal  vomiting.  More  frequent  than 
dt'(()ni})osition  in  the  small  intestine  is  fermentation  in  the  large  intestine, 


DIARRHEA  639 

because  in  many  forms  of  intestinal  dyspepsia,  starch-containing  and  cel- 
lulose-containing constituents  of  the  food — particularly  if  insufficiently 
masticated — find  their  way  into  the  colon,  and  there,  by  further  fermenta- 
tion, generate  gases  and  acids. 

We  can  scarcely  form  a  conception  as  to  the  volume  of  bacteria  present 
in  the  intestine.  J.  Strasburger  has  attempted  to  estimate  their  number 
in  the  feces  by  weighing,  and  found  that,  in  round  numbers,  about  one- 
third  (32.4  per  cent.)  of  the  total  solids  of  the  feces  in  adults  on  an 
easily  digested  food  consisted  of  bacteria.  As  the  feces  in  the  test  diet 
employed  by  Strasburger  (A.  Schmidt's  diet)  contain  upon  the  average 
24  grams  of  total  solids,  we  may  say  that  a  normal  adult  daily  excretes 
about  8  grams  of  dry  bacteria.  The  number  of  bacteria  corresponding  to 
these  8  grams  Strasburger  calculates  at  128,000,000,000,  while  A.  Klein  by 
a  previous  computation  found  only  about  9,000,000,000  (8,080,000,000). 

On  an  attempt  to  inoculate  plate  cultures  from  definite  portions  of 
the  feces  with  corresponding  dilutions  it  was  shown  that  the  overwhelming 
majority  of  bacteria  had  already  perished,  Eberle  could  only  develop 
upon  gelatin  4  to  5  per  cent.,  upon  agar  at  blood  temperature  10.6  per 
cent.,  of  the  bacteria  found  in  feces.  Among  those  capable  of  develop- 
ment the  majority  belonged  to  a  few  constantly  recurring  forms.  On  ad- 
ministering sterilized  food,  the  saprophytes  disappeared,  until,  finally,  only 
the  hacterium  lactis  and  bacterium  coli  could  be  cultivated  in  the  feces, 
therefore  those  bacteria  against  which  the  nursling  is  armed  with  pro- 
tective products  from  the  mother's  milk. 

What  are  the  bactericidal  substances  which  exert  such  immense  and 
destructive  power  upon  bacteria  in  the  intestinal  canal,  even  with  other 
food  than  mother's  milk?  Nucleinic  acid  of  the  lymphoid  cells  (Kossel) 
possesses  antiseptic  and  bactericidal  properties,  and,  in  another  article  in 
this  volume,  I  have  called  attention  to  the  importance  of  the  tonsils  and 
the  lymphatic  pharyngeal  rings  as  protective  organs.  Although  we  have 
as  yet  no  experimental  proof,  it  cannot  be  denied  that — apart  from  other 
functions — the  extensive  lymphatic  apparatus  of  the  intestinal  wall,  which 
is  extraordinarily  rich  in  follicles,  not  only  acts  as  a  filter  in  a  physical 
sense  but  also  chemically  forms  a  protective  process  for  the  fluids  of  the 
body. 

Antiseptic  action  must  be  admitted  for  the  free  hydrochloric  acid  of 
the  gastric  juice,  although  its  importance  is  far  less  great  than,  for  ex- 
ample, Bunge,  Kast,  and  others  have  assumed.  The  acme  of  digestion, 
during  which  time  free  hydrochloric  acid  in  the  normal  and  healthy 
stomach  possesses  a  concentration  which  permits  antisepsis,  is  reached 
several  times  during  the  day;  it  lasts  only  for  a  few  hours.  In  the  re- 
maining time  this  disinfecting  action  of  hydrochloric  acid  is  absent  from 
the  stomach.  Hence  numerous  bacteria,  without  suffering  particular 
damage,  have  an  opportunity  to  invade  the  intestine  from  the  stomach. 


640        DIARRHEA,  CATARRH,   AND   INTESTINAL  TUBERCULOSIS 

Finally,  the  biliary  acids  must  be  considered  as  antiseptic  agents  in 
the  intestine.  Maly  and  Emich  report  that  the  biliary  acids  set  free  'from 
the  cholates  by  the  hydrochloric  acid  of  the  gastric  juice,  particularly 
taurocholic  acid,  have  but  little  less  of  antiseptic  action  than  salicylic 
acid  and  phenol.  Naturally  the  disinfecting  power  of  free  biliary  acids 
is  only  active  while,  and  so  far  as,  the  chyle  in  the  small  intestine  is  of 
acid  reaction.  This  period,  however,  is  too  brief  to  permit  thorough  dis- 
infection. 

If  other  bactericidal  products  should  be  found  in  the  intestinal  juices, 
wc  must  assume  tliat  the  varieties  of  intestinal  bacteria  which  continue 
to  live  arc  those  which,  in  the  struggle  for  existence,  feed  upon  the  bac- 
toi'ia  which  constantly  enter  the  gastrointestinal  canal  by  means  of  the 
saliva  or  with  food  and  drink.  The  different  processes  of  this  struggle 
arc.  at  present,  entirely  beyond  our  knowledge.  But  the  fact  of  its  occur- 
rence is  proven  by  numerous  experiments. 

Thus  K.  Schiitz,  who  introduced  large  quantities  of  Metschnikoff's 
vibrios  directly  into  the  duodenum  of  dogs  through  a  fistula,  was  unable 
to  cultivate  this  germ  from  the  feces  provided  the  intestinal  activity  of 
the  animals  experimented  upon  was  normal  and  the  intestinal,  mucous 
membrane  uninjured.  Bienstock  fed  garden  earth  containing  tetanus 
germs  to  animals,  but  was  unable  lo  produce  tetanus  by  inoculation  experi- 
ments. 1'he  bacterium  coli  simultaneously  cultivated  with  diphtheria 
bacilli  in  meat  bouillon  prevented  the  development  of  the  latter,  yet  it  suc- 
cumbed to  other  microbes,  for  example,  to  streptococci  and  staphylococci. 

Processes  of  fermentation  and  decomposition  in  the  intestine  are 
strongly  influenced  by  the  food,  and  the  physiological  and  pathological 
processes  in  the  intestinal  canal  and  the  changes  in  the  fecal  discharges 
are  most  intimately  connected.  These  conditions  may  be  readily  investi- 
gated in  small  children. 

The  feces  of  healthy  nurslings  resulting  from  normal  breast  milk  are 
voided  two  to  five  times  daily,  have  an  acid  reaction,  and  an  acid  odor 
which  is  not  unpleasant.  They  are  of  a  yolk-yellow  color,  pappy,  and 
according  to  the  amount,  the  total  solids  form  1  to  1.3  per  cent,  of  the 
dried  food.  Intestinal  decomposition  increases  when  nurslings  are  nour- 
ished with  cow's  milk;  the  feces  are  of  lighter  color,  of  firmer  consistence, 
have  an  alkaline  reaction,  and  the  odor  of  feces  or  of  decomposition.  The 
amount  of  total  solids  rises  to  2-3.1  per  cent,  of  the  dried  food.  Fermen- 
tation and  decomposition  in  the  intestine  become  more  marked  when  chil- 
dren are  nourished  ad  libitum.  In  such  children  the  total  solids  of  the 
feces  rise  to  5.9-7.5  per  cent,  of  the  dried  food;  therefore  are  five  or 
six  times  as  great  as  those  of  nurslings  nourished  with  mother's  milk 
(Biedort). 

Infants  who  do  not  enjoy  the  blessing  of  mother's  milk,  and  who  are 


DIARRHEA  641 

"artificially"  nourished,  are  greatly  injured  by  over-feeding  and  over- 
loading the  stomach  and  intestines.  If  the  child's  stomach  is  not  relieved 
by  frequent  vomiting,  and  the  warning  given  by  profuse  evacuations  of 
feces  permeated  with  cheesy  clumps  and  of  disagreeable  odor  is  disre- 
garded, severe  intestinal  disturbances  soon  appear.  These  cheesy  masses 
readily  irritate  the  delicate  intestinal  wall  mechanically,  producing  more 
violent  peristalsis  and  the  premature  diarrheal  evacuation  of  constituents 
of  the  food  not  yet  absorbed  and  utilized.  Added  to  this  loss  of  nutrition, 
however,  is  the  baneful  factor  that  undigested,  superfluous  masses — the 
deleterious  residue  of  food  described  by  Biedert — promote  a  dangerous  in- 
crease of  bacteria  in  the  intestine  by  furnishing  a  suitable  culture  media 
for  the  generators  of  fermentation  and  decomposition  already  present 
there,  for  the  saprophytes  which  enter  with  the  food,  and,  under  some 
circumstances,  for  pathogenic  bacteria.  According  to  the  nature  of  the 
food,  a  surplus  of  products  of  fermentation  then  produces  acid  diarrhea ,  or 
an  abnormal  proteid  decomposition,  fetid  diarrliea.  Other,  often  severe, 
forms  of  diarrhea  which  threaten  the  life  of  young  children  by  intoxica- 
tion or  infection  are  produced  by  definite,  more  or  less  specific  kinds  of 
bacteria,  and  are  especially  influenced  by  season  and  climate,  particularly 
by  heat. 

Adults  who  have  no  accurate  knowledge  or  clear  conception  of  the 
requirements  of  the  body,  and  who,  either  from  a  love  of  eating  or  from 
habit,  overtax  their  digestive  organs  by  over-eating  or  by  flooding  them 
with  wine  and  beer,  and  who  thus  fill  the  lower  portions  of  the  intestines 
with  fermentative  and  decomposing  material,  suffer,  as  do  young  children, 
from  "  deleterious  residues  of  food  "  in  the  intestine. 

For  a  time  the  habit  of  over-distending  the  normal  digestive  organs 
produces  no  symptoms  other  than  profuse  and  frequent  compact  or  soft 
dejecta.  This  condition,  designated  by  earlier  authors  as  "  copropoesis," 
i.  e.,  increased  formation  of  feces,  polycopria,  is  readily  combined  with 
a  tendency  to  diarrhea,  which,  sooner  or  later,  passes  into  habitual  diarrhea 
that  may  continue  for  years  and  decades,  often  without  much  effect  upon 
the  general  nutrition  of  the  patient.  This  significant  "  copropoesis "  and 
the  tendency  to  diarrhea,  if  disregarded,  are  frequently  followed  in  the 
course  of  time  by  severe  injury  to  the  intestine  and  other  organs;  for  ex- 
ample, the  liver,  the  kidneys,  the  heart  and  the  vessels,  and  this  is  en- 
hanced by  advancing  age  and  by  certain  occupations,  for  example,  those 
necessitating  a  sedentary  life.  To  the  diarrhea  which  assumes  a  chronic 
form,  flatulency  is  added,  and  the  inflation  of  the  abdomen,  borborygmi 
in  the  intestines,  and  the  frequent  discharge  of  gas  of  a  very  disagreeable 
odor,  become  most  annoying.  The  constantly  distended  intestine,  espe- 
cially the  colon,  gradually  becomes  blunted  to  irritation  always  present 
and  loses  its  tone.  The  first  sign  of  flaccidity— which  precedes  long  torpor 
of  the  intestine— is  bloating  of  the  abdomen  and  the  over-distention  of 


642        DIARRHEA,   CATARRH,   AND   INTESTINAL  TUBERCULOSIS 

individual  portions  of  the  intestine  or  the  entire  colon  from  gas  (partial 
or  total  intestinal  atony).  This  flaccidity  is  not  necessarily  due  to  ad- 
vancing age,  for  it  may  occur  at  any  period  of  life,  and  an  abdomen 
enormously  distended  with  gas  is  especially  conspicuous  among  poorly 
nourished  children  who  suffer  from  chronic  diarrhea. 

Heavy  food  containing  little  of  nutritive  products  rich  in  residue, 
especially  of  a  vegetable  nature,  also  causes  overloading  and.  extreme 
irritation  of  the  intestine.  We  cannot  nourish  ourselves  with  just  enough 
pure  food  according  to  its  calory  value,  but  require  for  a  sense  of  satiety, 
and  especially  to  stimulate  peristalsis,  the  aid  of  food  containing  residue. 
If,  however,  the  fluids  of  digestion  are  insufficient  to  assimilate  and  absorb 
a  large  amount  of  nourishment  which,  however,  is  poor  in  nutritive  prod- 
ucts, tlie  undigested  residue  of  the  food  will  cause  irritation,  and  the 
produels  of  I)acterial  decomposition  will  give  rise  to  diarrheic  discharges 
which  in  the  course  of  time  are  followed  by  catarrh  and  flaccidity. 

The  ]ial)itual  overloading  of  the  intestine  and  the  consequent  chronic 
intestinal  dyspepsia  which  runs  its  course  with  diarrhea  are  opposed  by 
an  occnsional  form  of  acute  intestinal  dyspepsia  due  to  quantitative  errors 
in  diet.  Any  excess  in  eating  or  drinking  may  bring  this  about.  More  or 
less  severe  intestinal  disturbances  which  may  also  appear  without  pro- 
nounced symptoms  on  the  part  of  the  stomach  are  relieved  in  a  compara- 
tively short  time  if  the  intestinal  canal  becomes  empty  by  the  free  dis- 
charge of  gas  and  diarrheal  evacuations.  Without  any  excess  whatever, 
a  (jualifative  error  in  diet  may  be  made  unconsciously,  or  may  pass  un- 
noticed, and  the  error  in  nutrition  may  be  recognized  only  by  its  conse- 
quences. Here  individual  circumstances,  personal  susceptibility  of  the 
intestine  or  the  peculiarities  of  its  bacterial  flora  play  an  important  role. 
Some  intestines  are  so  irritable  that  diarrhea  ensues  on  the  slightest 
change  in  the  food,  and  simple,  non-irritating  foods,  which  others  always 
include  in  the  dietary,  act  like  purgatives.  I  do  not  refer  to  fresh 
fruits,  vegetables,  cucumbers,  sauerkraut  and  fermenting  drinks,  which 
are  known  to  possess  laxative  properties,  but  call  attention  to  milk,  for 
wliieh  some  persons  have  an  actual  idiosyncrasy,  and  to  which  adults  are 
often  more  susceptible  than  nurslings. 

But  the  assumption  of  an  abnormal  or  nervous  irritability  of  the 
intestine  will  not  explain  all  of  the  many  acute  and  chronic  forms  of 
diarrhea,  particularly  when  the  so-called  dyspeptic  intestinal  phenomena 
a])pt'ar  without  an  actual  error  in  diet.  After  the  ingestion  of  food 
liygienically  suitable,  and  when  the  stomach  functions  normally,  insuffi- 
ciently digested  chyle  may  be  washed  into  the  intestine  by  fluids,  such 
as  plain  water,  carbonated  water,  tea  or  coffee,  taken  while  eating  or 
soon  aft(n-ward,  and  intestinal  dyspepsia,  abnormal  fermentation,  the  gen- 
eration of  gas  and  diarrhea  are  frequently  the  consequences. 

Exceedingly  often  the  irritability  of  the  intestine  which,  even  with 


DIARRHEA  643 

ordinary  food,  causes  intestinal  dyspepsia  and  diarrhea,  is  the  consequence 
of  buccal  dyspepsia  or  gastric  dyspepsia.  A  disturbance  of  digestion  in 
the  mouth  is  due  to  insufficient  mastication  and  to  the  incomplete  admix- 
ture of  saliva  with  the  bolus,  and  occurs  in  all  the  affections  of  the  mouth, 
particularly  in  caries  of  the  teeth,  with  deficient  dental  prosthesis,  and, 
much  more  frequently,  from  the  bad  habit  of  bolting  the  food.  Even  an 
excellent  stomach  is  incapable  of  disintegrating  large  portions  of  food, 
nor  can  the  intestine  accomplish  this,  hence  it  suffers  from  the  mechanical 
irritation  of  the  fermenting  and  decomposing  foreign  body. 

The  various  gastric  dyspepsias  produce  intestinal  dyspepsia  and  diar- 
rhea in  many  ways.  Hypermotility  of  the  stomach,  even  when  the  secre- 
tory function  is  normal,  fills  the  intestine  to  repletion  with  insufficiently 
prepared  chyle.  When  there  is  a  disturbance  of  gastric  juice  secretion, 
or  a  decrease  or  absence  of  hydrochloric  acid,  as  in  achylia  or  apepsia, 
the  chyle  also  passes  from  the  stomach  into  the  intestine  insufficiently 
prepared.  If,  in  consequence  of  atonic  conditions  of  the  stomach — either 
with  a  normal  or  pathological  secretion  of  gastric  juice — hyperacidity 
develops  from  abnormal  fermentation,  even  the  upper  small  intestine 
simultaneously  contains  bacteria  and  large  quantities  of  those  acid  prod- 
ucts of  fermentation  whose  stimulating  effect  upon  peristalsis  has  been 
experimentally  proven  by  Bokai.  To  all  this  must  be  added  that,  with 
the  absence  of  hydrochloric  acid  in  the  gastric  juice,  the  specific  generator 
of  pancreatic  juice  secretion  is  absent,  and  this  renders  intostinal  digestion 
more  difficult.  In  the  undigested  portions  of  the  chyle  excessive  fermenta- 
tion and  decomposition  take  place.  After  what  has  been  said,  the  mouth 
and  the  stomach  may  be  quite  properly  designated  as  protective  organs 
for  the  intestine.  But  all  intestines  do  not  require  this  protection,  for 
frequently  intestinal  digestion  is  normal,  and  the  state  of  the  nutrition  is 
good;  often  even  constipation  is  present,  notwithstanding  these  functional 
disturbances  in  the  mouth  and  stomach. 

Just  as  in  the  intestinal  dyspepsias  which  have  so  far  been  described, 
in  which  products  of  fermentation  and  decomposition  of  the  intestinal 
bacteria  produce  diarrhea  by  chemical  irritation  of  the  walls  of  the  intes- 
tine, so  this  is  also  brought  about  by  the  products  of  metabolism  of  many 
pathogenic  microorganisms. 

The  greatest  irritation  to  the  intestinal  wall  is  caused  by  the  hacterial 
toxins  which  are  recognized  as  strong  poisons.  Toxic  diarrhea  in  conse- 
quence of  poisoning  from  meat,  sausage,  fish,  mushrooms,  potatoes,  beans, 
etc.,  is  more  rarely  observed  than  the  sporadic  forms,  those  occurring  in 
families  or  in  entire  districts,  the  so-called  diseases  of  the  masses.  The 
poisons  are  of  ectogenous  origin,  and  find  their  way  into  the  body  with 
tainted  food,  for  alJcaloids  of  decomposition  and  cadaveral  alkaloids,  so- 
called  ptomains,  do  not  develop  under  normal  conditions  of  intestinal 
decomposition  in  the  body.     Brieger  has  found  numerous  products  of  this 


644        DIARRHEA,  CATARRH,   AND  INTESTINAL  TUBERCULOSIS 

kind  in  decomposing  masses  of  meat.  He  observed  that  some  of  the 
bases  isolated  during  the  first  period  of  decomposition  (monamins  and 
diamins)  were  physiologically  indifferent,  and  some  slightly  toxic.  After 
llie  third  day  of  decomposition,  however,  more  poisonous  ptomains  or 
toxins  appear,  and,  on  prolonged  decomposition,  substances  of  extraordi- 
nary toxicity  (mydalein,  methyl-guanidin  and  others).  Even  under  patho- 
logical conditions,  ptomain  formation  very  rarely  occurs  in  the  intestinal 
canal  itself,  but  invariably  in  cholera,  and  in  a  peculiar  anomaly  of 
nietal)o]isni,  cystinuria  (Neumeister).  In  pure  cultures  of  the  cholera 
bacillus  and  of  the  Finkler-Prior  cholerine  bacillus,  after  twenty-four  hours, 
Rrieger  found  pentamethylendiamin,  aud  in  older  cholera  cultures  pu- 
trcscin,  cadaverin  and  methyl-guanidin.  Therefore,  intestinal  autointoxi- 
cation cannot  be  so  greatly  distributed  nor  so  important  as  Bouchard 
maintains,  although  Ave  refer  to  abnormal  processes  of  decomposition  in 
the  gastrointestinal  canal  many  general  symptoms  of  intestinal  dyspeptic 
(listurl)anco,  for  example,  lassitude  and  depression,  headache,  nausea  and 
vertigo. 

ETIOLOGY 

Chemical  substances  and  poisons  introduced  into  the  intestine  from 
without  irritate  the  intestinal  wall  just  as  do  products  derived  from  bac- 
teria, and,  by  increasing  peristalsis  and  the  flow  of  the  intestinal  juices 
(secretion  of  dilution),  produce  more  or  less  distressing  diarrhea,  hyper- 
emia and  inflammation. 

]\rost  of  the  milder  laxatives  act  only  by  stimulating  peristalsis,  espe- 
cially peristalsis  of  the  colon;  therefore,  they  free  only  the  colon  from 
feces  and,  at  most,  give  rise  to  fecal  diarrhea.  The  thin,  fluid  Ci;»mposi- 
tion  of  the  dejecta  is  due  to  its  rapid  propulsion  through  the  intestine, 
and  consequently  there  is  diminished  absorption  of  water.  If  we  desire 
to  induce  increased  secretion  of  the  intestinal  juices,  or  transudation  from 
tlic  blood  into  the  intestine  and  watery  diarrhea,  alkaline  salts  are  admin- 
istered in  liypertonic  solutions.  In  spite  of  the  existing  osmotic  differences 
in  ])ressure,  the  current  of  diffusion  from  the  intestine  is  only  in  the 
direction  of  the  vascular  tract  and  not  in  the  contrary  direction,  because 
(he  normal  intestinal  wall  is  impermeable  to  fluids  of  the  body  (0.  Cohn- 
licim).  Both  properties,  namely,  the  power  of  absorbing  the  intestinal 
coiiteiits  and  the  impermeability  of  the  intestinal  wall  to  the  fluids  of  the 
body,  may  be  destroyed  by  poisons  such  as  sodium  fluorid  and  arsenic,  or 
by  either  one  of  these.  Very  concentrated  solutions  of  salt  and  sugar  also 
injure  the  epithelium  of  the  intestine  so  that  the  processes  of  diffusion 
follow  only  physical  laws,  for  instance,  fluid  flows  into  the  intestine.  Thus 
tlie  intestinal  wall  is  irritated  or  the  epithelium  of  the  intestine  is  damaged 
l)y  various  spices,  drastic  purgatives,  acids  and  alkalies,  metallic  salts  and 
metalloids,    alcohol,   volatile  ethereal  oils,   some  vegetable   alkaloids   and 


DIARRHEA  646 

numerous  chemical  preparations  which  cannot  here  be  individually 
enumerated. 

Some  of  the  substances  mentioned  may  also  produce  diarrhea  ly  way 
of  the  blood,  for  example,  cathartic  acid  injected  subcutaneously,  colo- 
cynthin,  aloin  and  others.  _  Mercury,  the  mercurous  chlorid  of  which  is 
designated  mite  (hydrarg.  chlor.  mite),  has  a  more  highly  toxic  action 
from  the  blood  than  calomel  from  the  intestine.  Severe  intestinal  dis- 
turbance with  superficial  epithelial  destruction  or  deeply  invading  necrosis 
of  the  mucous  membrane  has  not  rarely  been  observed  from  the  external 
use  of  corrosive  sublimate,  for  example,  after  vaginal  and  uterine  douches. 
I  have  also  known  chronic  diarrhea  and  colitis  to  develop  in  surgeons 
from  the  frequent  disinfection  of  their  hands  with  solutions  of  corrosive 
sublimate,  and  to  be  kept  up  by  this  method.  The  laxative  effect  of 
tobacco  smoking  appears  to  be  due  to  the  fact  that  nicotin  is  absorbed  into 
the  circulation  from  the  oral  cavity  or  the  pharynx,  or  it  may  be  absorbed 
by  the  lungs  with  the  inspired  air.  Sometimes,  however,  the  effect  from 
tobacco  is  produced  so  rapidly — while  at  other  times  it  does  not  appear 
at  all  in  habitual  smokers — that  we  must  presuppose  a  suggestive  action. 

The  diarrheas  which  occur  at  the  onset  or  in  the  course  of  many  infec- 
tious diseases  are  due  to  the  circulation,  the  intestine  showing  no  patho- 
logical change.  In  this  category  we  include  the  loose  stools  observed  in 
septicemia,  in  pneumonia,  in  malaria,  in  influenza  and  erysipelas,  as  well 
as  those  which  take  place  in  cholera  and  from  putrid  poisoning.  The  diar- 
rhea which  occurs  in  nephritis  and  uremia  is  the  result  of  urea  excreted 
from  the  blood  into  the  intestine;  in  its  transformation  into  ammonium 
carbonate  this  is  very  irritating,  and  even  produces  corrosion  and  necro- 
sis. As  a  rule,  we  refer  to  nervous  influences  those  forms  of  diarrhea  in 
which  no  dietetic  errors  or  pathologic  conditions  in  the  intestine  can  be 
recognized.  Under  normal  conditions  the  digestive  processes  are  controlled 
only  by  the  gastrointestinal  nerves ;  but  these  communicate  with  the  pneu- 
mogastric  nerve  as  well  as  with  the  sympathetic,  with  the  cerebral  and 
peripheral  nervous  systems;  therefore,  by  these  avenues  abnormal  processes 
and  pathological  conditions  may  derange  the  intestinal  function.  These 
functional  disturbances  may  be  motor,  secretory,  or  sensory;  they  may 
continue  for  a  long  or  short  time,  may  recur  periodically  or  become  chronic, 
and  may  then  produce  clearly  defined  clinical  pictures,  for  example,  chronic 
diarrhea  and  peristaltic  unrest  of  the  intestine.  In  this  manner,  in  the 
stomach  as  well  as  in  the  intestine,  the  various  functions  individually  or 
collectively  are  abnormally  stimulated  or  inhibited.  This  intestinal  action 
may  show  variations,  one  function  may  be  increased,  another,  on  the  con- 
trary, may  be  inhibited  or  even  absolutely  arrested. 

We  are  most  familiar  with  the  effect  of  sudden  and  great  psychical 
stimulation  upon  the  motor  function  of  the  gastrointestinal  canal,  and  such 
disturbances  in  function  are  attributed  to  psychical  irritation  of  the  nerve 
42 


646        DIARRHEA,  CATARRH,  AND  INTESTINAL  TUBERCULOSIS 

tracts  which  increases  peristalsis  or  to  psychical  paralysis  of  the  nerves 
which  inhibit  intestinal  motion.  Not  infrequently,  by  fright,  anxiety,  or 
fear,  the  contents  of  the  stomach  are  thus  propelled  into  the  intestine  more 
rapidly  than  usual,  and  the  intestines  are  more  rapidly  evacuated. 

As  to  the  effect  of  these  involuntary  and  irresistible  intestinal  dis- 
charges, the  laity  in  Germany  have  improvised  characteristic  designations 
for  nervous  people  and  cowards.  Innumerable  examples  of  this  might  be 
quoted  from  daily  life;  I  shall  limit  myself  to  calling  attention  only  to 
the  increased  peristalsis,  the  desire  to  evacuate  the  bowels,  and  even  the 
diarrheic  discharges  (which  actually  take  place  even  with  repetitions) 
from  which  many  persons  of  both  sexes  suffer  during  the  excitement  of 
a  journey,  while  in  company,  before  an  appointment,  preliminary  to  mak- 
ing a  speech,  in  anticipation  of  going  to  court,  etc.  An  auto-suggestive 
effect  is  produced  by  the  mere  sensation  of  traveling  in  a  railroad  car 
without  toilet  facilities,  of  being  in  a  house  or  in  company,  etc.,  where  it 
may  be  inconvenient  to  attend  to  the  bowels. 

Diarrhea  due  to  the  irritation  of  the  skin  by  cold,  and  produced  reflexly, 
ib  nervous  diarrhea  only  in  a  certain  sense,  for  example,  when  it  follows 
cliilling  of  the  feet,  a  wetting,  sitting  upon  a  cold  seat,  or  taking  a  cold 
bath ;  it  may  also  arise  from  the  diseased  condition  of  organs  adjacent  to 
the  intestine,  especially  the  internal  genitalia  of  women,  and  in  genito- 
urinary diseases  of  men.  During  menstruation  diarrhea  dependent  upon 
affections  of  the  female  genitalia  shows  periodic  aggravation.  There  are 
also  diarrheas  which  depend  upon  organic  diseases  of  the  spinal  cord,  such 
as  the  intestinal  crises  with  diarrhea  which  periodically  appear  or  peri- 
odicall}^  show  aggravation. 

In  actual,  chronic,  uninterrupted,  continuous  diarrhea,  varying  only 
in  intensity,  I  advise  great  deliberation  before  making  a  diagnosis  of 
nervous  diarrhea.  I  do  not  deny  the  occurrence  of  chronic  diarrhea  having 
a  nervous  or  psychopathic  foundation,  but  I  believe  it  to  be  very  rare. 
In  many  cases  of  this  kind,  if  on  strict  diet,  clinical  observation  and  the 
regular  examination  of  the  feces  will  reveal  the  starting  point  of  the 
irritative  condition  somewhere  in  the  intestine,  or  external  to  it.  The 
sequels  of  a  former  perityphlitis,  a  pericholecystitis,  or  other  local  inflam- 
mation of  the  peritoneum,  must  here  be  borne  in  mind,  as  well  as  also 
tiibereulous  ulcers  in  the  rectum,  pol3^pi  situated  higher,  frequently  in 
women  old  and  neglected  lacerations  of  the  perineum  or  prolapse,  and 
in  children  enterozoa. 

Whether  the  very  persistent  and  exhausting  diarrheas  in  Graves'  dis- 
ease, like  the  tachycardia,  depend  upon  nervous  hypermotility  of  the  gastro- 
intestinal canal  or  whether  they  are  due  to  autointoxication  cannot  with 
our  present  knowledge  be  positively  decided. 


DIARRHEA  647 


SYMPTOMS 


As  a  rule,  the  symptoms  in  diarrhea  are  quite  uniform;  those  which 
have  preceded  or  may  follow  the  diarrheal  discharges  may  show  many 
variations,  and  those  observed  in  nervous  persons  may  bear  a  very  peculiar 
stamp. 

In  some  cases  the  patients  complain  only  that  the  intestinal  discharges 
are  more  frequent  than  usual,  that  their  consistence  is  abnormally  soft, 
or  more  or  less  fluid.  N"ot  rarely  the  preceding  intestinal  dyspepsia  pro- 
duces symptoms.  A  short  time  after  the  usual  meal,  often  even  during 
the  meal,  a  distention  of  the  abdomen  is  noted  and  is  exceedingly  unpleas- 
ant. This  is  followed  by  noticeable  motion  in  the  intestine,  often  only 
in  the  form  of  peristaltic  unrest,  such  as  gurgling  and  rumbling,  but  also 
often  as  increased  peristalsis  accompanied  by  slight  pain.  Other  painful 
sensations  may  now  and  then  be  felt  in  the  abdomen.  These  are  caused 
b}^  irritating  food  substances  or  abnormal  digestive  products,  and  indicate 
either  local  irritation  of  the  mucous  membrane — cutting  pains,  griping 
pains — or  spasmodic  contractions  of  the  muscular  layer  of  the  intestine 
occurring  in  portions  of  the  intestine  already  irritated,  or  they  are  due 
to  the  distention  of  isolated  intestinal  coils  by  gas  or  feces.  Both  spastic 
contraction  of  the  intestine  and  great  distention  of  the  same — the  former 
being  a  muscular  pain,  the  latter  a  peritoneal  pain — produce  "  bell3'-ache  " 
or  "  griping,"  and  when  this  becomes  intense  it  is  designated  "  colic." 
The  paroxysmal,  periodic  appearance  of  these  pains  is  characteristic; 
slight  at  first  they  increase  in  severity  and  become  most  intense;  the 
cessation  or  disappearance  of  the  pain,  which  resembles  "labor  pain" 
and  is  often  compared  with  it,  is  also  typical.  In  the  intervals  between 
the  attacks  the  pain  may  cease  and  the  patient  seem  restored  to  complete 
health;  sometimes,  however,  in  these  intervals  between  the  marked  colicky 
attacks,  a  greater  or  less  degree  of  sensitiveness  remains  until  the  irritating 
intestinal  contents  have  been  completely  evacuated.  • 

According  to  their  cause,  these  colics  have  been  designated  wind  colic 
(colica  fatulenta)  or  fecal  colic  (colica  st er cordis) .  Usually,  however, 
these  forms  are  combined.  In  these  colics,  the  pain  ameliorates  as  soon 
as  gases  or  feces  are  discharged,  the  attacks  are  less  frequent  and  the 
recurrences  less  severe.  Inversely,  however,  they  increase  in  intensity 
when  the  passage  of  gas  or  feces  is  prevented.  The  gases  discharged  may, 
according  to  their  nature,  produce  a  burning  sensation  which  may  continue 
for  some  time.  This  is  also  true  of  the  feces,  particularly  the  thin  ones 
mixed  with  undigested  fluids  which  corrode  the  anal  mucous  membrane. 

These  colics  may  be  of  such  intensity  as  to  cause  even  adults  to 
writhe;  in  debilitated  persons  they  sometimes  cause  syncope,  and  in  chil- 
dren they  frequently  lead  to  general  convulsions,  even  to  loss  of  con- 
sciousness. 


648        DIARRHEA,  CATARRH,  AND  INTESTINAL  TUBERCULOSIS 

If  we  remember  the  physiology  of  intestinal  movement,  and  particu- 
larly the  fact  that  tonic  contraction  results  from  a  local  irritation  of  the 
intestine  above  the  point  of  irritation,  and  that  in  consequence  of  this 
an  annular  constriction  forms  while  the  intestine  below  the  point  of  irri- 
tation l^ecomes  flaccid  and  dilated,  the  frequency  of  invagination  in  small 
children,  whose  intestine,  as  is  well  knovm,  is  much  more  irritable  than 
that  of  adults,  is  easily  explained.  As  a  matter  of  fact,  during  intestinal 
colic  in  children  invagination  of  the  small  intestine  and  of  the  colon  fre- 
quently occurs  and  is  chiefly  due  to  marked  local  irritation;  often  the 
colicky  pains  are  the  consequence  of  such  invaginations.  Spontaneous  re- 
covery no  doubt  takes  place  provided  such  invagination  is  but  slight ;  in 
other  cases  intussusception  of  greater  or  less  extent  supervenes,  and  by 
constriction  or  occlusion  of  the  intestine  may  threaten  life. 

Aside  from  complications  on  the  part  of  the  stomach  (the  intolerance 
of  wliicli  lov.anl  any  food  or  drink  may  cause  debility,  as  in  cholera  nostras) 
the  ell'ocl  of  diarrhea  upon  the  general  strength  and  nutrition  depends 
chiefly  upon  the  mimlx'r  and  size  of  the  evacuations  during  the  day.  The 
discliarge  of  deleterious  masses  from  the  gastrointestinal  canal  may  be 
bc7i(»ficial,  l)ut  since  not  these  alone  are  discharged  but  also  a  quantity  of 
nutritive  sul)Stances,  and  especially  much  of  the  fluid  of  the  body,  all 
])rofuse  diarrlieas  mean  a  loss  of  fluid  to  the  organism.  In  children  and 
debilitated  adults,  therefore,  diarrheas  produce  a  rapid  loss  of  strength 
because  such  persons  possess  but  little  reserve  material.  After  profuse 
diarrhea  the  turgescence  of  the  skin  rapidly  disappears;  the  skin  becomes 
flaccid  and  dry,  the  face  hollow,  the  nose  pointed,  and  the  eyes  are  sunken 
ill  their  cavities.  Corresponding  with  the  loss  in  water  through  the  intes- 
tine, the  amount  of  urine  decreases,  and  the  blood-pressure  in  some  cases 
is  so  much  reduced  that  the  pulse  becomes  imperceptible.  In  severe  cases 
in  adults  who  evacuated  from  two  to  three  liters  of  thin  fluid  feces  in 
twenty-four  hours,  I  have  seen  complete  anuria  which  only  disappeared 
when  repeated  subcutaneous  infusions  of  normal  salt  solution  were  given 
or  when  the  extreme  thirst  led  the  patients  to  supply  the  fluid  loss  by 
drinking.  As  a  rule,  a  restitutio  ad  integrum  rapidly  occurs  provided 
the  diarrhea  is  not  too  long  continued  and  is  not  due  to  severe  anatomical 
lesions. 

Nevertheless,  even  in  acute  diarrhea,  the  loss  of  fluid  with  the  numer- 
ous, watery  discharges  is  more  or  less  injurious.  The  feeling  of  exhaus- 
tion, tlie  cardiac  asthenia  in  diarrhea,  has  been  referred  to  the  lowered 
l)lood-])ressure  from  loss  of  fluid,  also  cramps  in  the  calves  and  the  appear- 
ance of  tonic  spasms  in  unilateral  and  symmetrical  muscles  of  the  extrem- 
ities, of  the  trunk,  and  of  the  face,  also  in  the  muscles  of  the  pharynx, 
larynx  and  eyes;  in  fact,  the  entire  picture  of  tetany,  including  all  its 
other  symptoms,  has  been  referred  to  inspissation  of  the  muscular  and 
nervous  tissue  from  losses  of  water  (Kussmaul,  Fleiner).     Other  authors 


DIARRHEA  649 

attribute  these  severe  musculo-nervous  disturbances  to  gastrointestinal 
processes  of  intoxication.  Their  etiology,  however,  has  not  yet  been  de- 
cided, as  no  similar  toxic  products  which  have  this  effect  have  yet  been 
proven  to  exist  in  the  gastrointestinal  canal  of  patients  with  diarrhea. 

In  most  cases  of  severe  diarrhea  there  is  a  loss  of  weight  even  if 
the  condition  persists  but  a  few  days.  This,  however,  is  rapidly  compen- 
sated if  no  severe  organic  disturbances  are  present,  because  the  loss  of 
weight  is  chiefly  dependent  upon  the  loss  of  water.  In  prolonged  or 
chronic  diarrhea,  the  condition  is  different.  Here,  in  the  course  of  time, 
added  to  the  loss  in  water  is  the  absence  of  resorption,  therefore  an  insuffi- 
cient ingestion  of  food,  and,  in  consequence  of  this,  a  utilization  of  the 
reserve  fund  of  fat,  glycogen  and  albumin  of  the  body,  therefore,  under- 
nutrition and  emaciation.  In  children  and  adults  the  latter  may  be  of 
alarming  extent;  moreover,  during  this  period  of  under-nutrition,  in  chil- 
dren the  general  growth  of  the  body  and  also  of  individual  organs  ceases, 
particularly  that  of  the  teeth  and  the  bones,  and  a  predisposition  to  other 
maladies,  especially  to  infectious  diseases,  rickets,  scrofulosis  and  tubercu- 
losis, is  established.  Besides  extreme  emaciation,  adults  with  severe  forms 
of  chronic  diarrhea  often  show  a  peculiar  form  of  glossitis,  apparently 
dependent  upon  atrophy  of  the  epithelium  at  the  tip  and  borders  of  the 
anterior  half  of  the  tongue,  and  atrophy  of  the  papilla  upon  the  dorsum 
of  the  tongue.  The  surface  of  the  tongue  is  free  from  coating,  it  is 
smooth  and  glistening  like  the  mucous  membrane  of  the  mouth,  and  very 
sensitive  to  chemical  and  mechanical  irritation.  Small  children,  and  adults 
greatly  weakened  by  disease,  particularly  the  senile,  not  rarely  succumb  to 
profuse  diarrhea.  In  consequence  of  the  great  loss  of  fluid  and  the  ex- 
cessive limitation  of  absorption,  chronic  diarrhea  sometimes  leads  to  severe 
forms  of  anemia,  to  cardiac  weakness  the  result  of  fatty  degeneration  of 
the  heart,  to  hydremia,  and  occasionally  to  albuminuria  which  finally  causes 
death. 

Middle-aged  men  who  eat  heartily  and  hastily,  and  who  are  accus- 
tomed to  drink  a  great  deal,  withstand  chronic  diarrhea  remarkably  well 
for  years  and  even  decades.  In  spite  of  three,  or  many  more,  soft,  diar- 
rheic  evacuations  daily,  their  general  nutrition  does  not  suffer;  on  the 
contrary,  they  increase  rather  than  lose  in  weight,  and  they  are  even  indif- 
ferent to  a  decided  degree  of  flatulence,  until,  from  atony  of  the  intestine, 
constipation,  flatulent  and  fecal  colic,  colitis  or  severe  complications  on  the 
part  of  other  organs  (for  example,  the  heart  or  the  kidneys)  and  atheroma- 
tosis, etc.,  are  superadded. 

The  reaction  of  intestinal  disturbances  upon  the  nervous  system  varies 
in  its  manifestations;  as  from  the  stomach  so  from  the  intestine  every 
abnormal  irritation  may  be  conducted  to  the  central  organs  of  the  nervous 
system  by  centripetal  tracts  in  the  pneumogastric  and  sympathetic  nerves. 
In  persons  of  neuropathic  tendency,  or  those  who   are   debilitated   and 


650        DIARRHEA,  CATARRH,   AND   INTESTINAL  TUBERCULOSIS 

anemic,  there  are  intestinal  neuroses  of  the  pneumogastric  nerve  which, 
similar  to  the  gastric  form,  disturb  cardiac  activity  and  the  respiration,  ancl 
produce  sensations  of  constriction,  a  feeling  of  anxiety,  and  vertigo.  This 
so-called  intestinal  vertigo,  which,  as  a  rule,  appears  suddenly  during  a 
diarrhea  of  brief  duration,  and  is  sometimes  synchronous  with  the  fecal 
movements,  may  come  in  severe  attacks  or  in  a  milder,  but  more  pro- 
tracted form;  the  latter  is  more  likely  to  be  induced  by  constipation  than 
by  diarrhea.  There  are,  however,  cases  of  paradoxical  constipation  not- 
withstanding profuse,  even  diarrheal  discharges,  and  these  conditions  are 
frequently  associated  with  such  attacks  of  vertigo.  In  connection  with 
intestinal  dyspeptic  disturbances,  the  pulse  invariably  becomes  irregular 
and  intermittent.  To  this  peristaltic  unrest  of  the  intestine,  which  may 
be  purely  nervous  or  psychical  but  is  usually  due  to  abnormal  intestinal 
irritation,  general  nervous  excitement  due  to  intestinal  action  is  added, 
as  well  as  noises  of  a  gurgling  character  which  at  night  prevent  sleep,  or 
cause  the  patient  to  awaken  in  a  state  of  nervous  anxiety  which  sometimes 
takes  the  form  of  definite  fears  (worms,  frogs,  etc.,  in  the  abdomen). 
Closely  allied  to  these  terrors  is  the  hypochondriac  depression,  originating 
in  sensations  produced  by  peripheral  irritation  of  the  sympathetic,  and 
referred  by  the  consciousness  to  fear,  which  constantly  centers  attention 
on  those  organs  and  parts  of  the  body  which  are  threatened.  Such  indi- 
viduals are  actually  tormented  by  their  sensations  and  imaginations;  they, 
however,  make  all  those  about  them  miserable,  not  less  so  their  physician, 
or,  more  correctly,  their  physicians,  who  are  annoyed  much  more  than  is 
necessary  by  their  patients  with  intestinal  hypochondriasis. 

Migraine  and  hemicrania  intestinalis,  or  hemicrania  dyspeptica,  are 
often  produced  by  diarrhea;  sometimes,  however,  migraine  ceases  with  the 
appearance  of  diarrhea.  The  conditions  are  similar  with  hyperesthesia  and 
neuralgia  of  other  localizations,  as  well  as  vasomotor  disturbances  which, 
in  a  certain  sense,  are  related  to  intestinal  dyspepsia,  such  as  urticaria, 
acute  and  chronic  erythema,  and  acne-like  eruptions  of  the  face,  whether 
tills  relation  be  established  by  the  nerve  tracts  or  by  the  circulation,  by 
reflex  action  and  irradiation  or  by  intoxication. 

DIAGNOSIS 

The  diagnosis  of  an  intestinal  affection  must  not  be  based  upon  the  rec- 
orrnition  of  one  particular  symptom  of  the  disease — for  example,  diarrhea 
constipation,  colic,  or  hemorrhage — but  a  number  of  problems  must  be  taken 
into  consideration.  In  diarrhea,  for  instance,  the  cause  and  the  seat  of 
the  disturbance  must  be  determined,  and  we  must  decide  whether  a  merely 
fuiu'tional  disturbance — hypermotility,  hypersecretion,  or  diminished  ab- 
sorption— is  the  basis  of  the  malady,  whether  this  functional  disturbance  is 
tlu'  (Expression  of  pathological  changes  in  the  intestinal  wall,  and  whether 


DIARRHEA  651 

these  are  of  substantive  character;  therefore,  whether  they  are  of  intes- 
tinal origin,  are  dependent  upon  disturbances  or  diseases  of  other  organs, 
or  are  due  to  general  constitutional  conditions.  If  the  latter,  the  organs 
directly  connected  with  the  intestine  must,  above  all,  be  investigated;  first 
the  oral  cavity  and  the  stomach,  then  the  liver  and  the  pancreas,  later 
the  peritoneum  and  the  organs  related  to  it,  and  especially  the  female 
genitalia,  then  the  nervous  system,  the  composition  of  the  blood,  the  organs 
of  circulation,  and,  finally,  the  kidneys.  The  clinical  examination  of  the 
entire  body  and  its  individual  organs  is  absolutely  necessary  to  determine 
the  origin  and  the  action  of  processes  of  disease  in  the  intestines.  Of  these 
we  actually  get  but  imperfect  knowledge,  and  this  chiefly  by  an  examina- 
tion of  the  feces,  which  occupies  the  same  position  in  the  diagnosis  of  intes- 
tinal diseases  as  the  examination  of  the  gastric  contents  in  the  diagnosis 
of  gastric  diseases,  the  examination  of  the  sputa  in  the  diagnosis  of  respira- 
tory diseases,  or  the  examination  of  the  urine  in  renal  diseases  and  in 
disturbances  of  metabolism. 

Examination  of  the  gastric  contents  and  the  intestinal  discharges  has 
not  as  yet  attained  such  popularity  in  practice  as  examinations  of  the  urine 
and  the  sputum.  The  methods  are  more  complicated  and  difficult,  never- 
theless the  pith  of  a  voluminous  literature  of  investigations  of  the  gastric 
contents  and  their  value  in  practice  is  infinitesimally  small  and  simple. 
Contrasted  with  a  pure,  scientific  coprology,  those  methods  of  examination 
of  the  feces  which  permit  a  positive  clinical  diagnosis  and  furnish  clear 
therapeutic  indications  are  just  as  simple.  First  among  these  methods  is 
coproscopy,  simple  inspection  of  the  feces.  When  the  unaided  eye  is  not 
sufficient  the  lens  and  the  microscope  should  be  employed,  or  even  chemical 
reagents.  Quantitative  analysis  of  the  feces  is  only  rarely  necessary  in 
practice,  although  its  value  in  solving  scientific  and  physiologic  ques- 
tions in  the  laboratory  cannot  be  overestimated. 

Like  everything  else,  coproscopy,  the  inspection  of  the  feces,  requires 
practice,  and,  if  we  expect  it  to  yield  results,  inspection  must  be  not  only 
occasional,  but  regular  and  continuous  until  the  diagnosis  becomes  abso- 
lutely clear  or  the  patient  ceases  to  be  under  observation.  In  order  to 
secure  any  reliable  data  from  the  examination  of  the  feces,  we  must  have 
a  knowledge  of  the  patient's  previous  diet.  WTien  the  findings  are  doubt- 
ful, the  question  will  arise  whether  other  foods,  drink,  or  drugs  have  been 
taken. 

For  example,  let  us  consider  a  profuse,  diarrheic  stool  in  which  large 
and  small  particles  of  solid  food  of  various  kinds  may  be  recognized  with 
the  naked  eye:  This  form  of  diarrhea  has  long  been  known  as  lientery. 
The  investigation  is  made  in  order  to  decide  which  constituents  of  the 
food  have  been  carried  or  propelled  rapidly  through  the  intestine,  and 
what  abnormal  products  the  intestine  has  contributed  to  the  fecal  admix- 
ture.    The  size  and  amount  of  the  undigested  particles  of  food  evacuated 


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652        DIARRHEA,  CATARRH,   AND   INTESTINAL  TUBERCULOSIS 

lead  us  to  suppose  that  an  abnormally  large  amount  of  food  was  eaten, 
that  it  was  hastily  swallowed,  i.  e.,  was  insufficiently  masticated.  Conse- 
quently, we  examine  the  teeth  of  the  patient,  order  a  reduction  in  the 
amount  of  the  food,  and  insist  that  in  the  preparation  of  the  food  in  the 
kitchen  it  be  more  finely  divided  by  hashing  or  other  mechanical  means, 
or  that  this  be  done  during  eating  either  by  artificial  or  natural  mastica- 
tion (a  masticator).  Coproscopy,  repeated  the  next  day,  may  reveal  a 
normal  condition.  Therefore,  there  was  no  actual  intestinal  disturbance  in 
the  previous  lientery  but  the  cause  was  merely  a  poor  condition  of  the 
teeth,  incomplete  mastication,  or  overeating. 

If  in  a  given  case,  notwithstanding  a  prescribed  diet,  undigested  parti- 
cles of  food  appear  in  the  feces,  this  variety  of  lientery  admits  of  quite  a 
different  interpretation.  We  now  investigate  the  character  of  these  unab- 
sorbed  constituents  of  the  food.  If  the  fecal  discharges  are  thin  this  is 
sometimes  very  easy,  for  the  solid  constituents  may  be  extracted  by  the  aid 
of  a  pipette  or  a  small  stick.  It  is  sometimes  advisable  to  receive  the  latter 
in  a  wire  net  or  fecal  sieve  (Boas).  Necessarily,  compact  feces  must  be 
carefully  broken  up  in  a  vessel  with  water  by  a  pestle. 

The  most  valuable  elements  in  our  food  are  albumin  (meat),  fat,  and 
carbohydrates,  while  the  residue  of  vegetables  is  of  subordinate  importance. 
Hence,  when  we  find  with  the  naked  eye  or  with  the  microscope  fragments 
of  food  in  the  feces  we  know  that  we  are  dealing  either  with  an  albumin 
(or  meat)  diarrhea  or  a  fat  diarrhea,  that  is,  albumin,  or  meat,  or 
connective  tissue  lientery  (proteorrhea)  or  a  fat  lientery  (steatorrhea). 
Accordingly,  with  the  relatively  rare  appearance  of  starch  in  the  feces,  we 
designate  the  affection  as  amylura  lientery  or  amylorrhea  (v.  Oefele). 

The  results  of  the  physiology  of  digestion  teach  us  that  albuminous 
products  are  digested  in  the  stomach  by  pepsin  and  hydrochloric  acid,  and 
in  the  intestine  by  the  proteolytic  ferment  of  the  pancreatic  juice  (trypsin), 
while  fat,  which  is  only  slightly  absorbed  in  the  stomach  (Volhard),  is 
chiefly  absorbed  in  the  small  intestine  by  the  steapsin  of  the  pancreatic 
juice.  The  carbonated  alkali  of  the  pancreatic  juice,  the  bile,  and  the 
fluids  of  the  small  intestine  combine  with  free  fatty  acids,  and,  by  giving 
off  carbonic  acid,  fatty  alkalies  or  soaps  develop  at  any  stage  between  the 
molecules  of  neutral  fat  which  have  not  as  yet  been  split  up.  Thus  a 
fine  emulsion  of  microscopically  small  fat  globules  is  formed  in  the  intes- 
tine. The  digestion  of  carbohydrates  begins  in  the  mouth  by  the  action 
of  the  ptyalin  of  the  saliva  during  mastication.  If  the  stomach  contents 
have  an  acid  reaction,  amylolysis  ceases  in  the  stomach ;  but  it  begins 
again  in  the  small  intestine  by  the  action  of  the  ptyalin  of  the  pancreatic 
juice. 

The  most  important  carrier  of  albumin  is  meat.  From  what  has  been 
previously  stated  we  know  that  the  presence  of  undigested  meat  in  the 
feces  indicates  a  disturbance  of  gastric  or  pancreatic  digestion  in  the  small 


JO 


DIARRHEA  653 

intestine,  and  a  careful  investigation  of  the  functions  of  the  stomach  in 
the  usual  manner  is  advisable.  The  result  will  show  whether  the  disturb- 
ance is  gastric  or  pancreatic,  and  whether  we  should  prescribe  hydrochloric 
acid  and  pepsin  or  a  preparation  of  pancreas.  To  complete  the  technic 
of  fecal  examination,  it  must  be  mentioned  that  the  passage  of  undigested 
meat  is  evidence  of  impaired  gastric  and  pancreatic  digestion.  Connective 
tissue,  according  to  Kiihne,  is  digested  in  the  stomach;  the  finding  of 
shreds  of  connective  tissue  in  the  feces  therefore  indicates  a  lack  of  gas- 
tric digestion,  HCl-anacidity,  achylia  gastrica,  or  apepsia.  Muscle  fibers 
are  digested  in  the  small  intestine  by  trypsin;  hence  the  macroscopic  recog- 
nition of  remains  of  muscle  or  well-retained  transverse  muscle  strias  by  the 
microscope  indicates  a  disturbance  of  digestion  in  the  small  intestine — defi- 
cient trypsin  digestion.  The  passage  of  undigested  remains  of  milk  in  the 
form  of  cheesy  flocculi  is  subject  to  the  same  interpretation. 

With  a  little  practice,  an  enormous  increase  of  fat  in  the  stool  may 
be  certainly  recognized  by  the  oily,  creamy  consistence,  the  pale,  grayish, 
yellow  or  grayish  white  fatty  gloss,  by  the  fact  that  the  feces  float  in  water, 
and  their  behavior  when  pulverized  (a  membrane  showing  a  play  of  colors). 
Under  the  microscope  such  feces  show  unsplit,  neutral  fats  in  globules,  and 
fatty  acids  and  soap  needles  in  profusion.  On  analyzing  these  findings,  we 
are  forced  to  consider  disturbances  in  the  flow  of  bile  and  in  bile  produc- 
tion; therefore,  diseases  of  the  liver  and  biliary  passages  (occlusion  of  the 
common  bile  duct,  jaundice),  derangement  of  the  pancreatic  secretion,  and 
actual  diseases  of  the  small  intestine.  Doubt  can  only  be  removed  by  clin- 
ical observation  combined  with  therapeutic  measures  (pancreatic  prepara- 
tions) and  chemical  examinations  of  the  urine  and  feces,  which  cannot  be 
considered  in  this  article. 

The  carbohydrates  of  the  food,  provided  this  is  properly  prepared  in  the 
kitchen  and  thoroughly  masticated,  are  usually  well  digested.  The  dis- 
covery of  food  particles  containing  starch  indicates,  therefore,  an  extremely 
rapid  propulsion  through  the  intestine.  Since,  however,  the  carbohydrates 
which  escape  digestion  and  absorption  ferment  and  rapidly  decompose  in 
the  intestine,  we  are  justified  in  concluding  from  the  presence  of  large 
quantities  of  acid  products  of  fermentation  (acid  reaction  of  the  feces)  or 
a  great  volume  of  gas  in  the  bowel  or  in  the  feces  (perhaps  A.  Schmidt's 
fermentation  test)  that  there  is  deficient  carbohydrate  digestion  in  the 
intestine.  The  absence  under  the  microscope  of  the  iodin  reaction  is  not 
always  conclusive ;  digestion  of  starch  may  be  deficient  and  the  reaction  for 
starch  in  the  feces  be  very  slight  provided  the  undigested  starch  has  been 
destroyed  by  fermentation. 

We  must  search  for  the  cause  of  poor  digestion  of  starch  in  the  im- 
proper preparation  of  the  food,  in  imperfect  mastication  and  insufficient 
admixture  with  the  saliva,  also  within  the  bowel  itself  (intestinal  fer- 
mentative dyspepsia). 


654        DIARRHEA,  CATARRH,   AND   INTESTINAL  TUBERCULOSrS 

The  treatment  of  acute  and  chronic  diarrhea  will  be  considered  in  the 
chapters  relating  to  intestinal  catarrh. 


n.   INTESTINAL  CATARRH 

Diarrhea  and  intestinal  catarrh  running  its  course  with  diarrhea  pre- 
sent in  common  the  disturbances  in  function  previously  described.  Often, 
therefore,  they  are  confounded  with  one  another.  This  error,  however,  is 
not  so  great  as  it  may  appear;  for  between  diarrhea  and  intestinal  catarrh 
there  is  often  a  difference  only  of  degree,  and  simple  diarrhea  may  precede 
true  intestinal  catarrh,  may  continue  as  a  functional  irritation,  and  cause 
a  catarrhal  inflammation  of  the  intestinal  mucous  membrane.  The  chief 
difference  between  diarrhea  and  intestinal  catarrh  consists  in  a  pathologic 
cliange  in  the  intestinal  wall  which  may  be  clinically  recognized  from  the 
admixture  of  mucus  to  the  diarrhcic  stools. 


ACUTE  INTESTINAL  CATARRH 

This  is  one  of  the  most  common  maladies,  and  occurs  in  man  at  every 
age,  Init  especially  in  small  children,  in  the  aged,  and  in  the  debilitated 
who  have  little  power  of  resistance.  Acute  intestinal  catarrh  is  usually 
a  primary  and  substantive  affection,  more  rarely  it  occurs  secondarily  and 
symptomatically  in  the  course  of  previously  existing  diseases. 

Etiology. — The  most  frequent  cause  of  intestinal  catarrh  is  the  abnor- 
mal nature  of  the  intestinal  contents  which  immoderately  irritate  the  intes- 
tinal mucous  membrane,  either  mechanically  or,  more  frequently,  chem- 
ically. Those  causal  factors  which  have  been  enumerated  for  the  develop- 
ment of  diarrhea  may  also  be  of  etiologic  importance  in  intestinal  catarrh. 
Among  the  normal  products  of  fermentation  and  decomposition  of  the 
intestinal  contents  which  are  of  great  importance  in  peristalsis,  we  men- 
tion also  those  which,  according  to  Bokai's  investigations,  not  only  pro- 
duce diarrhea,  but  also  spastic  contraction  of  the  muscles  of  the  intestine 
and  catarrh  and  inflammation  of  the  gastric  mucous  membrane.  The  same 
dietetic  indiscretions,  the  immoderate  eating  of  food  and  drinking  of  fluids, 
or  the  unsuitable  nature  of  these  and  their  injurious  effect  upon  the  body 
— briefly,  all  errors  in  diet  of  either  a  quantitative  or  qualitative  nature — 
may  in  the  one  case  produce  only  diarrhea,  and  in  another  give  rise 
to  intense,  catarrhal,  intestinal  symptoms.  Local  and  periodic  condi- 
tions whicli  increase  the  virulence  of  bacteria  may  favor  the  ectogenous 
(loeomposition  of  food,  so  that  the  toxic  action  of  the  abnormal  products 
of  decomposition  not  only  results  in  functional  irritative  symptoms  but 
also  in  pathological  changes  in  the  intestinal  wall.  In  the  intestine  itself 
a  foreign  vegetation  introduced  with  spoiled  food  may  replace  the  nor- 
mal   intestinal   flora   or  even   exceed  this  in   growth,   and   by  abnormal 


INTESTINAL  CATARRH  655 

decomposition  also  generate  products  in  the  intestinal  contents — therefore 
endogenous — which  damage  the  intestinal  mucous  membrane.  This  chyme 
infection  of  Escherich  is  the  opposite  of  intestinal  infection — ^the  direct 
damage  of  the  intestinal  wall  by  bacteria  and  other  specific  pathogenic 
agents. 

Many  infectious  diseases  begin  with  the  appearance  of  gastrointestinal 
catarrh,  which,  as  in  the  case  of  enteric  fever,  cholera,  and  dysentery,  may 
be  attributed  to  the  accumulation  and  development  of  specific  pathogenic 
microorganisms  and  their  effect  on  metabolism.  In  all  probability,  the 
majority  of  the  pathogenic  microorganisms  are  capable  of  producing  infec- 
tious intestinal  catarrh;  this  is  certain,  at  least,  of  staphylococci  and 
streptococci.  Similar  in  action  to  bacteria  are  amehw,  coccidia  and  infu- 
soria, which  are  common  in  the  tropics  and  find  entrance  to  the  intestine 
by  means  of  stagnant  or  decomposed  water.  Upon  entering  the  mucous 
membrane  they  cause  the  death  of  the  epithelium  by  a  poison  that  they 
develop,  and  even  in  the  deeper  layers  of  the  intestinal  wall  they  produce 
inflammation  and  necrosis  which,  in  the  severer  forms  of  enteritis,  lead  to 
ulceration.  Just  as  abscesses  develop  in  the  liver  by  means  of  the  portal 
vein  circulation  in  dysentery  and  in  some  forms  of  ameba  enteritis,  so 
may  metastatic  inflammation  and  septicemia  follow  infectious  intestinal 
catarrh.  The  conditions  are  the  reverse  in  other  infectious  diseases  which 
are  not  localized  in  the  intestine;  for  example,  in  puerperal  fever  and 
other  septic  processes,  also  in  the  dyscra^ias  which  are  the  consequence  of 
some  infectious  diseases  (tuberculosis,  syphilis,  malaria  and  pyemia,  as 
well  as  in  carcinomatosis  and  in  uremia)  by  producing  an  abnormal  com- 
position of  the  blood  or,  on  the  contrary,  the  excretion  of  definite  toxic- 
acting  products  into  the  intes'tinal  canal,  which  there  produce  intestinal 
catarrh. 

In  the  forms  of  disease  last  mentioned,  the  mucous  membrane  of  the 
entire  digestive  tract  may  be  the  seat  of  catarrhal  inflammation,  for  in 
catarrh  due  to  abnormal  intestinal  contents  the  localization  and  the  dis- 
tribution of  the  catarrh  depend  upon  the  extent  of  the  materia  peccans 
into  the  intestine,  the  length  of  time  it  retains  its  noxious  properties,  or 
where  it  assumes  this  virulent  nature. 

An  acute  gastric  catarrh  distributes  itself  within  the  upper  small  intes- 
tine, not,  as  was  formerly  assumed,  by  the  extension  of  the  inflammatory 
process  from  the  gastric  mucous  membrane  to  the  duodenal  mucous  mem- 
brane, but  by  the  propagation  of  the  same  irritating,  deleterious  agents. 
The  lower  portions  of  the  intestine  may  be  exempt  when  chyle,  which  is 
still  abnormal  in  the  duodenum  and  in  the  jejunum,  becomes  innocuous 
by  further  dilution  with  the  digestive  juices,  or  by  dilution  with  a  large 
amount  of  fluid  which  has  transuded  into  the  intestine,  or  when  it  is  coated 
with  mucus.  On  the  other  hand,  abnormal  processes  of  decomposition  may 
frequently  be  generated  in  the  deeper  portions  of  the  small  intestine  or  in 


056        DIARRHEA,  CATARRH,   AND   INTESTINAL  TUBERCULOSIS 

the  beginning  of  the  colon,  in  regions  where  the  conditions  are  more  favor- 
able for  the  existence  of  microbes  than  in  the  upper  portion  of  the  small 
intestine  or  in  the  stomach. 

Except  when  caused  by  abnormal  fermentation  and  decomposition, 
catarrh  of  the  colon  is  most  frequently  caused  by  the  abnormal  dryness 
and  hardness  of  the  feces,  by  their  prolonged  retention,  or  by  their  accu- 
mulation in  large  masses.  Owing  to  peculiar  local  and  functional  condi- 
tions, definite  areas  of  the  colon  are  predisposed  to  catarrhal  and  inflam- 
matory affections;  above  all,  the  cecum,  the  flexures  at  either  side  of  the 
abdomen,  and  the  sigmoid  flexure.  The  same  is  true  of  the  rectum;  but, 
besides  accumulated  feces  in  the  ampulla,  various  kinds  of  ingesta  produce 
catarrh  of  the  mucous  membrane,  as  do  also  enemata  which  irritate  ther- 
mically,  nutritive  enemata  which  irritate  by  their  concentration  or  by  the 
decomposition  of  food  products  which  they  contain,  and  drugs  which  are 
injected  into  the  rectum.  Occasionally  gonorrheal  virus  produces  a  severe 
catarrh  of  the  rectum.  Kefrigeration  must  frequently  be  considered  as  a 
cause  of  acute  intestinal  catarrh,  and  also,  finally,  intestinal  parasites  and 
foreign  bodies  which  find  their  way  into  the  intestine. 

Secondarily  or  syniptomatically  intestinal  catarrh  arises  in  other  patho- 
logical, structural  changes  of  the  intestinal  wall,  in  many  ulcers,  in  inflam- 
mation of  the  peritoneum,  and  in  local  and  general  circulatory  disturb- 
ances which  affect  the  intestinal  canal.  Abnormal  displacements  and  the 
fixation  of  individual  intestinal  coils,  also  invagination,  torsion,  and  incar- 
ceration, lead  to  stretching  and  compression  of  the  mesenteric  vessels,  and, 
consequently,  to  local  circulatory  disturbances,  changes  in  the  mucous  mem- 
brane, and  intestinal  necrosis.  In  all  of  these  conditions  it  is  true  that 
intestinal  catarrh,  as  such,  is  of  minor  importance. 

Pathology. — In  acute  intestinal  catarrh  the  pathological  lesions  are 
often  out  of  proportion  to  the  severity  of  the  clinical  symptoms,  especially 
in  the  cases  Avhich  run  a  rapid  course  and  in  which  severe  intestinal  infec- 
tions or  intoxications  have  caused  a  speedy  death.  In  these  instances, 
chemical  and  bacteriological  investigations  lead  to  more  accurate  conclu- 
sions than  the  autopsy  findings. 

When  a  catarrhal  enteritis  is  present  the  intestinal  tract  only  excep- 
tionally shows  inflammatory  change;  as  a  rule,  merely  isolated  portions 
are  diseased,  some  more,  others  less,  while  extensive  areas  of  the  intestinal 
canal  are  often  entirely  exempt.  The  diseased  mucous  membrane  may  be 
covered  with  a  slimy,  or,  more  often,  a  serous,  or,  at  other  times,  a  muco- 
purulent and  turbid  exudate  from  desquamated  epithelia  and  pus,  and  this 
may  sometimes  be  of  even  a  hemorrhagic  nature.  The  mucous  membrane 
Itself  is  flaky  or  diffusely  reddened  and  swollen,  is  more  markedly  infil- 
trated (han  normally,  often  showing  hemorrhagic  infiltration  or  permea- 
tion by  small  hemorrhages,  particularly  in  the  crests  of  the  mucous  mem- 
brane folds. 


INTESTINAL  CATARRH  657 

Many  intestinal  catarrhs  are  characterized  by  swelling  and  redness  of 
the  follicular  apparatus  (enteritis  follicularis).  The  solitary  follicles 
then  form  reddish  or  grayish  white  prominent  nodules,  and  on  the  agminate 
glands  (Peyer's  patches)  are  grayish  white  or  gray  elevations  surrounded 
by  a  hyperemic  area,  and  permeated  by  groove-like  depressions. 

Microscopically,  the  mucous  membrane  is  markedly  hyperemic,  and  fre- 
quently shows  a  very  defective  epithelial  coating  as  a  post  mortem  phe- 
nomenon. The  epithelia  still  present  have  undergone  a  mucoid  and  de- 
structive change,  the  supporting  tissue  and  the  submucosa,  according  to 
the  intensity  of  the  inflammation,  give  evidence  of  serous  transudation  and 
small  cell  infiltration,  while,  on  the  other  hand,  the  muscularis  is  slightly 
or  not  at  all  altered. 

In  accordance  with  the  localization  of  the  inflammation,  we  differen- 
tiate patliologically  between  duodenitis,  jejunitis  and  ileitis,  a  typhlitis 
(appendicularis  and  typhlitis  cecalis),  colitis  (even  sigmoiditis)  and  proc- 
titis.    Clinicallv,  these  differentiations  are  impossible. 

As  a  rule,  in  tlie  milder  forms  of  acute  intestinal  catarrh  complete 
recovery  occurs.  After  the  removal  from  the  intestinal  canal  of  all  dele- 
terious products  the  inflammatory  irritation  ceases  as  well  as  the  patho- 
logical secretions,  the  products  of  inflammation  are  absorbed,  and  the  epi- 
thelium which  has  been  destroyed  is  replaced  by  regenerative  proliferation 
of  the  epithelial  cells  retained  in  Lieberkiihn's  crypts. 

If  the  inflammatory,  irritation  is  long  continued,  or  if  it  recurs  rap- 
idly and  often,  chronic  intestinal  catarrh  may  develop  from  an  acute  form. 
More  intense  irritation  leads  to  severe  inflammation  of  the  mucous  mem- 
brane and  of  the  deep  layers  of  the  intestinal  wall,  to  necrosis  and  to 
ulceration.  Severe  infectious  and  toxic  forms  of  enteritis  not  rarely  result 
in  death,  and  they  form  the  chief  cause  of  the  enormously  great  mor- 
tality of  infants. 

Symptoms. — Among  the  clinical  symptoms  of  acute  intestinal  catarrh 
the  most  coinmon  are  intestinal  motor,  sensory,  and  secretory  irritative 
phenomena:  Diarrhea,  pain  and  the  admixture  of  mucus  to  the  feces.  In 
the  severe  infectious  and  toxic  forms  of  intestinal  catarrh  to  these  must 
be  added  the  general  symptoms  of  infection  and  of  intoxication  which  not 
infrequently  may  be  of  very  serious  nature  and  extremely  dangerous  to 
debilitated  persons. 

Among  the  symptoms,  diarrhea  and  the  pain  of  various  kinds  so  often 
combined  with  it  liave  been  described.  I  have  also  emphasized  that  an 
intense  irritation  of  the  colon  is  a  typical  characteristic  of  the  diarrhea. 
In  fact,  there  are  many  forms  of  catarrh  of  the  small  intestine  which  can- 
not be  recognized  except  by  those  who  make  it  a  rule  in  all  gastrointestinal 
affections  to  subject  the  feces  to  regular  and  minute  examination.  Duo- 
denal catarrh,  for  example,  may  be  masked  by  the  symptoms  of  gastritis, 
with  which  it  is  usually  associated  until  the  appearance  of  jaundice,  which 


658        DIARRHEA,   CATARRH,   AND   INTESTINAL  TUBERCULOSIS 

originates  from  the  duodenum.  Catarrh  may  also  be  of  the  jejunum  and 
of  the  ileum;  in  fact,  catarrh  limited  to  the  small  intestine  is  frequently 
unrecognizable  because  it  has  so  few  diagnostic  points  of  support.  It  is 
true  that  it  may  run  its  course  with  marked  disturbance  of  the  constitu- 
tional condition  and  local  difficulties,  but  diarrhea  is  absent,  or  present 
for  only  a  few  days,  when  the  colon  also  becomes  irritated  and  the  seat 
of  catarrlial  inflammation.  Nothnagel  has  described  as  jejunal  diarrhea 
a  condition  in  which  feces  are  evacuated  which  are  of  the  same  composi- 
tion as  the  contents  of  the  jejunum:  Odorless  masses  with  unaltered  con- 
stituents of  the  food  and  unaltered  bile,  and  permeated  with  mucus.  Such 
diarrheas  occasionally  occur.  Much  more  frequently,  however,  catarrh  of 
the  jejunum  and  catarrh  of  the  upper  ileum  run  their  course  without  diar- 
rhea, at  least  for  a  time.  Not  rarely  we  observe  in  such  cases  irritative 
symptoms  which  usually  precede  diarrhea — increased  peristalsis,  rolling 
movements,  borborygmi  and  pain — but  the  diarrhea  does  not  occur  for 
some  time.  Notwithstanding  this — probably  in  consequence  of  the  too 
rapid  propulsion  through  the  small  intestine  of  the  undigested  remains 
of  food — abnormal  fermentation  generates  in  the  large  intestine  an  in- 
creased gas  formation  which  causes  some  distress,  and  which  may  be 
clinically  recognized  until,  after  more  or  less  time,  diarrhea  supervenes. 
In  the  evacuated  feces  insufficiently  digested  fragments  of  food  will  prob- 
ably be  found,'  but  often,  at  the  onset  of  diarrhea,  no  unaltered  bile.  Only 
in  catarrh  of  the  small  intestine  and  colon  combined,  which  runs  its  course 
with  frequent  diarrhea,  is  bile  again  passed  in  an  unaltered  condition.  In 
such  feces  we  sometimes  find,  besides  unaltered  bile,  also  other  digestive 
juices,  or,  at  least,  their  ferments,  pepsin  and  trypsin.  On  exposure  to  the 
air  their  bilious  tint  occasionally  changes  and  becomes  greenish,  or  leek- 
colored. 

Ahdominal  pain  is  common  in  most  cases  of  intestinal  catarrh.  This  is 
usually  dull,  sometimes  of  a  burning  or  cutting  character,  and  may  be 
continuous  or  increase  and  decrease  periodically.  This  may  spread  over 
tlie  entire  abdomen,  or  may  be  localized  in  the  region  of  the  navel,  espe- 
eially  if  the  small  intestine,  in  particular,  is  implicated.  Acute  catarrh  of 
the  colon  appears  to  cause  much  greater  pain  than  that  of  the  small  intes- 
tine; the  pain  is  localized  in  the  ileo-cecal  region,  in  the  flexures  of  the 
hypochondriac  regions,  and  in  the  sigmoid  flexure,  or  is  often  confined  to 
the  transverse  colon  or  may  extend  throughout  the  entire  course  of  the 
colon. 

Pains  of  the  greatest  intensity  may  be  caused  by  a  simple  mucous 
mrmhrane  catarrh  of  the  appendix;  very  frequently  this  suggests  per- 
foration; however,  peritoneal  phenomena  and  fever  do  not  follow,  and  if, 
in  such  cases,  as  a  precaution,  the  appendix  is  resected,  the  slight  change 
in  the  mucous  membrane  of  the  excised  appendix  is  surprising.  It  may 
not  be  out  of  place  to  emphasize  the  fact  that  the  vermiform  appendix  is 


INTESTINAL  CATARRH  659 

predisposed  to  extremely  painful  colics  which  appear  upon  the  slightest 
irritation. 

Diarrheal  discharges  from  the  large  intestine  also  cause  periodic  attacks 
of  colic  which  are  frequently  of  great  intensity.  As  already  stated,  these 
are  attributable  to  spastic  contracture  of  the  annular  musculature  of  the 
intestine  or  to  the  great  distei»tion  of  certain  portions  of  the  intestine  by 
gas  or  feces  (incarcerated  gas,  wind  colic),  while  the  non-spasmodic  intes- 
tinal pains  are  to  be  ascribed  to  chemical  irritation  of  the  sensory  nerves 
of  the  intestinal  wall.  In  many  intestinal  catarrhs  pain  is  absent;  the 
diarrheic  stools  are  forcibly  ejected  from  the  bowel. 

Pboctitis. — Acute  proctitis  is  accompanied  by  peculiar  pain  which  in 
mild  cases  shows  itself  by  a  more  or  less  distressing  sensation  of  burning, 
often  by  ineffectual  attempts  to  evacuate  the  bowels,  and,  in  severe  cases, 
appears  in  the  form  of  spasmodic  tenesmus.  Not  infrequently — although 
but  little  fecal  matter  is  discharged — the  mucous  membrane  of  the  rectum 
to  a  greater  or  less  extent  protrudes  from  the  anus  as  a  tumor,  or  tumor- 
like mass,  almost  ectropic.  Occasionally,  as  in  colica  spastica,  spasm  of 
the  anal  sphincter  appears  and  may  continue  for  some  tim6,  giving  rise 
to  severe  pain,  and  preventing  evacuation.  Often  in  acute  proctitis  mucus 
alone  is  discharged,  sometimes  of  a  glassy  or  shreddy  character,  occasion- 
ally also  in  peculiar  globular  or  cluster-like  masses;  when  there  is  severe 
tenesmus,  besides  mucus  blood  also  invariably  appears  in  the  dejecta. 
Often  hemorrhagic  mucus,  or  blood  alone,  is  noted  without  ulcerations 
being  necessarily  present  in  the  rectal  mucous  membrane. 

In  acute  intestinal  catarrh  the  general  systemic  disturbances  vary 
extraordinarily.  Eobust  persons  who  have  no  fever  very  often  pass  through 
an  attack  without  being  confined  to  bed;  the  evacuations,  which  often 
amount  to  ten  or  twenty  during  the  day,  are  very  distressing,  as  well  as 
the  feeling  of  soreness  about  the  anus  and  the  lassitude  which  is  attribu- 
table to  the  great  loss  of  fluid  and  the  impossibility  of  taking  sufficient 
nourishment,  but,  in  a  few  days,  the  difficulty  passes  away.  In  severe 
cases  there  is  a  sensation  of  extreme  illness  which  renders  the  patient  in- 
capable of  attending  to  his  work,  and  confines  him  to  bed;  so  fulminant 
do  the  symptoms  appear  that  a  severe  infectious  disease  or  an  intoxication 
is  supposed  to  be  present  until  the  diagnosis  becomes  clear. 

Fever  is  more  commonly  observed  and  is  also  higher  in  children  than 
in  adults;  the  onset  and  course,  however,  conform  to  no  distinct  type. 
In  the  toxic  forms  of  acute  intestinal  catarrh,  the  temperature  is  apt  to 
be  subnormal. 

Other  symptoms  frequently  observed  as  accompaniments  of  dyspeptic 
disturbances,  such  as  headache,  lassitude,  nausea,  anorexia,  coated  tongue, 
thirst,  an  eruption  of  herpes  about  the  lips,  urticaria,  pains  in  the  limbs, 
also  cramps  in  definite  muscle  groups,  and  cramp  in  the  calves,  are  noted 
also  in  acute  intestinal  catarrh.     In  severe  cases  typical  attacks  of  tetany 


C60        DIARRHEA,  CATARRH,   AND  INTESTINAL  TUBERCULOSIS 

and  delirium  are  now  and  then  observed.  In  children  the  nervous  disturb- 
ances of  acute  enteritis  are  particularly  severe  and,  at  the  onset  of  the 
disease,  tubercular  meningitis  may  be  simulated. 

Corresponding  in  ratio  with  the  losses  of  water  by  the  copious  bowel 
discharges,  at  the  height  of  an  attack  of  acute  intestinal  catarrh  the  excre- 
tion of  urine  is  very  deficient,  and  the  daily  amount  voided  is  much  re- 
duced; often  anuria  may  last  for  a  day  or  even  longer;  during  this  time 
blood-pressure  is  decidedly  lessened,  the  pulse  is  small  and  often  irregular. 
With  the  reestablishment  of  diuresis,  albumin  may  often  be  found  in  the 
urine  as  well  as  casts,  both,  however,  only  temporarily. 

Upon  examination  the  patients,  particularly  children,  are  found  apa- 
thetic and  apparently  seriously  ill.  As  a  rule,  very  little  can  be  demon- 
strated objectively  except  the  frequent  diarrheic  discharges  at  the  onset  of 
the  disease.  Enlargement  of  the  spleen  has  now  and  then  been  observed 
in  infectious  catarrh.  The  abdomen  is  usually  unchanged,  at  times  sorae- 
wliat  retracted,  at  other  times  distended.  Through  the  thin  abdominal 
walls  we  occasionally  perceive  the  motions  of  the  intestine,  or  they  may 
be  felt  with  a  palpating  hand,  or  rumbling  is  heard  in  the  abdomen  and 
portends  another  intestinal  evacuation.  As  a  rule,  the  entire  abdomen  is 
sensitive  to  pressure,  but  it  may  be  so  in  only  limited  areas;  gurgling  is 
readily  produced  in  the  ileo-cecal  region.  Profuse  accumulations  of  fluid 
and  intestinal  contents  here  and  there  cause  dulness  upon  percussion.  The 
comparatively  rapid  change  in  the  symptoms  will,  however,  soon  show  how 
erroneous  is  the  assumption  of  a  peritoneal  exudate  or  an  ascites. 

In  no  other  malady  is  the  destructive  action  of  the  affection  so  dis- 
tinctly apparent,  and  in  relatively  so  brief  a  time,  as  in  severe  acute 
(gastro-)  enteritis.  In  severe  cases  striking  changes  may  take  place  be- 
tween one  visit  and  another.  A  blooming  child  may  be  changed  to  a 
pitiable  object,  the  previously  full,  round  face  may  be  emaciated,  a  for- 
merly strong  heart  may  be  flaccid  and  weak.  Just  as  rapidly,  however, 
a  change  for  the  better  may  supervene  when  the  profuse  discharges  cease 
and  copious  draughts  of  fluid  have  quenched  the  thirst  of  the  body  and 
its  tissues. 

Course  of  the  Disease. — In  adults  the  course  of  acute  intestinal  catarrh 
is  usually  favorable,  provided  there  is  no  severe  alimentary  intoxication. 
Unfortunately,  at  the  onset  of  an  acute  enteritis  we  do  not  always  know 
that  it  is  the  primary  effect  of  an  infectious  disease — occasionally  the 
latter  is,  in  fact,  the  case,  under  which  circumstances  only  in  the  further 
course  of  the  disease  do  the  characteristic  symptoms  of  specific  infection, 
influenza,  articular  rheumatism,  enteric  fever,  or  cholera,  appear.  If, 
lunvever,  there  is  no  reason  to  suspect  these  affections,  the  prognosis  in 
adults  is  always  favorable.  In  a  few  days  the  affection,  whose  severity 
is  usually  limited  to  the  excessive  number  of  bowel  evacuations  daily, 
has   run  its  course,  and  although  convalescence  may  be  somewhat   pro- 


INTESTINAL  CATARRH  661 

tracted  the  duration  of  the  disease  is  rarely  more  than  one  or  two  weeks. 
Only  in  little  children  is  acute  enteritis,  particularly  gastroenteritis,  a 
severe  disease  which  greatly  influences  the  general  mortality. 

In  persons  of  any  age  severe  acute  intestinal  catarrh  not  rarely  leaves 
an  irritative  condition  of  the  colon  which  expresses  itself  by  a  tendency 
to  diarrhea,  and  may  persist  for  a  considerable  time. 

Diagnosis. — The  diagnosis  of  acute  intestinal  catarrh  is,  as  a  rule,  very 
easy;  but  the  localization  of  the  catarrh,  and,  in  some  cases  which  run 
their  course  with  severe  constitutional  symptoms,  the  decision  of  the  ques- 
tion, whether  the  disease  is  an  infection  or  intoxication,  may  be  difficult. 

In  practice,  usually,  no  line  of  demarcation  is  drawn  between  diarrhea 
and  intestinal  catarrh,  and,  indeed,  the  designation  intestinal  catarrh 
appears  to  be  the  more  popular  one  for  the  cases  under  consideration. 
The  chief  characteristic  of  catarrh,  however,  is  the  admixture  of  mucus 
with  the  feces,  and  this  cannot  be  overlooked  if  the  investigation  of  the 
feces  is  at  all  thorough. 

We  regard  mucus  as  a  pathological  secretion,  the  presence  of  which 
in  a  given  case  clearly  indicates  that  the  limits  of  a  purely  functional 
disturbance  have  been  exceeded,  and  that  pathological  changes  have  taken 
place  in  the  intestinal  wall;  namely,  catarrh  and  inflammation.  The 
differential  diagnosis  between  diarrhea  and  intestinal  catarrh  can,  there- 
fore, he  made  only  hy  coproscopy. 

Mucus  is  a  glycoproteid  which  upon  splitting  becomes  a  proteid  and 
a  carbohydrate.  This  splitting  may  be  produced  chemically  (by  boiling 
with  a  5  per  cent,  hydrochloric  acid  solution)  after  which  the  albumin 
body,  as  well  as  the  carbohydrate,  may  be  demonstrated  by  reagents. 
It  takes  place  in  the  stomach  as  well  as  in  the  small  intestine;  therefore, 
mucus  is  digestihle. 

Consequently  sputum  that  has  been  swallowed,  mucus  from  the  phar- 
ynx, from  the  esophagus,  or  from  the  stomach  never  reappears  in  the 
feces;  therefore,  mucus  found  in  the  feces  must  originate  in  the  intestine. 
But  mucus  is  also  digested  in  the  upper  portion  of  the  small  intestine; 
in  the  colon,  however,  it  is  certainly  not.  Hence  it  is  possible  that  mucus 
originating  from  catarrh  of  the  upper  small  intestine  disappea,rs  wholly 
or  entirely  in  digestion,  provided  it  is  not  too  rapidly  propelled  into  the 
lower  portion  of  the  intestine  and  voided  with  profuse  diarrheal  discharges. 

An  admixture  of  mucus  with  the  feces,  like  the  more  or  less  intimate 
admixture  of  blood,  indicates  a  somewhat  high  point  of  origin.  Flocculi 
of  mucus  intimately  combined  with  feces,  and  bile-stained,  denote  catarrh 
of  the  small  intestine.  This  sign  is,  however,  not  absolutely  certain,  for 
in  severe  diarrhea  unaltered  bile  may  pass  through  the  entire  intestinal 
canal  and  be  readily  recognizable  in  the  feces.  In  doubtful  cases,  Gmelin's 
test  or  Schmidt's  corrosive  sublimate  test  is  decisive  for  unaltered  biliary 
coloring  matter.  This  reaction  shows  an  abnormally  rapid  propulsion 
43 


662        DIARRHEA,  CATARRH,   AND   INTESTINAL  TUBERCULOSIS 

through  the  intestine  of  all  those  constituents  of  the  feces  which  are 
stained  with  unaltered  biliary  coloring  matter  (and  which  become  green 
with  Schmidt's  test). 

While  a  microscope  is  often  necessary  to  detect  small  mucus  flocculi 
(and  partly  digested  ones?)  from  the  upper  small  intestine,  mucus  from 
the  lower  small  intestine,  also  that  which  comes  from  the  colon,  even  when 
intimately  admixed  with  feces,  can  always  be  recognized  by  the  naked  eye. 
If  only  the  descending  colon,  the  sigmoid  flexure  and  the  rectum  are 
diseased,  the  mucus  masses  originating  from  these  areas  may  easily  be 
detached  from  the  feces;  they  will  rarely  show  staining  with  bile.  In 
acute  catarrh  of  the  rectum  and  the  descending  colon  pure  mucus  is 
sometimes  discharged.  An  admixture  of  blood  with  the  mucus  or  feces 
is  very  frequently  found  in  acute  proctitis  running  its  course  with  severe 
tenesmus  even  when  there  is  no  ulcerative  process  in  the  rectum. 

The  quantity  and  composition  of  the  mucus  admixed  with  the  feces 
varies  greatly;  between  the  finest  flocculi,  delicate  membranes,  and  large 
shreddy  membranes,  all  intermediate  stages  may  be  observed.  Amorphous 
mucus  gives  to  many  diarrheic  stools  a  gelatinous  composition;  sometimes 
amorphous  mucus  is  discharged  alone  as  a  glassy  mass.  The  uniform 
admixture  of  small  threads  of  mucus  with  diarrheic  stools  gives  to  them 
a  choppy  appearance  (thread-worms). 

In  the  descending  colon  and  rectum  the  mucus  sometimes  appears  in 
the  form  of  bands  or  tubes  corresponding  in  shape  with  these  portions 
of  the  intestine.  A  peculiar  globular  or  grape-like  appearance  of  the 
mucus,  which  to  the  inexperienced  sometimes  becomes  a  diagnostic  enigma, 
is  acquired  in  the  haustra  of  the  colon  or  the  ampulla  of  the  rectum  (in 
chronic  catarrh  more  frequently  than  in  acute,  especially  after  convales- 
cence has  set  in)  when  the  feces  which  are  propelled  by  peristalsis  toward 
the  anus  take  from  the  mucous  membrane  its  mucus  coating  and  roll  it 
up.  Admixture  of  mucus  with  the  feces  does  not  take  place  in  this  lower 
portions  of  the  intestine;  the  feces  then  are  covered  with  mucus — actually 
enveloped  in  it. 

Microscopic  examination  of  the  mucus  will  protect  us  from  a  possible 
confusion  with  the  remains  of  food,  and  at  the  same  time  it  reveals  the 
intensity  of  the  catarrhal  inflammation;  this  can  be  estimated  by  the  num- 
bers of  white  (and,  rarely,  of  red)  blood-corpuscles  admixed  with  the 
mucus.  A  plentiful  admixture  of  white  blood-corpuscles  to  the  mucus 
gives  this  a  purulent  character  which  may  frequently  be  recognized  macro- 
scopically. 

The  mucus  often  shows  a  hemorrhagic  discoloration,  even  with  only 
superficial  infiammation  of  the  intestinal  mucous  membrane.  Greater  ad- 
mixture of  blood  to  the  intestinal  discharges  almost  always  indicates  ul- 
cerative processes  in  the  intestine  or  rupture  of  continuity  of  the  mucous 
membrane  in  the  rectum  (fissures,  abrasions,  hemorrhoids).     Here  it  need 


INTESTINAL  CATARRH  663 

only  be  mentioned  that  profuse  hemorrhages,  even  without  ulcerative  proc- 
esses, may  take  place  in  the  gastrointestinal  canal ;  for  example,  in  hepatic 
cirrhosis  and  in  thrombosis  and  embolism  of  the  mesenteric  artery. 

The  causes  of  endemic  and  tropical  diarrhea,  of  many  acute  and 
chronic  catarrhs,  and  of  inflammations  of  the  intestinal  mucous  mem- 
brane are  to  be  found  in  the  protozoa  in  fresh  intestinal  mucus  or  that 
which  has  been  kept  warm.  Some  forms  of  dysentery  belong  to  this 
category,  also  amela  enteritis,  coccidia  and  infusoria  diarrhea.  In  his 
article,  "Dysentery  and  Ameba  Enteritis,"  which  I  should  here  like  to 
refer  to,i  G.  Hoppe-Seyler  has  described  these  conditions.  But  I  cannot 
here  enter  upon  the  bacteriologic  finding  of  the  specific  agents  of  many 
infectious  diarrheas  and  intestinal  infiammations,  neither  can  I  enumerate 
the  parasites  of  the  intestine,  the  existence  of  which  can  be  determined 
by  an  examination  of  the  feces. 

Treatment. — The  treatment  of  diarrhea  and  of  acute  intestinal  catarrh 
must  be  instituted  with  a  search  for  the  cause.  If  it  has  been  found  that 
abnormality  of  the  intestinal  contents  has  produced  the  affection  the  -first 
indication  in  the  treatment  is  the  removal  of  the  deleterious  intestinal 
contents. 

As  a  matter  of  fact  the  action  of  the  organism  is  based  on  the  same 
principles:  Diarrhea,  produced  refiexly,  is  an  attempt  on  the  part  of  the 
over-irritated  organ  to  relieve  itself,  and  this  is  further  promoted  by 
the  increased  excretion  of  fluid  and  the  inappetence,  also  reflexly  produced, 
which  prevents  the  placing  of  additional  labor  upon  the  digestive  organs, 
but  gives  them  rest;  thus  a  reserve  power  of  resistance  is  produced.  In 
fact,  many  diarrheas  and  catarrhs  are  self-limited  and  naturally  run  a 
rapid  and  favorable  course;  for  this  reason  we  should  not  interfere  with 
the  organism  in  its  attempt  at  self-aid:  Primo  die  quiescere  satis  est; 
neque  impetum  ventris  prohihere  (Celsus). 

We  aid  this  endeavor  of  the  body  by  rest  in  bed  and  the  administra- 
tion of  non-irritating  drinks  which  immediately  cleanse  the  stomach  and 
the  upper  part  of  the  small  intestine  and,  after  absorption,  also  the  tissues 
of  the  body,  especially  the  blood  and  the  kidneys,  thus  compensating  for 
the  loss  of  fluids  and  the  diarrhea  by  maintaining  diuresis.  By  washing 
out  the  colon  from  below  a  large  quantity  of  its  contents  can  be  more 
rapidly  evacuated  than  by  the  diarrhea,  and  thereby  we  limit  the  absorp- 
tion of  abnormal  products  of  decomposition,  and  give  the  irritated  organ 
longer  periods  of  rest,  even  if  we  do  not  always  by  these  means  succeed 
in  rapidly  controlling  the  diarrhea. 

Warm  infusions  of  herbs  which  contain  ethereal  oils  (phenol,  anise, 
chamomile,  or  peppermint)   long  enjoyed  a  great  reputation  in  diarrhea, 

'  See  "  Modern  Clinical  Medicine,"  "  Infectious  Diseases,"  D.  Appleton  &  Co., 
1905,  p.  681. 


664        DIARRHEA,  CATARRH,  AND  INTESTINAL  TUBERCULOSIS 

for  the  reason  that  they  taste  better  than  warm  water,  and  as  carminatives 
apparently  have  a  mild  action;  but  they  may  well  be  substituted  for  by 
warm  mineral  water  with  a  small  addition  of  table  salt,  by  weak  warm 
or  cold  tea,  and,  in  some  cases,  by  dilute  rice  water,  barley  water,  oatmeal 
water  or  albumin  water.  When  these  drinks  are  to  be  taken  for  several 
days  the  last  named  deserve  preference,  as  they  simultaneously  contain 
a  minimum  of  nourishment. 

The  quantity  of  fluid  that  is  to  be  administered  depends  upon  indi- 
vidual conditions;  it  should  be  sufficient  to  quench  the  thirst,  but  should 
not  be  given  in  excess. 

For  intestinal  irrigations,  besides  weak  infusions  of  peppermint,  chamo- 
mile, anise,  etc.,  the  most  suitable  fluids  are  saline  solutions  one-half  to 
three-quarters  per  cent.,  under  some  circumstances  with  the  addition  of 
0.5  to  1.0  of  salicylic  acid  to  the  liter  of  fluid.  Other  disinfectants  may 
be  used  for  this  purpose;  some  of  them  are  not  very  effective  as  the  solu- 
tion must  be  very  weak  in  order  not  to  injure  the  intestinal  epithelium, 
and  in  choosing  these  remedies  their  absorption  in  the  rectum  and  colon 
must  l)e  considered.  The  efficacy  of  the  washing  depends  largely  upon 
the  temperature  of  the  fluid,  which  should  be  of  the  same  temperature 
as  the  body,  and  the  quantity  employed  must  depend  upon  individual 
circumstances.  I  advise  that  the  patient  be  placed  in  the  left  lateral 
posture,  under  some  circumstances  the  pelvis  to  be  raised,  and  as  much 
of  the  lukewarm  fluid  to  be  introduced  with  low  pressure  (one-half  to 
one  meter)  as  can  be  borne  without  discomfort.  As  soon  as  there  is  a 
desire  to  evacuate  the  bowel  we  must  suspend  the  irrigation  and  the 
l^atient  should  be  permitted  to  discharge  the  fluid  injected.  In  children 
from  200  to  500  c.c,  in  adults  from  1  to  1|  liters  and  more  may  thus 
1)0  used. 

According  to  the  indications  of  the  case,  in  diarrhea  we  may  irrigate 
the  intestines  morning  and  evening,  or  even  three  times  a  day;  for  ex- 
ample, in  acute  diarrhea  combined  with  great  tenesmus.  In  other  instances 
a  single  washing  of  the  intestine  in  the  morning  or  in  the  evening  will 
suiricc.  In  so-called  nocturnal  diarrhea^  which  invariably  occurs  at  night 
and,  as  a  rule,  in  the  second  half  of  the  night  or  early  in  the  morning, 
it  is  advisable  to  give  a  chamomile  injection  in  the  evening,  shortly  before 
supper,  or  half  an  hour  after  going  to  bed.  Such  evening  injections  are, 
at  the  same  time,  the  most  effective  remedies  for  peristaltic  unrest  of  the 
intestine  which  prevents  or  interferes  with  sleep. 

Tlie  l)cst  instrument  to  employ  is  an  irrigator  or  glass  funnel  with  a 
conveniently  long  rubber  tube;  but  syringes  may  also  be  employed  if 
a  ])iece  of  rubber  tubing  20  to  30  cm.  in  length  is  inserted  between  the 
syringe  and  the  rectal  bulb  to  allow  for  a  possible  recoil  or  jerk  of 
the  syringe,  and  to  prevent  trauma  to  the  rectum.  Care  is  necessary 
ill  the  clioice  of  an  anal  tube;  the  best  are  those  made  of  hard  rubber  or 


INTESTINAL  CATARRH  665 

glass  which  have  an  olive-shaped  bulb  and  are  well  and  smoothly  rounded 
off,  and  the  rubber  rectal  tubes  to  be  attached  should  have  fenestra  that 
have  been  smoothly  rounded  off.  The  high  introduction  of  longer  tubes 
into  the  intestine  is  only  advisable  when  the  sphincter  will  not  contract, 
and  when  we  desire  to  dislodge  an  obstruction  with  the  rectal  tube;  for 
example,  in  a  retroflexion  of  the  uterus  or  in  the  case  of  perimetritic 
exudates.  Even  in  the  so-called  high  intestinal  injection,  a  high  intro- 
duction of  the  rectal  tube  is  unnecessary;  the  flow  of  the  fluid  into  the 
intestine  is  promoted  much  more  by  the  position  of  the  patient  than  by 
the  introduction  of  a  long  tube :  The  knee-elbow  position,  the  dorsal  decu- 
bitus with  the  shoulders  low  and  the  pelvis  high,  perhaps  even  the  placing 
of  the  patient  upon  a  modern  operating  table  which  permits  the  maximum 
high  position  of  the  pelvis. 

Occasionally  we  thoroughly  cleanse  the  rectum  and  the  sigmoid  flexure, 
sometimes  even  the  left  flexure  of  the  colon  or  the  entire  colon,  by  irri- 
gating the  intestine  with  a  tube  and  funnel,  similarly  as  in  gastric  lavage, 
raising  and  lowering  the  funnel  and  occasionally,  after  emptying  the 
funnel,  adding  more  fluid.  The  intestine,  however,  is  more  susceptible 
than  the  stomach,  and  the  observance  of,  at  least,  the  same  precautions 
as  in  washing  the  other  organ  is  necessary. 

If  the  injurious  intestinal  contents  cannot  be  removed  by  washing  from 
below,  it  is  advisable  to  try  mild  laxatives.  The  number  of  remedies  to 
choose  from  is  great,  therefore  individual  indications  may  be  considered. 
Young  children  bear  calomel  in  small  doses  (0.01-0.03  several  .times  daily) 
very  well.  In  adults  several  (2  or  3)  large  doses  (0.1-0.2)  given  at  short 
intervals  are  sometimes  of  great  value  in  diarrhea,  although  even  with 
these  doses  ^  we  must  reckon  with  the  frequent  intolerance  of  mercury. 
In  doubtful  cases  a  good  dose  (20  to  30  grams)  of  castor  oil  is  given, 
or  rhubarb,  cascara  sagrada,  laxative  tea  or  lemonade  (citrate  of  magne- 
sia), a  teaspoonful  of  Glauber  salt,  Epsom  salt,  sodium  subsulphate  or 
Carlsbad  salt  dissolved  in  about  a  quarter  of  a  liter  of  water. 

The  second  indication  in  the  treatment  of  acute  diarrhea  and  intestinal 
catarrh  is  to  produce  non-irritating  intestinal  contents.  As  a  rule,  we 
should  be  in  no  haste  to  bring  about  such  a  change.  Fluids  that  are 
easily  absorbed,  water,  tea,  thin  meat  broth,  rice  water,  and  various  min- 
eral waters  with  a  small  addition  of  brandy  or  red  wine  are  sufticient 
until  hunger  reappears  or  weakness  becomes  noticeable.  In  the  choice 
of  foods  the  results  of  the  examination  of  the  feces  must  be  considered, 

and  at  first  those  foods  must  be  avoided  which  coproscopy  shows  to  be 

— ,— 

*  I  particularly  desire  to  emphasize  that  the  belief  that  calomel  disinfects  the 
intestine  is  erroneous.  Schiitz  proved  in  his  experimental  animals  that  by  calomel 
— in  contrast  with  castor  oil — the  bactericidal  properties  of  the  intestine  were  inhib- 
ited, and  Strasburger  found  more  bacteria  in  diarrheic  stools  after  calomel  than  in 
those  produced  by  castor  oil. 


666        DIARRHEA,  CATARRH,   AND  INTESTINAL  TUBERCULOSIS 

insufficiently  digested  or  difficult  of  absorption.  If  we  are  dealing  espe- 
cially with  fermentative  diarrhea,  those  substances  which  produce  fermen- 
tation— principally,  therefore,  the  starches — must  be  at  first  avoided  and 
an  albumin  diet  given,  or,  mostly  in  fetid  diarrhea,  an  albumin  diet  should 
be  avoided  or  should  be  permitted  to  but  a  very  limited  extent,  and 
carbohydrates  given  instead,  perhaps  in  the  form  of  gelatinous  soups,  milk 
soups,  or  cream  soups. 

In  the  acute  diarrhea  of  little  children,  albumin  water,  thin  gelatinous 
soups  which  are  made  with  water,  or  veal  broth  may  for  a  few  days 
substitute  for  milk.  Young  infants  should  have  a  wet  nurse,  or,  if  this 
cannot  be  arranged  for,  sterilized  milk  suitably  diluted  with  oatmeal 
gruel  is  the  best  food.  For  larger  children  racahout  and  other  fine 
starches  (arrowroot,  avena,  maizena,  mondamin  and  rice  flour)  with  milk, 
or  milk  and  oatmeal  gruel,  may  be  given.  A  gelatinous  mixture  prepared 
by  toasting  equal  parts  of  rolled  barley  and  candied  sugar  and  then  boiling 
for  a  long  time  in  water  is  very  concentrated,  possesses  a  high  nutritive 
value,  is  easily  taken,  and  well  borne.  The  quantity  of  food  is  to  be 
cautiously  increased,  as  well  as  the  concentration  of  the  milk  and  other 
foods;  for  a  time,  however,  we  adhere  strictly  to  the  calory  requirement 
of  the  youthful  organism,  and  avoid  overloading  the  intestine. 

In  adults  also  we  must  carefully  regulate  the  nutrition;  generally, 
however,  they  may  more  rapidly  return  to  the  ordinary  diet  than  children. 

Treatment  hy  drugs  is  indicated  when  a  strict  diet  combined  with 
rest  and  intestinal  lavage  has  proven  unsuccessful.  It  is  a  great  mistake 
to  resort  to  drugs  at  the  onset  of  the  malady.  This  is,  above  all,  true  of 
opium,  which  is  the  best  remedy  with  which  to  lessen  or  inhibit  intestinal 
activity.  If  this  is  done  while  noxious  material  is  still  in  the  intestine, 
the  organism  is  not  only  deprived  of  its  natural  power  of  self-aid  by 
increased  peristalsis,  but  it  is  damaged  and  the  course  of  the  disease  is 
thereby  protracted. 

I  believe  it  advisable  to  give  such  a  dose  of  opium  as  is  just  sufficient 
to  quiet  the  motor  and  secretory  irritability  of  the  intestine,  and  to  repeat 
this  dose  at  proper  intervals.  Occasionally  larger  doses  may  be  given  at 
night  to  secure  rest  for  the  patient. 

A  direct  antirirritant  effect  is  produced  upon  the  mucous  membrane 
by  gelatinous  fluids :  Gum  arable,  decoction  salep,  decoction  of  althea,  and 
also  emulsions  of  oil  and  milk  of  almonds.  These  substances  may  be 
administered  even  with  the  addition  of  opium.  In  catarrh  of  the  rectum 
and  of  the  lower  colon  we  may  also  employ  these  directly  as  injections; 
enemata  of  starch  (retained  enemata),  perhaps  with  the  addition  of  a 
few  drops  of  opium,  have  a  remarkably  soothing  effect  upon  the  colon; 
they  mechanically  protect  the  membrane  as  does  mucus,  and  do  not  de- 
compose— at  least,  do  not  become  fetid — and  even  appear  directly  to  coun- 
teract decomposition. 


INTESTINAL  CATARRH  667 

Oil  and  the  preparations  of  bismuth  also  mechanically  protect  the  bowel 
if  in  proper  suspension  in  water  or  oil,  and  injected  as  small,  retained 
enemata.  When  there  is  painful  tenesmus  and  spasm  of  the  anus  the 
local  application  of  opium  or  other  antispasmodics  (extract  of  belladonna) 
in  the  form  of  suppositories  is  indicated;  sometimes  a  simple  suppository 
of  cacao  butter  is  sufficient,  for  the  melted  cacao  butter  covers  the  irritated 
mucous  membrane  with  an  oily  surface,  and  protects  and  quiets  it. 

Anod}Tie  and  chemical  effects  are  produced  in  the  intestine  by  alkalies 
and  alkaline  earths,  as  they  neutralize  the  fatty  acids  in  the  small  intes- 
tine. The  fatty  acid  salts  irritate  the  intestinal  membrane  much  less  than 
free  fatty  acids.  This  explains  the  constipating  effect  of  chalk  water  and 
calcium  carbonate,  as  well  as  the  anodyne  property  of  Hufeland's  chil- 
dren's powders  (pulv.  magnes.  c.  rheo.)  which,  in  small  doses,  allay 
abdominal  pain,  expel  gas,  and  regulate  the  bowels,  but  in  larger  doses 
have  a  laxative  effect. 

As  constipating  remedies  antidiarrheics  and  astringents  are  still  fre- 
quently resorted  to,  particularly  tannic  acid  and  tannic  acid  combinations, 
both  by  mouth  and  as  enemata  (tannin,  tannalbin,  tannigen)  ;  also  the 
vegetables  containing  tannic  acid  (lign.  campech.,  Colombo,  ratanhia,^  cate- 
chu, whortleberries,  red  wine,  cocoa,  acorn,  acorn  cocoa) ;  the  metals,  above 
all,  bismuth  (bismuth  subnitrate,  bismuth  salicylate,  bismutose),  lead 
acetate,  and  silver  nitrate  are  valuable.  In  acute  cases,  however,  we  usually 
refrain  from  using  the  last  named  remedies. 

It  was  supposed  for  a  time  that  a  disinfectant  action  upon  the  intes- 
tinal contents  could  be  produced  by  creosote,  salol,  naphthalin,  benzonaph- 
thol  and  numerous  other  combinations  from  the  group  of  creasols  and 
naphthols.  I  have  seen  no  noteworthy  results  from  these  or  other  intes- 
tinal antiseptics,  or  from  calomel  in  large  doses.  Limitation  of  fermenta- 
tion and  decomposition  in  the  intestine  is  best  attained  by  the  application 
of  the  principle  of  asepsis;  namely,  the  intestinal  contents  which  have 
begun  to  decompose  are  expelled  from  the  intestine  as  thoroughly  as 
possible  without  producing  irritation  therein,  and  until  this  cleansing 
process  has  been  accomplished  the  ingestion  of  food — for  a  few  days — is 
to  be  limited  to  easily  absorbable  material  which  will  leave  but  little 
residue,  and,  if  possible,  to  a  fluid  diet :  Tea,  meat  broth,  gelatinous  soups. 
In  a  few  days  an  increase  of  food  may  be  permitted  without  any  danger 
of  a  relapse. 

In  conclusion,  I  must  issue  a  warning  against  the  artificial  arrest  of 
diarrheas  and  intestinal  catarrhs  due  to  the  excretion  of  toxic  substances 
from  the  blood  into  the  intestine.  Paramount  among  these  is  the  diarrhea 
in  nephritis,  the  arrest  of  which  with  opium  and  similar  remedies  may 
bring  about  severe  uremia. 


668        DIARRHEA,   CATARRH,   AND  INTESTINAL  TUBERCULOSIS 


CHRONIC  INTESTINAL   CATARRH 

Chronic  intestinal  catarrh,  like  the  acute  form,  may  appear  as  a  pri- 
mary and  substantive  affection.  Frequently,  however,  it  is  either  second- 
ary or  of  a  symptomatic  nature. 

Etiologfy. — The  causes  of  idiopathic  chronic  intestinal  catarrh  are,  as 
a  rule,  identical  with  those  which  produce  acute  catarrh  except  for  the 
difference  that  the  baneful  agents  mentioned  here  act  not  only  once  and 
intensely,  but  that  this  effect  is  produced  repeatedly  or  continuously.  It 
happens  by  no  means  rarely  that  the  chronic  form  develops  from  acute 
enteritis;  that,  therefore,  also  a  single  and  transitory  but  active  poison, 
an  indiscretion  in  diet,  severe  refrigeration,  or  an  infection,  may  be  the 
cause  of  chronic  intestinal  catarrh.  Above  all,  I  desire  to  refer  to  the 
clironic  catarrh  of  the  colon  which  persists  after  tropical  diarrhea  and 
tropical  enteritis.  To  mention  an  example  from  the  present  time,  our 
soldiers  who  returned  from  China  without  having  had  severe  forms  of 
dysentery  (although  quite  a  large  number  had  persistent  irritation  of  the 
colon  which  in  the  cases  observed  by  me  proved  to  be  chronic  colitis) 
showed  impairment  of  health  for  a  long  time  although  they  did  not 
become  chronic  invalids.  More  frequently  chronic  intestinal  catarrh  sets 
in,  without  an  acute  stage  of  onset,  as  the  consequence  of  oft-repeated 
and  continuous  injury  to  the  intestine,  by  improper  food  and  an  inju- 
dicious mode  of  life,  by  the  prolonged  use  of  powerful  purgatives,  and 
by  constitutional  anomalies. 

"  Morhorum  fere  omnium  causa  est  stomachi  infirmitas "  is  particu- 
larly true  of  the  different  forms  of  chronic  intestinal  catarrh.  Not  only 
does  weakness  of  the  stomach  impair  the  bowel,  but  also  that  factor 
which  has  damaged  the  stomach.  In  this  connection  the  poor  condition 
of  the  teeth,  their  insufficient  use  in  mastication,  the  incomplete  admix- 
ture of  the  food  with  saliva,  and  the  bolting  of  food  must  be  again 
referred  to.  We  must  also  consider  all  the  functional  disturbances  and 
organic  diseases  of  the  stomach  which  influence  the  chemical  preparation 
of  the  gastric  contents,  above  all,  gastric  dyspepsia,  achylia,  and  apepsia, 
which  run  their  course  with  deficiency  in  hydrochloric  acid  and  pepsin. 
To  these  must  be  added  chronic  catarrh  of  the  stomach,  hypermotility 
wliicli  causes  the  chyle  to  be  too  rapidly  propelled  from  the  stomach  into 
the  intestine,  and  gastric  atony,  in  which  condition  the  chyle  of  the 
stomach  undergoes  an  abnormally  acid  fermentation,  and  thus  enters  the 
l)owel.  Even  gastric  ulcer,  which,  by  HCl-hyperacidity  and  hyperpepsia, 
makes  gastric  digestion  so  rapid,  and  also  by  HCl-hyperacidity  reflexly 
stimulates  pancreatic  digestion,  may  induce  chronic  colitis  as  a  compli- 
cation if  the  chyle  (which  should  be  wholly  absorbed  and  thus  leave  but 
little  nutritive  material  in  the  intestine  for  the  bacteria  of  fermentation 
and  decomposition)  accumulates  in  the  colon,  and  if  constipation,  which 


INTESTINAL  CATARRH  669 

almost  invariably  accompanies  gastric  nicer,  then  irritates  the  mucous 
membrane.  Necessarily,  however,  none  of  the  previously  mentioned  gas- 
tric disturbances  need  secondarily  damage  the  intestine,  for,  to  a  certain 
extent,  and  frequently  for  a  long  time,  intestinal  digestion  may  compen- 
sate for  derangement  of  gastric  digestion. 

The  same  is  true  of  those  disturbances  originating  in  the  liver  and 
the  pancreas  which  I  have  already  mentioned. 

Pathology. — Pathologico-anatomical  changes  in  the  structure  of  the 
intestinal  wall,  and  to  a  less  extent  tuberculous,  dysenteric,  typhoid  and 
carcinomatous  ulcers,  the  cicatrices  (arising  from  the  former)  which  pro- 
duce stenotic  tumors,  and  peritoneal  adhesions  which  limit  peristalsis, 
abnormally  fix  the  individual  intestinal  coils,  or  produce  changes  in  their 
position,  and  thus  hinder  the  propulsion  of  feces ;  these  changes  are  almost 
invariably  associated  with  intestinal  catarrh,  which,  while  sometimes  lim- 
ited to  the  vicinity  of  the  primary  lesion,  occasionally  may  be  distributed 
over  extensive  areas  of  the  bowel.  In  fact,  any  condition  may  be  com- 
bined with  an  impediment  to  the  propulsion  of  feces,  whether  this  be 
due  to  organic  changes  in  the  intestinal  wall,  to  functional  disturbance 
of  intestinal  peristalsis  (habitual  constipation),  or  whether  it  is  caused 
mechanically  by  pressure  or  external  torsion  upon  the  bowel  (uterine  and 
ovarian  tumors,  hypertrophy  of  the  prostate,  peri-  and  parametritic,  peri- 
typhlitic,  pericholec5^stitic,  perigastric  or  pericolitic  adhesions,  indurations 
and  pseudo-membranes),  and  may  give  rise  to  chronic  intestinal  catarrh. 
We  must  mention  also  as  causes  of  chronic  intestinal  catarrh  the  circu- 
latory disturbances  which  produce  chronic  venous  hyperemia  of  the  intes- 
tinal mucous  membrane.  Among  the  more  common  of  these  conditions 
is  chronic  intestinal  catarrh  from  abdominal  plethora  which  is  the  con- 
sequence of  a  sedentary  mode  of  life.  Furthermore,  intestinal  catarrh  is 
common  as  the  consequence  of  stasis  of  the  portal  vein  circulation,  in 
hepatic  cirrhosis  and  constriction  of  the  portal  vein,  in  valvular  disease 
of  the  heart  and  chronic  myocarditis,  in  chronic  diseases  of  the  lungs  and 
pleurae,  and  in  chronic  simple  and  tuberculous  peritonitis. 

In  conclusion,  parasites  now  and  then  produce  chronic  irritation  and 
catarrh  of  the  intestine. 

The  pathological  changes  produced  by  chronic  intestinal  catarrh  are 
chiefly  manifested  in  the  mucous  membrane,  but  the  submucous  tissue  and 
the  muscularis  are  often  also  implicated,  much  more  frequently  revealing 
inflammatory  hyperplasia  than  a  degenerative  atrophy. 

The  mucous  membrane  is  hyperemic  and  shows  cellular  infiltration; 
consequently  it  is  swollen,  and  covered  with  mucus  or  muco-purulent 
masses.  In  some  areas  it  is  grayish  red,  livid,  rusty  brown,  or  it  may 
show  a  slaty  gray  pigmentation.  The  submucosa  is  thickened  and  infil- 
trated; Serous  transudation  is  evident.  The  connective  tissue  is  prolif- 
erated ;  the  gland  ducts  are  often  elongated,  and  occasionally  denote  cystic 


670        DIARRHEA,  CATARRH,   AND  INTESTINAL  TUBERCULOSIS 

degeneration  from  constriction.  The  muscularis  is  sometimes  hypertro- 
phied  and  thickened.  In  differentiating  these  conditions,  however,  the 
contraction  of  the  intestine  must  be  borne  in  mind,  for,  if  this  is  in- 
creased, it  readily  simulates  hypertrophy,  and  an  abnormal  distention  of 
the  lx)wel  may  be  easily  mistaken  for  atrophy  of  the  various  layers  of  the 
intestinal  wall.  At  the  ileo-cecal  valve  a  chronic  inflammatory  thickening 
of  all  these  layers,  especially  of  the  musculature,  may  bring  about  stenosis 
of  tlie  lumen,  which  resembles  pyloric  stenosis  due  to  chronic  inflamma- 
tion and  may  be  the  cause  of  invagination. 

The  question  of  intestinal  atrophy,  especially  atrophy  of  the  intestinal 
mucous  membrane,  has  been  much  discussed  of  late  since  Gerlach,  Heub- 
ner  and  others  designated  intestinal  atrophy  as  a  frequent  post  mortem 
phenomenon.  Whether  a  vital  pathologic  atrophy  of  the  mucous  mem- 
brane can  be  absolutely  denied  must  be  decided  by  renewed  investigations 
as  soon  as  possible  after  death. 

Fatty  degeneration  of  the  muscular  fibers,  more  conspicuous  in  the 
longitudinal  than  in  the  circular  fibers,  has  been  noted  now  and  then 
in  chronic  intestinal  catarrh,  but,  as  a  rule,  it  is  rare;  it  has  been  de- 
scribed by  Kussmaul,  Maier,  and  E.  Wagner.  There  are  but  few  isolated 
observations  of  sclerotic  and  fatty  degeneration  of  the  intestinal  nerves, 
the  ganglia  and  fibers  of  Meissner,  and  of  Auerbach's  plexuses. 

The  functional  disturbances  of  the  intestine  produced  by  chronic  in- 
testinal catarrh  are  prominent  in  the  clinical  picture;  associated  with 
these  are  disturbances  of  nutrition  and  blood  formation  as  well  as  other 
constitutional  symptoms. 

Symptoms. — While  in  acute  intestinal  catarrh  diarrhea  is  characteristic 
as  a  motor  irritative  factor,  in  chronic  intestinal  catarrh  this  is  rare,  and 
constipation  is  the  rule.  In  explanation  of  this  it  has  been  assumed  that, 
under  the  influence  of  pathologic  processes  in  the  intestinal  wall  in  chronic 
catarrh,  the  muscularis  of  the  intestine  suffers  functionally  by  the  pro- 
duction of  atony,  or  from  an  organic  damage  by  degenerative  atrophy. 
But  with  chronic  catarrhal  inflammation  frequently  no  change  can  be 
observed  in  the  musculature  of  the  intestine.  Therefore  neither  atony 
nor  atrophy  of  the  intestinal  muscularis  will  explain  the  constipation 
in  chronic  catarrh.  Nothnagel  has  assumed  that  the  cause  is  sluggishness 
of  the  intestines,  a  lessening  of  the  automatic  activity  of  the  nervous 
apparatus  of  the  intestinal  wall,  due  to  the  pathologic  processes  of  chronic 
catarrh,  especially  to  chronic  venous  hyperemia.  But  this  decrease  in 
automatic  activity  does  not  simultaneously  decrease  the  irritability  of  the 
nervous  apparatus  of  the  intestine  to  external  influences.  This  is  evident 
from  the  periodical  and  spontaneous  occurrence  of  brief  or  more  prolonged 
diarrhea,  produced  by  errors  in  diet,  drugs  or  fecal  accumulation.  Be- 
sides, in  chronic  intestinal  catarrh  due  to  local  irritation,  not  infrequently 
large  or  small  portions  of  the  intestine  may  assume  a  state  of  spastic 


INTESTINAL  CATARRH  671 

contracture  in  which  tonic  spasm  of  the  muscularis  is  indicated  by  severe 
pain  (colica  spastica).  This  spasmodic  contracture  may  cause  the  reten- 
tion of  fecal  masses  in  the  greater  portion  of  the  colon  (spastic  consti- 
pation). 

When  constipation  is  absent  in  chronic  catarrh  of  the  intestine,  abnor- 
malities of  the  bowel  movements  may  be  observed,  and  this  is  true  even 
when  the  bowels  are  apparently  regular.  These  abnormalities  are  shown 
by  the  composition  of  the  feces,  which  are  of  pappy  or  semi-fluid  con- 
sistence M^th  an  admixture  of  mucus,  by  the  evacuation  of  undigested 
particles  of  food,  and  by  an  abnormally  fetid  odor  in  consequence  of 
decomposition  of  the  pathologic  secretions  of  the  bowel. 

In  other  cases  of  chronic  intestinal  catarrh  constipation  and  diarrhea 
alternate  in  a  certain  regularity  and  periodicity.  Without  apparent  cause, 
after  one  or  several  days  of  constipation,  diarrhea  occurs  spontaneously, 
continues  from  one  to  several  days,  then  ceases,  and  constipation  reap- 
pears. Nothnagel  has  compared  this  alternation  of  constipation  with 
diarrhea  to  the  variations  of  the  Cheyne- Stokes  respiration,  and  assumes 
that,  in  the  cases  in  question,  constipation  was  originally  present  and 
persisted  until  by  stasis  of  the  feces  in  the  colon  a  condition  of  irritation 
was  produced  which  resulted  in  diarrhea.  The  irritation  ceased  after  the 
complete  evacuation  of  the  intestine,  and  constipation  reappeared. 

With  these  exceptions,  intercurrent  diarrheas  are  usually  due  to  some 
deleterious  agent  which,  by  irritating  the  intestinal  wall,  increases  the 
intensity  of  the  catarrh;  often  nervous  influences  are  the  cause.  Pro- 
longed diarrhea,  on  the  other  hand,  indicates  a  complication  of  the  intes- 
tinal catarrh  with  ulcerative  processes. 

N^ow  and  then  I  have  observed  in  chronic  intestinal  catarrh  a  peculiar 
abnormality  in  the  fecal  evacuations,  which  resembles  the  condition  in 
ischuria  paradoxa.  A  movement  of  the  bowels  occurred  daily,  even  regu- 
larly, the  feces  being  soft,  and  the  patients  never  complained  of  consti- 
pation. 

Nevertheless,  fecal  masses  were  retained  in  the  intestine  and  gradually 
increased  so  that  they  formed  large  fecal  tumors.  Years  ago,  when  I  was 
an  assistant  in  the  Pathological  Institute,  I  held  an  autopsy  upon  a  case 
of  this  kind  and  found  in  the  colon  a  fecal  mass  weighing  4  kilograms. 
In  the  sigmoid  flexure,  where  the  largest  fecal  tumor  was  situated,  there 
was  an  extensive  pressure  necrosis  of  the  mucous  membrane,  also  pressure 
ulcers  one  of  which  had  perforated.  Up  to  the  time  of  death  the  patient 
in  question  had  daily  evacuated  thin  stools  which  had  been  regarded  as 
sufficient.  Among  other  cases  of  this  kind,  my  most  recent  one  is  inter- 
esting. It  occurred  in  a  medical  student  who  had  severe  colicky  pains  and 
a  most  offensive  diarrhea,  the  thin  fecal  discharges  being  sometimes  in- 
voluntary and  soiling  his  bed  and  body  linen  most  disagreeably;  he  was 
treated  in  the  Clinic,  and  had  also  been  treated  elsewhere  unsuccessfully, 


672        DIARRHEA,  CATARRH,   AND  INTESTINAL  TUBERCULOSIS 

with  opium.  When  I  examined  this  unfortunate  man,  I  found  a  fecal 
tumor  of  about  the  size  of  a  child's  head  bulging  from  the  rectum,  the 
sphincter  of  which  was  open.  Manually  I  removed  as  much  of  this  as 
was  possible  without  anesthesia.  Five  days  later  this  procedure — although 
diarrhea  was  still  present — had  to  be  repeated  because  on  the  removal  of 
the  fecal  tumor  another  formed.  After  this  the  pains  and  the  accom- 
panying disturbances  of  the  bladder  ceased,  and  the  bowels  were  regulated 
by  injections  of  oil.  Field  has  described  such  a  condition  under  the  name 
of  cumulative  constipation,  and  Courtade  as  latent  constipation.  From 
its  analogy  to  ischuria  paradoxa,  I  believe  that  this  might  well  be  desig- 
nated as  constipatio  paradoxa,  that  is,  a  retention  of  feces  notwithstanding 
existing  diarrhea.  A  very  intelligent  patient  who  suffered  from  this 
paradoxical  retention  of  feces  quite  aptly  designated  her  disease  as  "  con- 
stipating diarrhea."  The  condition  reminds  us  of  some  cases  of  chronic 
intestinal  catarrh  and  constipation  in  which  liquid  bowel  discharges  follow 
tlie  ingestion  of  fruit,  the  use  of  some  laxatives  and  mineral  waters,  and 
also  occur  in  a  mineral  spring  treatment,  but  do  not  relieve  the  patient 
by  a  salisfactory  emptying  of  the  bowel. 

The  paifi  in  chronic  intestinal  catarrh  is  usually  insignificant;  never- 
theless there  are  irritable  forms,  particularly  of  catarrh  of  the  colon — 
colitis  muco-membranacea — in  which  the  patients  suffer  greatly  from  pain 
and  persistent  colic,  similarly  as  in  nervous  mucous  colic.  In  catarrh 
of  the  colon  the  pains  radiate  to  the  small  of  the  back,  to  the  hips  and 
to  the  thighs,  and  very  often  to  the  entire  back,  and  are  lessened  or 
entirely  relieved  by  the  evacuation  of  the  accumulated  fecal  masses.  The 
latter  is  true  not  only  of  some  cases  of  sciatica  but  also  of  other  neuralgias. 

In  other  instances  the  patients  are  greatly  annoyed  by  periodic  or 
long-continued  disagreeable  sensations  in  the  abdomen,  and  these  some- 
times engender  a  peculiar,  melancholic  state  of  depression.  These  sensa- 
tions are  chiefly  localized  in  the  hypochondria  or  the  region  of  the 
flexures  of  the  colon,  but  are  also  noted  in  other  areas  of  the  abdomen 
and  the  pelvis  (the  designation  hypochondriasis,  now  employed  only  for 
certain  depressing  psychical  conditions,  was  originall)'  applied  to  some 
localized  affections  in  which  the  colon  was  presumed  to  be  especially  im- 
plicated). These  disagreeable  sensations  appear  to  be  due  to  movements 
in  the  colon  which  are  manifested  in  the  way  described;  that  is,  they 
are  increased  after  the  ingestion  of  food,  before  and  after  a  passage  from 
the  bowels,  while  frequently  the  patient  is  at  ease  so  long  as  the  intestine 
is  at  rest,  i.  e.,  while  there  is  constipation.  Besides  the  formation  of  other 
chemically  irritant  products  of  fermentation  and  decomposition,  abnormal 
gas  production  is  probably  the  cause  of  increased  intestinal  unrest,  and  rum- 
bling, gurgling,  or  splashing  sounds  are  heard  not  only  by  the  patient 
but  by  those  about  him.  The  patients  feel  as  though  the  fluid  contents 
of  the  intestine  were  forced  from  one  part  of  the  abdomen  to  another, 


INTESTINAL  CATARRH  673 

or  as  if  the  intestines  were  filled  with  gas  which  could  find  no  vent. 
Patients  with  disease  of  the  intestine  who  have  become  hypochondriacs 
often  torment  themselves  with  strange  fancies  as  to  the  cause  of  these 
sensations  and  sounds;  these  imaginations  correspond  with  the  remedies  to 
which  they  resort  to  ameliorate  the  condition,  especially  the  dietetic 
penance. 

In  undernourished  persons  with  a  thin,  flaccid  abdominal  wall,  peristal- 
tic movements  of  the  intestine  are  often  visible  and  palpable.  In  these 
cases  inflation  of  the  abdomen  from  gas  is  rarely  absent ;  often  it  is  gen- 
eral, at  other  times  limited  to  individual  portions  of  the  intestine.  The 
passage  of  flatus  usually  brings  relief,  but  the  opposite  condition  is  most 
impleasant  to  the  patient.  The  accumulation  of  gases  in  the  bowel  causes 
much  discomfort,  disturbance  of  sleep,  a  feeling  of  unrest  and  anxiety, 
a  sense  of  constriction,  arrhythmia  and  intermittent  pulse,  cardiac  palpa- 
tion which  is  often  combined  with  precordial  distress  and  difficulty  in 
respiration.  Not  infrequently  intestinal  gas  becomes  incarcerated  in 
dilated  coils  of  intestine,  and  produces  intense  colicky  pains  (wind  colic 
from  overdistention  of  the  intestinal  wall). 

In  other  cases  of  chronic  intestinal  catarrh  the  abdomen  is  retracted, 
the  colon  in  certain  areas  or  in  its  greatest  extent  is  contracted,  may  then 
be  felt  as  a  baud,  and  is  painful  to  the  touch.  Upon  palpation  the  sigmoid 
flexure  may  usually  be  felt  as  a  cylindrical  band  which  rolls  under  the 
palpating  finger.  Sometimes  only  one  portion  of  the  colon  is  contracted 
while  other  parts  are  flaccid  or  even  meteorically  distended. 

The  nutrition  always  suffers  in  chronic  colitis,  but  especially  when  the 
small  intestines  are  markedly  implicated  and  less  so  when  the  disease  is 
chiefly  confined  to  the  colon.  Catarrh  widely  distributed  throughout  the 
small  and  large  intestines  causes  extreme  emaciation  and  debility.  The 
best  known  forms  of  this  are  atrophia  infantum,  pedatrophia,  or  tabes 
mesenterica,  the  sequel  of  chronic  intestinal  catarrh  in  children  in  which, 
in  contrast  with  the  enormously  distended  belly,  the  patients  are  emaciated 
and  withered  to  a  skeleton,  and  with  their  sad,  deeply  sunken  eyes,  small, 
senile  faces,  and  dry,  discolored,  withered  skin  they  present  a  pitiable 
picture  of  suffering  and  human  helplessness. 

In  adults  this  general  disturbance  of  nutrition  is  rarely  so  marked  as  in 
children;  but  I  have  repeatedly  known  middle-aged  persons  to  succumb 
to  intestinal  catarrh  and  chronic  diarrhea  which  were  the  results  of  trop- 
ical enteritis.  The  dirty  gray  discoloration  of  the  skin  in  some  persons 
with  chronic  constipation  which  accompanies  intestinal  ca1,arrh  is  typical. 
This  "constipation  tint''  may  be  readily  differentiated  from  that  of 
anemia,  cachexia,  jaundice,  and  also  from  Addison's  disease.  To  what 
alteration^  in  the  composition  of  the  blood  it  is  due  cannot  always  be  deter- 
mined with  the  ordinary  methods  of  blood  examination.  Dyscrasic  intoxi- 
cation may  be  presumed,  but  cannot  always  be  certainly  proven. 


674        DIARRHEA,  CATARRH,   AND  INTESTINAL  TUBERCULOSIS 

Anemic  conditions  are  found  in  chronic  intestinal  catarrh,  especially 
when  the  property  of  absorption  in  the  small  intestine  is  diminished. 
While,  however,  in  this  condition  of  hyponutrition  we  are  dealing  chiefly 
with  oligemia,  in  colitis  there  is  a  destruction  of  red  blood-corpuscles,  prob- 
ably due  to  toxic  products  of  decomposition,  particularly  when  the 
condition  is  accompanied  by  constipation.  Inspissation  of  the  blood 
with  an  apparent  increase  of  the  erythrocytes  to  6,000,000  or  more  and  a 
corresponding  increase  of  hemoglobin  I  have  observed  at  various  times  in 
prolonged  diarrhea  due  to  chronic  gastrointestinal  catarrh;  tetany  as  a 
complication  was  noted  in  only  one  case.  Severe  progressive  anemia  which 
was  formerly  referred  to  atrophy  of  the  intestinal  mucous  membrane  is  com- 
paratively rare  in  chronic  intestinal  catarrh.  In  such  cases  Eisenlohr 
described  degeneration  of  a  dyscrasic  nature  in  the  posterior  and  lateral 
columns  of  the  spinal  cord  which  was  very  similar  to  that  I  found  in 
Addison's  disease. 

The  Urine. — In  chronic  intestinal  catarrh  the  condition  of  the  urine 
depends  mainly  upon  the  relation  of  intestinal  absorption  to  intestinal  ex- 
cretion. In  severe  diarrhea  the  daily  amount  of  urine  voided  may  fall  to 
that  of  transitory  anuria;  constipation  does  not  decidedly  influence  the 
amount.  Albuminuria  occurs  in  disturbances  of  intestinal  digestion,  and 
is  not  infrequent  in  abnormally  increased  decomposition  in  the  colon;  in 
fact  this  latter  condition  plays  a  role  which  is  not  to  be  underestimated  in 
considering  the  etiology  of  nephritis  as  well  as  that  of  many  diseases  of  the 
liver  and  the  blood. 

Disturbance  of  gastric  digestion  is  rarely  absent  in  chronic  intestinal 
catarrh,  often  being  the  cause  of  the  latter,  and  frequently  its  consequence. 
The  gastric  dyspepsia  resulting  from-  intestinal  catarrh  appears  to  cause 
greater  subjective  disturbance  than  a  primary  gastric  affection.  In  many 
cases  it  is  difficult  to  say  whether  the  digestive  symptoms,  such  as  loss  of 
appetite,  a  disagreeable  taste,  a  coated  tongue,  pressure  and  fulness  in  the 
abdomen,  discomfort  after  eating,  eructations,  flatulence  and  nausea,  are  to 
Ije  attributed  to  the  stomach  or  to  the  intestine.  I  believe  a  coated  tongue 
is  more  frequently  due  to  intestinal  than  to  gastric  disturbance,  and  most 
often  results  from  constipation. 

Various  nervous  symptoms  are  to  be  regarded  partly  as  reflex  phenom- 
ena from  the  intestine,  and  partly  as  due  to  the  absorption  of  toxic  sub- 
stances formed  by  abnormal  processes  of  decomposition  in  the  intestine. 
To  this  category  belong  the  oft  recurring  headache,  the  migraine  and 
other  forms  of  neuralgia,  vertigo,  psychical  depression,  disinclination  for 
mental  or  physical  exertion,  a  feeling  of  weakness  and  lassitude,  drowsiness 
or  insomnia,  arrhythmia  and  intermittent  pulse,  tachycardia,  as  well  as 
tetany  and  the  otlier  spasmodic  conditions  which  are  the  consequence  of 
constij)ation  and  which  are  especially  observed  in  small  children  and  feeble, 
easily  irritated  persons. 


INTESTINAL  CATARRH  675 

The  appearance  of  fever  in  chronic  intestinal  catarrh  indicates  a  com- 
plication with  ulcerative  processes  and  the  implication  of  the  peritoneum  in 
the  inflammation. 

Diagnosis.— The  diagnosis  of  chronic  intestinal  catarrh  can  be  based 
only  upon  the  results  of  the  examination  of  the  feces,  for  the  history,  the 
subjective  symptoms,  and  the  general  phenomena,  even  the  clinical  inves- 
tigation of  the  abdominal  organs,  are  not  conclusive;  the  demonstration  of 
mucus  in  the  feces  is  alone  decisive. 

The  fundamental  laws  for  the  examination  of  the  feces  and  their 
application  have  been  described  in  the  preceding  sections  of  this  article. 
They  are  generally  applicable,  and  therefore  may  be  employed  in  chronic 
catarrh  of  the  intestine,  at  least  in  that  form  running  its  course  with 
diarrhea.  To  complete  my  description,  however,  /  must  enter  somewhat 
more  minutely  into  the  condition  of  the  feces  in  chronic  intestinal  catarrh 
which  runs  its  course  with  constipation. 

In  this  affection  the  bowel  movements  are  often  found  to  be  immod- 
erately large.  From  this  fact  we  may  differentiate  copropoesis  or  poly- 
copria,  provided  these  large  masses  are  regularly  voided  for  a  long  time; 
where  this  is  not  the  case,  but  small  portions  and  then  occasionally  very 
large  ones  are  passed,  the  evacuations  are  insufficient  and  there  is  conse- 
quently fecal  accumulation. 

When  the  fecal  masses  voided  are  invariably  large — large  in  compari- 
son with  the  ingested  food — ^there  is  poor  assimilation,  insufficient  absorp- 
tion in  the  small  intestine,  and  profuse  excretion  of  digestive  juices  and 
pathologic  products  from  the  intestinal  wall.  Accurate  investigation  of  the 
feces  for  undigested  remains  of  food  permits  the  recognition  of  their  nature 
and  the  seat  of  the  disturbance,  and  simultaneously  indicates,  as  has  already 
been  stated,  the  advisability  of  testing  the  function  of  the  stomach,  and 
also,  perhaps,  the  glycogenetic  function  of  the  liver  (alimentary  glyco- 
suria). A  decision  as  to  the  proper  quantity  of  the  feces,  aside  from  their 
form  and  composition,  requires  much  practice  (repeated  weighing  of  the 
total  solids  of  the  feces,  which  is  alone  decisive,  is  impracticable)  and  pre- 
supposes an  exact  knowledge  of  the  previously  ingested  food,  its  quantity, 
composition  and  preparation.  We  have  here,  it  is  true,  a  constantly  vary- 
ing but,  nevertheless,  in  its  composition  and  nutritive  value,  an  average  diet 
(already  referred  to  in  my  "Text-Book  of  the  Diseases  of  the  Digestive 
Organs"),  a  similar  form  of  nutrition  for  all  patients  under  observation 
until,  from  the  requirements  of  the  individual  case,  deviations  from,  addi- 
tions to,  restrictions  in,  or  substitutes  for  this  normal  diet  become  necessary. 
As  the  feces  of  all  patients  are  examined  separately  from  day  to  day,  and 
are  preserved  for  subsequent  and  necessary  tests,  it  is  easy  to  determine 
patliologic  change  in  a  bowel  movement,  any  alteration  in  the  form,  the 
consistence,  or  quantity,  also  any  abnormal  admixture;  even  individual 
peculiarities  may  be  at  once  recognized.     I  believe  it  to  be  important  to 


676        DIAHRHEA,  CATARRH,  AND  INTESTINAL  TUBERCULOSIS 

resort  to  coproscopy  in  every  case,  not  only  once  or  occasionally,  but  regu- 
larly and  until  in  a  given  case  we  have  arrived  at  a  definite  conclusion  in 
regard  to  the  digestive  processes,  not  only  the  intestinal  but  also  the  gas- 
tric, not  only  the  digestibility  of  the  chief  articles  of  food  but  also  of  a 
great  number  of  foods.  This  method  of  clinical  observation,  of  the  study 
of  the  ingestion  of  food,  and  of  the  examination  of  the  excreta,  which,  in 
the  main,  I  learned  from  my  revered  master,  Kussmaul,  and  which  I  have 
elaborated  systematically,  has  been  for  years  of  such  service  that  the  use 
of  Scli-midt's  test  diet  to  test  the  function  of  the  intestine  has  become 
unnecessary.  My  method  has  the  additional  advantage  that  it  can  be 
adhered  to  for  a  long  time,  i.  e.,  as  long  as  necessary,  while  the  other 
method  is  practicable  for  only  a  few  days.  I  do  not,  however,  mean  to 
disparage  the  importance  and  value  of  Schmidt's  teachings,  and  advise  the 
employment  of  his  test  diet  whenever  the  study  of  the  nutrition  and  the 
investigation  of  the  digestive  processes  cannot  be  carried  out  in  the  manner 
I  have  indicated.  I  also  advise  the  physician  not  to  be  content  with  a 
single  examination,  or  a  single  analysis,  of  the  feces  in  order  to  make  a 
diagnosis.  The  demonstration  of  connective  tissue,  meat,  fat,  or  mucus  in 
the  feces  aids  us  materially  in  differentiation,  just  as  does  the  demonstra- 
tion of  albumin  or  sugar  in  the  urine,  or  of  bacilli  in  the  sputum.  But, 
as  a  matter  of  fact,  such  demonstration  points  out  only  where  and  how 
subsequent  clinical  researches  are  to  be  begun  and  further  developed. 

By  a  fecal  examination  we  are  enabled  to  recognize,  in  the  given  case, 
whether  the  chronic  catarrh  is  localized  in  the  small  intestine  or  in  the 
colon.  IMost  frequently  the  colon  alone  is  attacked,  or  the  colon  simul- 
taneously with  the  lowest  portion  of  the  small  intestine. 

From  the  appearance  of  the  intestinal  discharges,  as  well  as  from  the 
subjective  symptoms,  various  types  of  chronic  (colon)  intestinal  catarrh 
may  be  differentiated :  Flaccid,  atonic  or  asthenic  forms,  and  nervous, 
irrital)le  forms.  The  first  usually  run  their  course  with  constipation; 
in  this  atonic  constipation  the  bowel  movement  is  dry  and  compact,  and 
consists  of  adherent  clumps  or  cylinders  of  immoderately  large  caliber,  also 
of  isolated,  irregularly  formed  particles  of  varying  size,  and  of  fecal  balls 
from  the  size  of  a  nut  to  that  of  an  apple.  These  fecal  clumps  are  not 
always  formed  in  the  rectum  (in  the  ampulla  of  which  they  may  attain  their 
greatest  bulk)  or  the  flexures,  but  often  much  higher,  in  the  colon  or  even 
in  the  cecum.  In  chronic  catarrh  of  the  colon,  running  its  course  with 
atonic  constipation,  the  abdomen  is,  as  a  rule,  uniformly  distended.  On 
tlie  other  hand,  when  the  entire  colon  is  atonic  and  filled  with  gases  and 
feces  it  is  asymmetric,  and  only  partially  so  when  but  a  portion  of  the 
colon  is  diseased.  If  the  abdominal  walls  are  thin,  the  accumulated  fecal 
masses  may  be  felt  in  the  flexures  or  the  cecum,  and  also  in  other  por- 
tions of  the  large  intestine,  as  doughy  tumors,  in  rare  cases  as  hard, 
gIol)iil;u-  or  cylindrical  tumors,  and  in  the  colon  they  may  frequently  be 


INTESTINAL  CATARRH  677 

displaced  toward  the  anus.  These  atonic  forms  of  constipation  and  catarrh 
of  the  colon  are  found  at  all  ages,  not  rarely  even  in  children.  Occasion- 
ally the  impacted  fecal  masses  may  cause  very  painful  attacks  of  colic. 

The  irritable  forms  of  chronic  catarrh  of  the  colon  are  characterized 
by  a  tendency  to  diarrhea  and  colic.  But  many  cases  of  irritable  catarrh 
of  the  large  intestine  run  their  course  with  constipation  of  that  type  I 
have  described  as  spastic  constipation.  In  these  cases,  an  irritation  affect- 
ing the  motor  function  of  the  muscularis  of  the  colon,  a  spastic  contracture 
which  implicates  large  portions  of  this  organ,  causes  the  retention  of  the 
compact  fecal  masses,  and  constricts  and  compresses  them;  or  the  subse- 
quent peristalsis  in  high  portions  forces  the  compact  mass  through  the 
spastically  contracted  portions  of  the  intestine.  In  this  spastic  constipation 
— which  may  also  occur  without  colitis — the  composition  of  the  feces  is 
extremely  characteristic.  The  masses  are  cylindrical  and  of  small  caliber, 
often  only  of  the  thickness  of  a  lead-pencil  or  of  the  little  finger;  some- 
times they  are  very  long,  and  in  the  chamber  they  assume  a  spiral  shape 
like  the  shell  of  a  snail.  Sometimes,  however,  they  are  so  short  that  their 
total  amount  appears  to  be  wholly  insufficient.  Balls  of  small  caliber, 
masses  resembling  the  feces  of  sheep,  are  sometimes  formed  in  the  haustra 
but  are  not  always  characteristic  of  spastic  constipation,  for  they  may  be 
discharged  simultaneously  with  fecal  cylinders  of  large  caliber,  or  may  be 
superficially  embedded  in  these. 

In  some  cases  of  colitis  the  types  of  constipation  which  have  been 
described  appear  side  by  side,  and  atony  and  spasm  in  different  areas  of 
the  colon  may  alternate. 

Mucous  Colic. — The  severest  form  of  catarrh  of  the  colon,  and  at  the 
same  time  the  most  irritable,  I  shall  designate  as  colitis  muco-memhranacea. 
The  views  of  physicians  in  regard  to  this  common  and  stubborn  disease 
have  for  a  long  time  been  far  asunder,  as  is  best  proven  by  Whitehead's 
report:  Of  120  authors  who  have  written  concerning  it,  less  than  6  have 
given  it  the  same  name.  Some  lay  the  greatest  stress  upon  the  intestinal 
symptoms,  others  upon  the  nervous  phenomena.  Cruveilhier,  Trousseau, 
Habershon,  Ijeube  and  others  emphasized  its  association  with  other  inflam- 
matory affections  of  the  colon,  especially  with  chronic  catarrh;  v.  Leyden, 
Guttmann  and  others  assume  that  the  condition  is  due  to  a  specific  inflam- 
matory process  similar  to  that  which  is  generated  in  croupous  chronic  bron- 
chitis (Litten)  and  in  dysmenorrhea  membranacea  (Wernich).  In  con- 
trast with  this,  many  other  authors  believe  the  affection  to  be  a  neurosis 
of  the  bowel,  probably  a  secretory  neurosis  accompanying  other  general 
neuroses.  Nothnagel,  who  was  later  supported  oy  Ewald  and  many  other 
adherents,  especially  emphasizes  that  the  affection  chiefly  attacks  nervous 
and  hysterical  women  and  hypochondriacal  men,  these  presenting  the  clin- 
ical picture  of  colitis  muco-membranacea.  In  accordance  with  this  concep- 
tion, Nothnagel  proposed  that  we  discard  the  names  colitis  and  enteritis 
44 


678        DIARRHEA,  CATARRH,  AND   INTESTINAL  TUBERCULOSIS 

for  this  affection,  and  substitute  the  designation  colica  mucosa^  mucous 
colic}  In  attempting  to  relieve  or  cure  colitis  membranacea,  while  cor- 
recting the  general  nutritive  disturbances  and  regulating  the  intestinal 
functions,  I  have  so  frequently  seen  the  accompanying  nervous  symptoms 
of  this  disease  also  improve  or  entirely  disappear  as  to  be  convinced  that 
these  nervous  symptoms  are  in  many  instances  merely  secondary  and 
symptomatic,  and  in  the  overwhelming  majority  of  cases  the  actual  clin- 
ical picture  of  colitis  membranacea  is  caused  by  a  severe  inflammatory 
affection  of  the  colon,  a  malady  which  originates  in  the  colon  itself,  or  in 
its  immediate  vicinity  and  in  some  manner,  by  way  of  the  peritoneum, 
attacks  the  colon.  Nevertheless  cases  remain  in  which  only  a  colica  mucosa, 
therefore  a  sensory  and  secretory  neurosis  of  the  intestine,  is  present; 
however,  these  cases  in  my  experience  do  not  form  the  rule. 

Colitis  muco-membranacea  may  occur  at  any  age;  it  is  most  frequent 
in  middle  life,  rarer  in  childhood  and  in  the  aged.  Women  are  most  sub- 
ject to  the  disease,  particularly  such  as  suffer  from  enteroptosis,  dysmen- 
orrhea or  other  sexual  ailments;  sometimes  these  develop  after  abdominal 
operation,  perhaps  in  consequence  of  adhesions. 

In  the  periods  between  the  attacks  most  patients  present  the  symptoms 
of  simple  catarrhal  colitis  with  constipation.  Periodically  these  symptoms 
are  intensified  by  increasing  constipation,  and  culminate  in  a  typical  attack 
of  colic,  in  colitis  muco-membranacea,  at  the  acme  of  which  a  passage  of 
mucus  occurs;  this  must  be  regarded  as  critical  inasmuch  as  subsequently, 
and  particularly  after  a  profuse  evacuation  of  feces,  there  is  rapid  and 
conspicuous  improvement,  and  even  relative  euphoria  for  some  time. 

The  colic  begins  with  a  feeling  of  constriction,  of  burning  or  rawness 
in  the  epigastrium,  the  left  hypochondrium,  or  the  left  lumbar  region; 
this  gradually  increases  to  severe  spasmodic  or  neuralgic  pain  of  varying 
intensity  which  continues  for  hours  or  even  days,  being  sometimes  accom- 
panied by  reflex  phenomena  of  diverse  character  (spastic  constipation). 
In  some  cases  vomiting  occurs  during  this  time;  also,  although  rarely, 
sliglit  rises  in  temperature  and  albuminuria;  often  we  note  palpitation  of 
the  heart,  pulsation  of  the  abdominal  aorta,  and  a  rapid,  tense  pulse. 
Finally,  there  is  an  evacuation  of  the  bowels  in  which  the  quantity  and 
composition  of  the  admixed  mucus  is  conspicuous.  Often  mucus  alone 
is  discharged. 

The  mucus  discharged  reveals  nothing  especially  characteristic  since 
in  simple  catarrh  of  the  colon  also  mucus  may  be  passed  in  the  form  of 
shreds,  tubes,  globular  or  grape-like  masses.  But  in  colitis  muco-mem- 
branacea the  composition  of  the  mucus  is  significant;  it  is  hard  and 
tough,  much  coarser  than  that  usually  discharged  in  intestinal  catarrh, 
is  membranous,  and  not  dissimilar  to  croupy  membranes  although  it  con- 

1  See  the  article  by  Hoppe-Seyler  in  this  volume. 


INTESTINAL  CATARRH  679 

tains  no  fibrin.  There  is  unquestionably  no  desquamation  of  the  intes- 
tinal mucous  membrane,  as  was  formerly  assumed  by  some  authors.  On 
the  contrary,  a  process  of  coagulation  causes  the  peculiar  change  in  the 
mucus.  Intestinal  epithelia  and  round  cells  in  great  numbers  adhere  to 
these  mucus  shreds.  Only  when  these  are  absent,  and  when  in  the  inter- 
vals free  from  attack  no  signs  of  intestinal  catarrh  are  apparent,  when, 
therefore,  no  mucus  is  discharged,  can  a  purely  nervous  enteropathy,  in  the 
sense  of  a  secretory  neurosis  or  an  enteralgia,  be  considered. 

We  should  never  be  content  with  the  proof  of  a  catarrh  and  the  pres- 
ence of  accompanying  nervous  symptoms  or  sequels  of  a  colitis,  for,  in  most 
cases,  especially  the  severe  ones,  the  diagnosis  is  only  confirmed  when, 
by  a  minute  study  of  the  conditions  and  by  a  clinical  examination,  per- 
haps under  anesthesia,  the  cause  and  the  origin  of  the  secondary  colitis 
have  been  determined. 

There  are  rare  cases  of  colitis  muco-membranacea  in  which  the  malady 
terminates  with  a  single  attack  (Nothnagel)  ;  usually,  however,  the  affec- 
tion is  chronic  and  very  tenacious.  Many  authors  believe  that  colitis 
muco-membranacea  is  extremely  difficult  to  cure  or  even  incurable 
(A.  Clark).  In  my  experience  the  prognosis  is  no  worse  than  that  of 
other  chronic  intestinal  catarrhs,  especially  if  treated  in  an  institution 
where"  by  persistent  and  suitable  curative  methods  excellent  results  may 
be  attained.  It  is  true  there  are  cases  of  severe  secondary  chronic  colitis 
which  can  be  relieved  only  by  internal  remedies,  and  are  curable  only  by 
gynecological  or  surgical  treatment. 

Treatment. — The  treatment  of  chronic  intestinal  catarrh  is  designed  to 
regulate  the  nutrition  and  the  action  of  the  bowels  so  that  any  irritation 
which  may  produce  or  increase  inflammation  in  tjie  intestinal  wall  is 
prevented,  and  an  opportunity  is  given  the  bowel  gradually  to  recover 
its  tone. 

In  regard  to  diet  it  is  very  difficult  to  establish  general  rules,  as  the 
peculiarities  of  each  individual  case  must  be  borne  in  mind.  The  food 
products  which  are  easily  digested,  have  a  high  nutritive  value,  and  leave 
but  little  residue,  are  very  numerous.  We  must  discriminate  from  among 
these,  and  decide  which  are  best  borne  by  the  diseased  intestine,  which,  at 
the  same  time,  will  sufficiently  maintain  the  normal  strength,  or  so  improve 
a  reduced  or  weakened  organism  that  it  may  again  become  strong.  In 
many  cases,  especially  such  as  occur  in  the  debilitated,  which  run  their 
course  with  marked  irritability  of  the  intestines,  it  is  advisable  to  begin 
the  treatment  with  a  few  days  of  rest  in  bed  and  liquid  diet.  As  soon 
as  possible,  however,  and  while  avoiding  anything  that  will  demand  too 
great  exertion  of  the  digestive  organs,  I  give  the  previously  mentioned 
normal  diet— a  mixed  diet  in  which  special  preference  is  given  to  foods 
cooked  with  flour — since  by  the  amount  and  composition  of  the  feces  these 
permit  us  most  easily  to  recognize  deviations  from  the  normal.     If,  after 


680        DIARRHEA,  CATARRH,  AND  INTESTINAL  TUBERCULOSIS 

investigation  by  a  functional  test  of  the  stomach  and  the  examination  of 
ihe  feces,  disturbances  in  digestion  become  apparent,  these  are  combated 
by  the  administration  of  hydrochloric  acid,  pepsin,  pancreatin  or  pankreon, 
and  papain,  and,  if  these  are  unsuccessful  or  insufficient,  changes  in  the 
diet  must  be  instituted  to  prevent  the  undigested  and  unabsorbed  constitu- 
ents of  the  food  from  being  propelled  into  the  intestine,  where  they  may 
produce  irritation  or  processes  of  fermentation  and  decomposition,  or  main- 
tain these.  Abnormal  decomposition  necessitates  a  limitation  of  albu- 
minous diet,  particularly  of  meat;  abnormal  fermentation,  a  limitation  of 
carboliydrates  and  foods  containing  cellulose,  and  the  corresponding  substi- 
tution for  tliese  of  other  foods. 

The  irritative  forms  of  chronic  colitis — such  as  run  their  course  with 
diarrliea  or  spastic  constipation  and  colic — require  a  diet  which  lessens 
irritation.  In  the  torpid,  atonic  forms  of  intestinal  catarrh,  foods  which 
iiieehanically  or  chemically  stimulate  peristalsis  are  to  be  employed,  pro- 
vided that  by  their  use  we  do  not  over-irritate  the  intestinal  mucous  mem- 
brane. 

As  the  type  of  a  diet  which  will  lessen  irritation,  the  dietary  employed 
in  ulcer,  in  gastric  ulcer,  may  be  mentioned.  But  it  must  be  remembered 
that  an  exchisive  milk  diet  is  less  well  borne  in  intestinal  disease  than  in 
gastric  disease  (some  forms  of  tropical  diarrhea,  however,  form  an  excep- 
tion to  this  rule,  and  are  occasionally  cured  by  a  milk  diet).  Therefore, 
when  milk  is  not  well  borne  we  modify  the  diet,  and  give  milk  diluted 
with  oatmeal  gruel  or  barley  water,  cooked  with  fine  flour  or  with  one 
of  the  numerous  infant  foods,  racahout,  hygiama,  oatmeal,  cacao,  etc.,  or 
with  the  many  mixtures  of  flour  found  in  commerce,  these  to  be  given  in 
a  fluid  or  pappy  form,  and  then,  step  by  step,  we  pass  to  a  more  abundant 
diet  suited  to  the  individual  case;  for  a  time,  however,  mechanical  prepara- 
tion of  the  food  must  be  insisted  upon  (disintegration  with  a  meat 
chopper). 

In  diarrhea  some  foods  and  fluids  enjoy  a  certain  reputation  because 
they  have  a  constipating  effect;  for  example,  barley  water,  rice,  cacao, 
eggs,  tea,  red  wine,  whortleberries,  and  the  juice  of  stewed  pears.  In  the 
case  of  tea  this  is  not  always  true.  Neither  is  it  with  red  wine  and 
veal,  and,  in  the  main,  not  to  speak  of  individual  peculiarities,  we  may 
say  tliat  all  foods  appear  to  have  a  constipating  effect  which  are  dissolved 
and  absorbed  in  the  gastrointestinal  canal,  and  therefore  leave  but  little 
residue. 

In  contrast  with  this  there  are  many  foods  and  luxuries  which  stimu- 
late the  intestinal  function,  increase  peristalsis,  and  even  have  a  laxative 
effect,  naturally  varying  with  the  individual.  Cold  water  will  stimulate, 
but  much  more  so  carbonated  waters,  lemonade,  beer,  grape  juice,  asti, 
and  champagne.  Sugar  and  drinks  containing  sugar  (sugar  water),  honey, 
milk  sugar,  stewed  fruits,  marmalade,  fruit  jellies,  etc.,  produce  fermenta- 


INTESTINAL  CATARRH  681 

tion  in  the  gastrointestinal  canal  and  by  the  action  of  their  acids  stimulate 
peristalsis.  The  effect  of  buttermilk  and  of  kefyr,  of  sauerkraut  and  many 
fruits,  may  be  referred  to  their  acid  effect  as  well  as  to  the  development 
of  gas.  Besides  the  direct  action  of  its  acid,  with  sound  fruit  the  indirect 
effect  of  its  sugar  must  be  considered.  Sour  wines  and  salad  have  a 
similar  action,  and  the  latter,  besides,  has  the  same  property  as  many 
vegetables  and  contains  numerous  undigestible  constituents  (cellulose) 
which  mechanically  irritate  the  intestine  inasmuch  as  they  are  not  de- 
composed by  bacteria,  and  thus  they  distend  the  intestine.  The  foods 
which  mechanically  stimulate,  such  as  the  heavy  varieties  of  bread  con- 
taining bran — bran  bread,  brown  bread,  ration  bread  (brown  Tommy), 
Graham  bread,  Eademann's  DK  and  Simon's  bread,  etc. — favorably  as 
these  act  in  atonic  conditions  of  the  intestine,  are  little  indicated  in  the 
irritable  forms  of  intestinal  catarrh;  for  example,  in  colitis  muco-mem- 
branacea  and  spastic  constipation.  The  same  may  be  said  of  unripe, 
unpeeled  fruit,  of  the  skins  and  seeds  of  grapes  and  many  other  fruits, 
of  heavy  varieties  of  cabbage  and  the  legumes  when  insufficiently  boiled. 

Food  rich  in  fat  (cream,  butter,  fatty  meat,  fatty  sauces  and  salads, 
farinaceous  foods  cooked  in  fat)  in  most  persons  stimulate  intestinal 
peristalsis;  generally,  however,  with  the  exception  of  milk,  cream  and 
butter,  it  is  difficult  to  digest  and  is  a  standard  for  testing  the  so-called 
"  digestive  strength "  of  the  stomach.  Coffee,  tea,  tobacco,  and  brandy 
are  judged  according  to  their  individual  effects;  the  same  is  true  of 
very  salty  or  spiced  delicatessen  and  the  like.  The  irritation  they  produce 
in  the  intestinal  wall  varies;  gradually,  however,  the  digestive  organs 
become  accustomed  to  them,  but  subsequently  the  mucous  membrane  and 
musculature  of  the  intestines,  the  liver,  the  vascular  system,  the  kidneys 
and  nervous  system  begin  to  suffer.  Very  few  luxuries  and  delicatessen 
are  suitable  in  dietetic  treatment. 

Artificial  food  preparations,  I  believe,  should  be  used  only  occasion- 
ally, for,  as  permanent  constituents  of  the  dietary,  food  which  is  daily 
prepared  afresh  in  the  kitchen  is  preferable  for  the  healthy  as  well  as 
for  the  sick. 

The  same  thought  and  discrimination  should  be  exercised  in  regu- 
larly supplying  the  body  with  food  as  is  devoted  to  the  regular  evacuation 
of  the  intestinal  contents. 

In  chronic  intestinal  catarrh  accompanied  by  diarrhea,  regular  and  long- 
continued  intestinal  irrigations  in  the  manner  described  are  advisable. 
Besides  lukewarm  chamomile  infusion  or  lukewarm  saline  solution,  for 
this  purpose  mild  mineral  waters  (Ems  water,  Carlsbad  water  diluted  with 
an  equal  part  of  warm  water)  come  into  question,  also  dilute  solutions  of 
salicylic  acid  (1:1,000)  or  very  dilute  lysol  solution  (1  or  2:2,000). 
From  solutions  of  tannin  (5: 1,000),  of  ichthyol,  silver  nitrate  (0.5: 1,000) 
and  other  solutions  of  silver  I  have,  as  a  rule,  seen  no  better  results  than 


682        DIARRHEA,  CATARRH,   AND   INTESTINAL  TUBERCULOSIS 

from  suitable  washings  with  chamomile  water  and  mineral  waters  of 
proper  temperature,  provided  the  cause  of  the  diarrhea  was  not  in  the 
lowest  portion  of  the  intestine.  I  have  never  employed  long  tubes  for 
intestinal  irrigations  if  the  sphincter  ani  retained  its  tone.  In  laceration 
of  the  peritoneum  alone  are  we  justified  in  attempting  to  reach  a  point 
above  the  sphincter  tertius,  but  in  deep-seated  stenoses  we  must  try  to 
pass  the  stenosed  area  by  means  of  long,  soft,  rectal  tubes. 

These  watery  enemata  may  also  be  employed  in  chronic  intestinal  ca- 
tarrh which  runs  its  course  with  constipation  and  retention  of  feces. 
There  is  no  disadvantage  from  their  continued  use  provided  the  quantity 
of  fluid  is  no  larger  than  is  necessary  to  produce  evacuating  peristalsis. 
But  the  frequent,  or  even  regular,  employment  of  so-called  high  intestinal 
injections  of  2,  3  or  more  liters  is  not  justifiable,  and  I  have  repeatedly 
heard  patients  state  that  their  intestinal  disorders,  particularly  of  the 
atonic  form,  were  aggravated  by  these  forced  injections.  On  the  other 
hand,  it  cannot  be  denied  that  large  injections  into  the  intestine,  if  well 
borne,  are  particularly  beneficial  in  cases  of  secondary  colitis  in  which  old 
peritoneal  adhesions  hinder  the  passage  of  feces.  Inflammatory  processes 
in  the  pelvis,  even  those  which  have  run  their  course,  in  some  women 
prevent  the  employment  of  even  small  injections  on  account  of  the  pain 
they  produce;  that  is,  the  quantity  of  water  which  can  be  injected  into 
the  intestine  without  causing  pain  is  insufficient  to  stimulate  an  active 
peristalsis;  the  same  is  true  in  many  cases  of  spastic  constipation. 

The  most  effective  and,  at  the  same  time,  the  mildest  treatment  is 
by  oil  enemata,  which  Kussmaul  and  I  employed  in  all  affections  of  the 
colon  running  their  course  with  constipation.  Ten  years  ago  I  described 
their  use,  technic  and  physiologic  effects  {Berliner  hlin.  Wochenschr., 
1893,  Nr.  3  u.  4),  and  since  that  time  the  method  has  been  extensively 
and  most  successfully  employed  in  hospital  and  private  practice. 

The  oil,  lukewarm  olive  oil,  poppy-seed  oil,  or  sesame  oil,  if  of  proper 
temperature  and  carefully  injected,  penetrates  high  up  into  the  intestine, 
similarly  to  the  oil  in  the  wick  of  a  lamp.  The  passage  of  the  oil  is 
favored  by  placing  the  patient  in  a  proper  posture — usually  the  left  lateral 
position  or  the  dorsal  decubitus  with  raised  pelvis,  under  some  circum- 
stances even  the  knee-elbow  position — by  the  pendular  movement  of  the 
intestines,  and  by  the  physical  composition  of  the  oil  (absorption). 

Primarily  the  oil  lessens  the  irritability  in  the  intestine,  perhaps  acting 
like  ointment  upon  a  wound:  It  coats  the  intestinal  mucous  membrane 
and  protects  it  from  pressure  and  friction,  loosens  from  it  the  mucus  and 
adherent  feces,  limits  the  absorption  of  fecal  fluid  in  the  dissolved  prod- 
ucts of  decomposition  at  the  oiled  areas  of  the  intestinal  wall,  and  thereby 
prevents  a  marked  inspissation  of  the  feces. 

There  is  no  special  difficulty  in  retaining  the  oil  in  the  intestine  for 
hours.     While  so  retained,  free  oleic  acid  is  split  off  by  the  action  of 


INTESTINAL  CATARRH  683 

bacteria,  by  the  intestinal  juices  higher  up  in  the  intestine,  and  also  by 
other  undecomposed  digestive  juices,  particularly  by  bile,  and  this  causes 
a  marked  increase  in  the  activity  of  the  acid  contained  in  the  oil  (0.34—3.97 
per  cent.).  The  oil  which  has  become  acid  (simultaneously  with  the 
split-off  glycerin,  the  soaps  formed  from  the  oleic  acid,  and  the  alkali 
of  the  intestinal  juices)  stimulates  the  bowel  in  a  manner  closely  corre- 
sponding to  intestinal  peristalsis,  and  as  soon  as  it  reaches  the  necessary 
degree  of  acidity  for  a  chemo-reflex  causes  an  evacuation.  It  also  acts 
upon  the  excretion  of  bile  and  intestinal  fluid,  the  oleic  acid  split  off 
having  a  reflex  action.  Only  a  small  portion  of  oleic  acid  is  saponified 
and  absorbed,  for  at  least  as  much  oil  is  evacuated  as  was  injected  into 
the  intestine. 

The  exceedingly  mild  effect  of  the  oil  may  be  explained  by  the  theory 
that  the  oil  in  the  intestine  acts  only  as  an  evacuant  after  it  has  loosened 
the  fecal  masses  from  the  intestinal  wall  and  has  rendered  them  pliable 
and  smooth,  so  that  a  comparatively  slight  peristaltic  action  is  sufficient 
for  their  expulsion.  The  undecomposed  oil  present  in  excess  produces 
no  further  irritation  of  the  mucous  membrane,  at  least  patients  rarely 
complain  of  any  such  subsequent  effects  from  the  oil  as  follow  the  taking 
of  laxatives;  on  the  contrary,  the  evacuations,  as  a  rule,  promote  their 
comfort.  Diarrhea  rarely  occurs  after  enemata  of  oil,  although,  when  the 
effect  of  the  oil  is  at  its  height,  evacuations  may  occasionally  take  place 
several  times  during  the  day. 

When  the  decomposed  oil  and  the  feces  have  been  expelled  from  the 
colon  by  one  or  several  evacuations,  the  previously  described  chemism  again 
affects  the  retained  oil  which  adheres  to  the  mucous  membrane  of  the 
bowel.  If  the  quantity  of  oil  is  small,  a  long  time  will  be  necessary  to 
stimulate  peristalsis  and  to  form  oleic  acid,  glycerin  and  quantities  of 
soap.  The  number  of  evacuations  will,  however,  become  less  until,  finally, 
an  additional  amount  of  oil  will  be  necessary  to  regulate  the  bowels. 

According  to  this  view,  and  wherever  indicated,  a  treatment  with  oil 
may  be  instituted  which  will  meet  the  individual  circumstances  of  the 
case.  This  indication  is  found  in  all  forms  of  constipation,  particularly 
in  such  as  run  their  course  with  irritative  symptoms,  but  especially  in 
inflammatory,  catarrhal  and  ulcerative  processes  of  the  colon  immaterial 
whether  these  are  accompanied  by  peritoneal — non-perforating — symptoms 
or  not.^ 

The  dose  of  oil  employed  in  the  enemata  depends  upon  the  size  of 
the  patient  and  the  seat  of  the  pathologic  focus  in  the  intestine.  For 
adults  the  first  injection  should  contain  from  200  to  400  grams,  for  chil- 
dren 50  to  100  grams  of  oil  at  the  temperature  of  the  body;  this  is 


1  Other  indications  and  individual  points  are  given  in  the  original  article,  quoted 
above,  in  the  Berliner  klin.  Wochenschr.,  1893,  Nr.  3  u.  4. 


684        DIARRHEA,  CATARRH,  AND  INTESTINAL  TUBERCULOSIS 

permitted  to  flow  from  an  irrigator,  or  through  a  funnel  or  good  syringe 
(not  a  bulb  syringe)  while  the  patient  is  in  the  left  lateral  posture — ^the 
bed  or  sofa  to  be  previously  protected  with  a  rubber  sheet  or  other  suitable 
material — the  syringe  is  then  attached  to  the  anal  nozzle  by  means  of  a 
black  rubber  tube  20  cm.*  long,  and  the  oil  is  permitted  to  flow  slowly 
into  the  rectum.  After  the  injection  of  the  oil  the  patient  remains  in 
the  same  position  for  about  a  half  hour,  then  for  one  or  two  hours  longer 
upon  his  back,  preferably  in  bed,  until  an  evacuation  occurs.  Should  this 
waiting  be  prolonged,  or  should  the  patient  be  uncomfortable  from  the 
prolonged  retention  of  the  oil  in  the  intestine,  which  is  apt  to  be  the  case 
when  there  is  flatulence,  the  oil  may  be  evacuated  after  four,  six  or  eight 
hours  by  an  injection  of  chamomile  or  anise  water,  or  even  with  simple 
lukewarm  water.  These  enemata  of  oil  should  be  repeated  daily  until 
the  intestine  is  empty,  until  all  the  old,  hardened  fecal  masses  are  passed, 
or,  still  better,  until  the  oil  has  had  its  maximum  effect,  which  is  signal- 
ized l)y  the  passage  of  thin,  semi-solid  feces,  occasionally  still  containing 
undecomposed  bile.  Then  a  pause  of  one,  two  or  more  days  is  made  until 
oil  no  longer  appears  in  the  evacuations,  and  the  feces  again  show  a 
tendency  to  dryness,  or  until  an  evacuation  fails  to  take  place  daily. 

There  are  cases  in  which  a  few  enemata  of  oil,  even  a  single  injection, 
will  permanently  remove  the  difficulties  due  to  fecal  accumulation.  But 
in  chronic  catarrh  of  the  colon  running  its  course  with  constipation  the 
oil  treatment,  as  a  rule,  must  be  continued  for  weeks  or  even  months  until 
the  catarrh  has  been  relieved  as  well  as  the  functional  disturbance.  In 
these  cases,  after  the  first  complete  evacuation  of  the  intestine  an  injection 
of  oil  is  given  regularly  every  day  or  on  alternate  days,  and  only  after 
improvement  appears  is  the  oil  to  be  used  more  rarely,  perhaps  twice  or 
even  once  a  week,  until  permanent  recovery  is  brought  about. 

In  such  cases  it  is  advisable  to  give  the  oil  enema  at  night  in  bed 
just  before  the  patient  goes  to  sleep.  We  should  begin  with  200  to  300 
grams,  and  subsequently  use  doses  according  to  their  effect;  if  the  patient 
is  disturbed  at  night  by  a  desire  to  evacuate  the  bowels,  less  oil  should  be 
given  the  next  time  so  that  the  evacuation  may  occur  at  a  convenient 
morning  hour.  To  secure  this  result  small  quantities  of  oil,  100  grams, 
50  grams,  or  even  less,  are  often  sufficient.  There  are,  however,  cases  in 
which  the  oil,  while  retained  during  the  night  in  the  intestine,  fails  to 
produce  an  evacuation  in  the  morning,  and  we  must  then  resort  to  a 
pimple  enema  or  other  remedies.  It  cannot  be  denied  that  prolonged  oil 
treatment  sometimes  produces  disagreeable  results,  for  example,  the  un- 
conscious or  involuntary  passage  of  the  oil.  These  disagreeable  features, 
however,  may  be  avoided  by  better  technic  in  giving  the  enema,  by  proper 
dosage,  and  other  slight  precautions;  where  this  is  not  the  case  we  must 
return  to  the  vse  of  laxatives  for  the  proper  regulation  of  the  bowels. 

We  differentiate  between  mildly  acting  (lenitive)  and  powerfully  acting 


INTESTINAL  CATARRH  685 

(drastic)  laxatives.  In  chronic  colitis  and  other  irritative  conditions  of 
the  intestine  mild  remedies  only  should  be  employed,  and  these  may  be 
given  in  small  doses  for  a  long  time  without  injurious  effect.  Chief 
among  these  remedies  are  rhubarb  (powder,  tablet,  or  pills)  for  adults 
and  manna  for  children,  also  tamarinds,  cortex  ranguls,  senna,  cascara 
sagrada,  sulphur,  magnesia,  compound  licorice  powder  and  aloes  in  small 
doses.  Among  the  drastic  remedies:  Scammonium,  jalap,  colocynth,  and 
podophyllin  are  more  rarely  employed,  and  usually  only  as  additions  to 
increase  the  action  of  more  mildly  acting  drugs.  If,  in  stubborn  cases, 
we  are  compelled  to  resort  to  more  powerful  laxatives,  we  add  to  the  pill 
ingredients  which  lessen  irritation,  for  instance,  extract  of  hyoscyamus 
or  extract  of  belladonna,  both  of  which  have  an  anodyne  effect  without 
influencing  the  peristalsis.  In  spastic  constipation,  atropin  subcutaneously 
or,  for  long-continued  use,  in  solution  by  mouth  is  very  beneficial : 

I^  Atropin  sulphate 0.03 

Aqua  menth.    pip 20.00 

M.  D.     S. :  Seven  to  ten  drops  three  times  daily. 

Where  no  dyspeptic  conditions  complicate  chronic  intestinal  catarrh  and 
the  stomach  will  tolerate  it,  excellent  results  are  often  obtained  from  the 
regular  use  of  small  doses  of  castor  oil  or  olive  oil  given  by  the  mouth. 
Whether  the  newer  remedies,  purgen,  purgatin,  exodin  and  others,  are 
satisfactory  for  protracted  use  is  questionable.  Even  California  fig  syrup 
has  a  highly  irritating  effect;  at  all  events,  it  is  not  so  mild  as  the  name 
would  lead  us  to  suppose. 

The  aperient  spring  waters  and  the  so-called  neutral  salts  occupy  a 
special  position  among  laxatives :  Magnesium  sulphate,  Glauber  salt,  sodium 
chlorid,  magnesium  carbonate  and  citrate,  artificial  and  natural  Carlsbad 
salt,  and  sodium  hyposulphite.  They  not  only  promote  fecal  evacuations, 
but  also  the  discharge  from  the  intestine  of  non-absorbed  constituents  of 
the  food,  and  cause  an  effusion  of  fluid  into  the  gastrointestinal  canal, 
an  absorption  of  water,  and  the  stimulation  of  the  glandular  elements  of 
the  mucous  membrane  to  increased  activity.  Usually  the  artificial  salt 
solutions  are  taken  in  too  concentrated  a  form;  therefore,  on  prolonged 
use,  the  epithelium  of  the  stomach  and  intestine  suffers  from  their  h)rper- 
tonic  influence.  For  this  reason,  I  emplpy  solutions  of  salt  only  occa- 
sionally, and  for  long-continued  use,  and  as  an  adjunct  to  the  oil  treat- 
ment, prefer  the  natural  mineral  waters. 

The  choice  of  a  mineral  spring  depends  upon  the  indications  given 
by  the  functional  test  of  the  stomach  and  the  intestine.  The  hot  springs 
and  heated  natural  waters  (either  alkaline,  muriatic,  or  alkaline  muriatic) 
by  their  heat  lessen  irritation,  and  therefore  are  rather  constipating,  while 
the   cold   waters,   especially   those  which   contain   carbonic   acid,   have   a 


686        DIARRHEA,   CATARRH,   AND  INTESTINAL  TUBERCULOSIS 

stimulating  effect  upon  peristalsis.  True  spa  treatment  often  fails  to 
cure  the  severe  forms  of  chronic  colitis.  I  have,  however,  known  great 
benefit  to  follow  the  treatment  at  Kissingen,  Homburg,  Tarasp,  Carlsbad, 
Wiesbaden,  and  other  resorts,  provided  the  use  of  the  waters  was  instituted 
after  the  most  acute  disturbances  had  been  relieved  by  treatment  in  a 
sanatorium  or  at  home,  especially  by  the  oil  cure. 

In  the  majority  of  cases  of  chronic  intestinal  catarrh  of  gastric  origin, 
also  in  the  numerous  secondary  complications  which  involve  the  stomach, 
systematic  local  treatment  of  this  organ  by  lavage  (early  in  the  morning 
upon  an  empty  stomach)  is  very  advantageous.  The  effect  of  lavage  upon 
the  appetite,  upon  the  functions  of  the  stomach,  upon  the  upper  small 
intestine,  upon  the  liver,  upon  the  blood  and  the  kidneys,  and  last,  but 
not  least,  upon  the  morale  of  the  patient  is  so  well  known  that  I  need 
not  enter  into  details;  in  diarrhea  alone  does  gastric  lavage  occasionally 
have  an  unfavorable  effect,  and  in  these  cases  it  should  never  be  employed. 

A  number  of  other  remedies  indirectly  influence  the  pathologic  proc- 
esses in  the  intestine  and  the  disturbances  in  function  dependent  upon 
these.  Heat,  for  example,  is  beneficial  by  lessening  irritation  (warmth 
of  the  bed  and  rest  in  bed)  ;  hot  dry  cloths,  hot  bottles,  thermophores, 
moist  heat  l)y  means  of  compresses  (cataplasms)  are  all  useful  for  re- 
lieving abdominal  pain  and  colic.  As  a  rule,  patients  with  disease  of  the 
intestine  and  particularly  those  who  suffer  from  diarrhea  and  whose  nutri- 
tion has  been  damaged  require  a  great  amount  of  heat.  They  are  easily 
chilled;  when  the  physician  advises  them  to  wear  an  abdominal  binder 
they  follow  the  advice  with  excessive  eagerness.  In  the  winter  there  is 
no  objection  to  wearing  a  flannel  binder,  but  usually  the  wearing  of  these 
bandages  does  harm  rather  than  good,  since  they  weaken  the  skin  which 
steadily  becomes  more  susceptible  to  the  effect  of  cold. 

Cold  applied  to  the  skin,  reflexly  stimulates  peristalsis.  Its  hydro- 
therapeutic  employment  in  cases  of  catarrh  combined  with  intestinal  atony 
produces  remarkably  good  results;  for  this  purpose  Sitz  baths  of  brief 
duration,  bathing  of  the  abdomen,  friction,  half-baths,  douches,  river  and 
sea  baths,  may  all  be  employed  to  relieve  constipation.  Besides,  by  im- 
proving the  circulation,  these  procedures  have  a  curative  effect  upon  the 
intestinal  catarrh  which  may  even  be  increased  by  the  addition  of  salt 
to  the  bath;  therefore,  salt  baths,  mineral  baths  and  peat  baths  are 
advisable. 

In  suitable  cases  electricity  may  also  be  employed:  The  anode  of  the 
galvanic  current  for  the  amelioration  of  pain  which  originates  from  spastic 
conditions  and  neuralgia;  faradization  of  the  abdominal  wall  to  stimulate 
intestinal  movements. 

Massage  is  indicated  in  some  of  the  cases.  When  there  are  irritative 
conditions  in  the  intestine  and  the  peritoneum,  pains,  spastic  constipation, 
and  the  presence  of  hard  fecal  masses  in  catarrhally  inflamed  portions  of 


INTESTINAL  TUBERCULOSIS  687 

the  intestine,  massage  is  contraindicated,  while  in  the  atonic  and  torpid 
conditions  which  mark  some  cases  of  chronic  colitis  brilliant  results  are 
sometimes  attained  by  massage.  Vibration  massage  is  usually  less  harmful 
than  manual,  and  is  often  well  borne  when  the  latter  is  contraindicated. 
We  cannot,  however,  be  certain  of  its  advisability,  for  apparently,  like 
many  of  these  procedures,  it  presupposes  more  or  less  psychical  suscep- 
tibility. 

Medico-mechanical  treatment  and  gymnastic  exercises  combined  with 
spa  and  bath  cures  are  very  useful  for  the  constipation  of  chronic  colitis. 

Besides  these  auxiliary  methods  of  treatment,  in  the  severe  forms  of 
secondary  colitis  (colitis  muco-membranacea)  which  originate  from  in- 
flammatory processes  in  the  pelvis  and  abdominal  organs,  gynecological 
measures  must  be  considered:  Vaginal  treatment,  rectal  treatment  by 
bougies,  under  some  circumstances  even  laparotomy  for  the  purpose  of 
breaking  up  peritoneal  adhesions  or  the  extirpation  of  tumors  or  diseased 
organs,  for  example,  of  an  ovary,  of  the  uterus,  or  of  the  tubes.  I  am 
not  yet  ready  to  relate  my  experiences  with  thiosinamin  injections  in 
cases  of  peritoneal  adhesions  which  developed  after  abdominal  operations, 
but  the  subject  is  a  promising  one. 


m.     INTESTINAL  TUBERCULOSIS 

Tuberculous  infection  of  the  intestines  is  caused  by  tubercle  bacilli 
which  reach  the  mouth  in  some  manner  and  are  swallowed.  Frequently 
the  infection  is  self-conveyed  by  the  sputum  of  a  tuberculous  individual, 
who  swallows  it  and  thus  introduces  numerous  tubercle  bacilli  into  the 
intestine;  but  the  tuberculous  sputum  of  others  may  be  directly  thrown 
into  the  mouth  of  a  healthy  person  by  coughing,  or  it  may  be  conveyed  frona 
the  lips  of  a  patient  to  a  healthy  person  in  the  form  of  the  finest  particles. 
Dried  tuberculous  sputum  in  the  air  contains  bacilli  which  upon  inspira- 
tion do  not  all  reach  the  deep  respiratory  passages  and  the  lungs,  but 
may  adhere  to  the  wall  of  the  buccal  cavity  and  be  swallowed  with  the 
saliva.  Little  children  playing  with  earth  frequently  introduce  tubercle 
bacilli  into  the  mouth  with  their  dirty  fingers  as  well  as  with  toys  and 
other  articles  which  they  lick  or  bite.  From  tuberculous  wounds,  with 
soiled  fingers,  instruments  or  any  other  object,  children  as  well  as  adults 
may  introduce  the  tuberculous  poison  into  the  mouth. 

A  mode  of  infection  the  importance  of  which  was  for  a  long  time  under- 
valued, and  subsequently  for  a  time  exaggerated,  is  by  means  of  food  and 
drink  containing  bacilli  (feeding  tuberculosis).  Since  the  discovery  of 
the  tubercle  bacillus  by  Robert  Koch,  bacteriologic  investigation  has  re- 
vealed a  number  of  microorganisms  resembling  tubercle  which  at  first  were 
considered  to  be  different  in  nature  but  are  now  known  to  be  a  more  or 
less  common  variety  of  one  fundamental  form;  they  have  developed  by 


688        DIARRHEA,  CATARRH,   AND   INTESTINAL  TUBERCULOSIS 

adapting  themselves  to  new  conditions  of  existence.  If,  therefore,  the 
tubercle  bacilli  of  mammals,  of  birds,  and  of  reptiles  are  considered  to 
be  identical,  the  importance  of  infection  by  means  of  food  is  greatly 
enhanced.  But  the  view  of  v.  Behring  that  "  infant's  milk,"  i.  e.,  cow's 
milk  given  to  nurslings  as  a  substitute  for  mother's  milk,  "is  the  main 
cause  of  the  development  of  tuberculosis  "  is  far  fetched ;  he  should  have 
said,  the  main  cause  of  primary  intestinal  tuberculosis.  Between  the 
latter  and  pulmonary  tuberculosis  there  is  a  wide  difference.  And  although 
we  cannot  doubt  that  tubercle  bacilli,  like  many  other  bacteria,  may  per- 
meate the  intestinal  wall  of  the  young  without  causing  demonstrable 
changes  at  the  point  of  entrance,  yet  such  bacilli  fail  to  reach  the  fluids 
of  the  body  and  to  infect  the  lungs — in  particular,  as  well  as  other  organs 
— by  means  of  the  blood,  but  they  infect  the  regional  lymph-glands  in 
those  areas  of  the  intestine  which  they  traverse,  and,  after  penetrating 
to  the  roots  of  the  portal  vein  circulation,  also  the  mesentery  and  the  liver. 

Primary  enterogenous  hepatic  tuberculosis  is  very  rare  in  man;  pri- 
mary enterogenous  tuberculosis  of  the  mesenteric  lymph-glands — with  or 
without  tuberculous  lesion  of  the  intestine  at  the  point  of  invasion — is, 
however,  much  more  frequent,  but,  compared  with  pulmonary  tuberculo- 
sis, is  still  relatively  rare.^  Enterogenous  infection  cannot,  therefore,  be 
the  main  source  of  (pulmonary)  tuberculous  development.  Otherwise,  we 
must  assume  that  the  bacilli  not  only  pass  unhindered  through  the  intes- 
tine but  also  through  the  great  regional  lymph-gland  apparatus  of  the 
intestine  in  the  mesentery.  That  the  latter  is  not  the  case  is  distinctly 
evident,  but  rather  from  the  pathology  of  lymph-gland  tuberculosis,  espe- 
cially tuberculosis  of  the  mesenteric  gland,  than  from  the  histology  and 
physiology  of  the  lymph-glands.  I  do  not,  however,  deny  the  possibility 
that,  as  tuberculosis  advances  from  the  mesenteric  lymph-glands,  the  path- 
ologic process  may  implicate  the  intrathoracic  lymph-glands  and  finally 
attack  the  lungs;  but  this  occurrence  is  exceptional  and  by  no  means  the 
rule.  The  same  might  be  said  of  the  primary  lesion  of  tuberculosis  in 
the  lymphatic  apparatus  of  the  nasopharyngeal  space,  of  tuberculosis  of  the 
pharyngeal  and  palatine  tonsils  and  the  lymphatics  of  the  neck;  but  this 
digression  leads  us  too  far  afield. 

In  contrast  with  the  enterogenous  development  of  intestinal  tubercu- 
losis, hematogenous  intestinal  tuberculosis  in  the  form  of  miliary  tuber- 
culosis and  tuberculous  metastases  is  of  much  less  importance.  On  the 
direct  transference  of  the  tuberculous  pathologic  process  from  a  diseased 
organ  to  the  neighboring  intestine  and  its  peritoneal  coat,  the  primary 
focus  of  disease,  as  a  rule  (for  example,  a  fungus  coxitis,  genital  tubercu- 
losis, or  caries  of  the  vertebra),  becomes  prominent  in  the  clinical  picture. 

1  The  opinions  of  authors  as  to  the  frequency  of  primary  intestinal  tuberculosis 
are  far  asunder;  the  prevalence  of  tuberculosis  among  cattle  varies  within  wide 
limits    (7  to  45  per  cent.)  according  to  the  r^on  where  this  prevails. 


INTESTINAL  TUBERCULOSIS  689 


PATHOLOGY 

Pathologico-anatomically  tuberculosis  belongs  to  the  most  common  of 
intestinal  affections.  We  differentiate  primary  or  substantive  intestinal 
tuberculosis  from  the  secondary  form  which  occurs  in  consequence  of 
earlier  tuberculous  disease  of  other  organs,  particularly  of  the  lungs.  In 
point  of  frequency,  secondary  intestinal  tuberculosis  preponderates  greatly 
over  the  primary  form.  A  definite  opinion  as  to  the  absolute  frequency 
of  primary  intestinal  tuberculosis  cannot  be  obtained  at  this  time  even 
from  the  material  collected  by  Heller,  v.  Hansemann,  Lubarsch  and  others. 
Experience  indicates,  however,  that  primary  feeding  tuberculosis,  which, 
besides  primary  intestinal  tuberculosis,  includes  also  primary  tuberculosis 
of  the  tonsils  and  the  lymphatics  of  the  neck,  primary  mesenteric  gland 
tuberculosis  and  primary  (isolated)  peritoneal  tuberculosis,  is  not  a  rare 
affection  in  infants  and  children. 

When  tubercle  bacilli  collect  in  a  tissue,  an  inflammatory  focus  devel- 
ops and  the  chemical  poisons  generated  by  the  bacilli  at  first  damage  and 
destroy  ^  the  preexisting  tissue  cells,  by  chemotaxis  they  cause  an  accumu- 
lation of  leukocytes,  and  in  the  healthy  tissue  cells  in  the  neighborhood 
of  the  port  of  invasion  which  do  not  as  yet  contain  bacilli  they  produce  a 
reactive  inflammation.  Soon,  however,  the  descendants  of  the  proliferative 
tissue  cells,  the  epithelioid  and  giant  cells,  succumb  to  the  action  of  the 
adherent  poison  produced  by  the  bacilli,  and  simultaneously  obliterate  pre- 
existing vessels  and  prevent  the  formation  of  new  ones. 

Thus  the  process  of  destruction  advances  farther  and  farther  from  the 
point  of  invasion. 

Tubercle  bears  the  stamp  of  an  inflammatory  granulation  proliferation, 
and  differs  only  from  other  granulations  by  having  a  nodular  form  and 
by  remaining  without  vessels  (Ziegler).  In  the  main,  the  morphologic 
changes  in  the  tissues  produced  by  tubercle  bacilli  are  of  varying  kinds; 
simple  exudative  inflammation,  suppuration,  and  the  formation  of  granu- 
lation tissue  and  caseation  may  combine  in  such  different  ways  as  to  cause 
various  anatomical  pictures  (Orth).  Nodules  may  even  be  absent  in  the 
tuberculous  inflammatory  foci,  in  which  case  the  decision  as  to  tuberculosis 
can  be  made  only  by  the  tubercle  bacilli. 

The  chief  seat  of  the  disease  is  the  lymphadenoid  apparatus  of  the 
intestine,  especially  the  lower  small  intestine,  the  upper  colon,  and  the 
region  of  the  ileo-cecal  valve.  But  any  portion  of  the  digestive  tract,  from 
beginning  to  end,  may  be  affected  by  tuberculosis. 

In  the  manner  already  described,  ulcers  may  sooner  or  later  develop 
from  the  tubercles  of  the  solitary  or  agminate  glands;  these  are  either 
round,  longitudinal,  or  irregular  and  sinuous.     The  ulcers  spread  prefer- 

1  Karl  Weigert's  "  Shiwa." 


690        DIARRHEA,  CATARRH,  AND  INTESTINAL  TUBERCULOSIS 

ably  in  the  direction  of  the  vascular  division,  therefpre  vertically  to  the 
longitudinal  axis  of  the  intestine;  thus  the  annular  or  girdle-like  ulcers 
develop. 

The  borders  of  the  tuberculous  ulcers  are  usually  infiltrated,  the  mar- 
gins are  elevated,  and  often  undermined  and  permeated  by  the  character- 
istic and  more  or  less  caseous  and  decomposed  nodules.  The  latter  are 
found  also  upon  the  base  of  the  ulcer,  which  may  be  of  varying  depth,  the 
floor  being  formed  by  the  submucosa,  the  muscularis,  and  even  by  the 
serosa.  At  the  autopsy  we  invariably  recognize  the  seat  of  tuberculous 
intestinal  ulcers  even  from  without  by  the  redness  and  thickening  of  the 
serosa  and  its  permeation  by  small  nodules.  This  circumscribed  tubercu- 
lous peritonitis  commonly  favors  the  formation  of  adhesions  and  the  exten- 
sive agglutination  of  diseased  portions  of  the  intestine  with  other  organs 
covered  by  the  peritoneum  and  the  abdominal  wall,  and  renders  the  per- 
foration of  tuberculous  intestinal  ulcers  a  relatively  rare  occurrence;  when 
it  does  occur  it  is  less  dangerous  because  the  succeeding  peritonitis  is  sac- 
culated. Where  there  is  no  serous  covering  of  the  intestine,  as  in  the 
rectum,  ulcerative  tuberculosis  leads  to  perirectal  abscesses  and  subse- 
quently to  internal,  external,  and  complete  anal  fistula. 

Tuberculous  granulation  proliferation  may  terminate  in  caseation  and 
ulcerous  decomposition  as  well  as  in  induration,  according  to  the  action 
of  the  bacterial  toxins  and  the  composition  of  the  base  on  which  they 
develop,  and  also  perhaps  the  constitution  of  the  patient  (Ziegler).  Hence 
wo  find  in  one  case  extensive  and  advancing  ulceration  in  the  intestine,  in 
another,  on  the  contrary,  a  conspicuous  tendency  to  cicatrization  and  indu- 
ration by  connective  tissue  proliferation.  Undoubtedly  the  cicatrization 
of  a  tuberculous  ulcer  must  be  regarded  as  a  favorable  process  and  indica- 
tive of  a  cure.  This  healing  tendency  may,  however,  in  one  sense  be  a 
disadvantage  to  the  organism,  for,  as  pyloric  stenosis  may  develop  in  con- 
sequence of  the  cicatrization  of  a  gastric  ulcer  at  the  pylorus,  so  by  the 
cicatrization  of  an  annular  tuberculous  ulcer  of  the  intestine  constric- 
tion of  the  intestine  and  severe  disturbances  in  function  may  be  brought 
about.  Such  cicatricial  stenoses  in  the  intestine  occur  simultaneously 
with  tuberculous  ulcers;  I  have  repeatedly  seen  them  multiple  in  the 
same  case. 

Tlie  most  extreme  constrictions  of  the  intestine  are  the  ring-shaped, 
cicatricial  stenoses  which  originate  from  annular  ulcers,  and  are  very 
often  short.  The  cicatrices  which  project  spur-like  into  the  lumen  of  the 
intestine  and  encompass  only  a  portion  of  its  circumference,  at  least  in 
the  small  intestine,  do  not  decidedly  affect  the  permeability  of  the  latter. 
Nikoljski  draws  the  contrast  between  tuberculous  and  fibrinous  tuberculous 
stricture  which  does  not  originate  from  an  ulcer — consequently  does  not 
permit  the  recognition  of  cicatricial  formation  upon  the  mucous  mem- 
brane— but  arises  from  simple  connective  tissue  proliferation  in  consequence 


INTESTINAL  TUBERCULOSIS  691 

of  tuberculous  infection  of  the  intestine — peribasillary  sclerosis.  A  third 
form  of  tuberculous  intestinal  stenosis  is  the  so-called  hypertrophic  stric- 
ture which  is  characterized  by  great  thickening  of  the  intestinal  wall,  a 
thickening  which  involves  all  of  the  layers,  the  mucous  membrane 'by 
polypus  proliferation,  the  submucosa  and  muscularis  by  hypertrophy,  and 
the  serosa  by  a  decided  connective  tissue  development  which,  by  its  permea- 
tion with  masses  of  fat,  increases  the  resemblance  to  a  tumor.  The  dif- 
ferential diagnosis  between  carcinoma  and  tuberculosis  may  be  perplexing 
even  after  extirpation  of  the  stenosing  tumor,  until  the  microscope  decides 
the  question — as  in  one  of  my  cases.  In  this  hypertrophic  form  of  tuber- 
culous intestinal  stenosis  the  submucosa  with  its  vessels  is  most  markedly 
implicated;  some  authors  consider  hypertrophic  intestinal  tuberculosis  as 
of  hematogenous  origin  (Nikoljski). 


SYMPTOMS 

The  clinical  phenomena  of  intestinal  tuberculosis  are  manifold,  and 
in  the  advanced  stages  very  peculiar. 

The  initial  stage  of  the  affection  almost  always  eludes  observation, 
although  it  cannot  be  assumed  that  the  inflammatory  processes  succeeding 
tuberculous  infection  of  the  intestine  run  their  course  without  creating 
functional  disturbances   (pre-tuberculous  diarrhea?). 

From  indistinct,  dyspeptic,  intestinal  disturbances  which  in  children, 
and  not  rarely  in  adults,  are  accompanied  by  a  febrile  movement,  in  the 
course  of  time,  often  very  slowly,  well  developed  clinical  pictures  are 
formed  which  correspond  to  the  advancing  pathologic  changes  in  the  intes- 
tinal wall  and  the  mesenteric  lymph-glands;  these,  in  many  cases,  bear 
a  relation  to  the  symptom-complex  of  chronic  intestinal  catarrh  with  those 
anomalies  in  regard  to  the  bowel  movements  which  have  been  described. 
As  a  rule,  however,  Just  as  in  the  pathological  processes  in  the  intestinal 
wall,  ulcerative  symptoms  predominate.  In  every  case  peritoneal  irri- 
tative phenomena  may  be  superadded,  either  transitorily  or  permanently. 

The  symptoms  of  subacute  and  chronic  intestinal  catarrh,  especially 
the  increased  excretion  of  mucus,  may  be  due  to  the  inflammatory  process 
in  the  intestinal  wall.  Often,  however,  in  compact  as  in  diarrheic  intes- 
tinal discharges,  mucus  is  absent,  while  the  intensity  of  other  irritative 
symptoms  does  not  permit  us  to  assume  the  cessation  of  the  inflammatory 
processes.  Periodically  mucus  in  greater  masses  is  often  admixed  with 
the  feces.  In  such  cases  the  increased  excretion  of  mucus  is  not  always 
the  sign  of  an  exacerbating  tuberculous  inflammation,  for  functional  dis- 
turbances accidentally  produced  by  a  long-existing  ulcer,  above  all  spas- 
tic contracture  and  fecal  retention,  may  often  produce  in  the  mucous 
membrane  of  the  affected  intestinal  area  a  great  excretion  of  mucus,  an 
irritative  condition  resembling  colica  mucosa. 


692        DIARRHEA,  CATARRH,  AND  INTESTINAL  TUBERCULOSIS 

In  their  nature  and  intensity  the  ulcerative  symptoms  of  intestinal 
tuberculosis  depend  much  less  on  the  extent  of  surface  and  the  depth  of 
the  tuberculous  ulcerative  process  than  on  the  intensity  of  the  irritation 
of  the  exposed  intestinal  nerves  upon  the  floor  of  the  ulcer.  If  these  are 
absent  in  ulcerated  areas,  it  may  happen  that  numerous  and  comparatively 
large  tuberculous  ulcers  in  the  small  intestine  as  well  as  in  the  colon  run 
their  course  entirely  latent,  often  causing  no  functional  disturbance,  while 
in  other  cases  an  isolated  ulcer  in  the  colon,  if  this  implicate  an  impor- 
tant nerve  branch,  may  produce  the  most  severe  irritative  symptoms.  The 
latter  may  be  of  a  motor,  sensory  or  secretory  nature;  to  these  must  be 
added,  as  other  symptoms  of  ulcer,  hemorrhages  and  peritoneal  and  peri- 
rectal inflammations. 

The  motor  irritative  phenomena  are  most  frequent  in  intestinal  tuber- 
culosis. Diarrhea  is,  therefore,  the  most  common  symptom  of  intestinal 
tuberculosis,  and,  when  persistent,  the  possibility  of  intestinal  tuberculosis 
must  always  be  considered  unless  other  symptoms  indicate  a  different  affec- 
tion. In  cases  of  tuberculous  intestinal  ulcers  we  now  and  then  see  typical 
spastic  constipation  combined  with  the  previously  mentioned  painful  evac- 
uations of  mucus  which  resemble  mucous  colic.  The  distress  is  often 
localized  in  the  ileo-cecal  region,  and  at  first  is  usually  attributed  to  an 
acute  affection  of  the  appendix.  Violent  tenesmus,  often  combined  with 
the  passage  of  blood,  is  produced  by  tuberculous  ulcers  of  the  rectum.  In 
some  cases  the  irritation  of  the  rectum,  and  even  that  of  the  sigmoid  flex- 
ure, simulates  the  picture  of  nervous  hyperesthesia  of  the  intestine.  Small 
masses  of  dejecta  which  reach  the  rectum  produce  an  irresistible  desire  to 
relieve  the  bowels,  and  this  is  frequently  repeated  at  short  intervals  to  the 
great  distress  of  the  patient.  Since  in  these  cases  the  evacuations  are  very 
small  in  amount,  not  rarely  there  is  a  paradoxical  retention  of  feces,  a 
constipation-diarrhea. 

Peristaltic  unrest  accompanied  by  loud  intestinal  rumblings  is  an  almost 
invariable  symptom  in  the  chronic  diarrhea  of  intestinal  tuberculosis;  if, 
however,  it  continues  after  the  diarrhea  ceases,  or  is  more  marked  during 
the  periods  of  constipation,  this  increased  peristaltic  unrest  is  often  the 
first  sign  of  a  beginning  stenosis  of  the  intestine.  Added  to  it  in  the 
course  of  weeks  and  months  are  peristaltic  pains  which  occur  at  more  or 
less  regular  intervals,  often  every  few  minutes,  with  a  characteristic  ten- 
sion of  that  portion  of  the  intestine  anterior  to  the  obstruction.  I  shall 
later  discuss  this  symptom  of  intestinal  constriction. 

The  diarrhea  of  intestinal  tuberculosis  is  frequently  associated  with 
pain;  and  the  previously  mentioned  spasmodic  state  of  the  intestine,  the 
contracture  as  well  as  the  over-distention  sometimes  intercurrent  with  the 
former  but  also  occurring  without  it,  is  often  marked  by  excessive  pain. 
During  or  before  defecation,  when  hard  feces  pass  through  the  ulcerated 
intestinal  area,  there  is  often  true  ulcer  pain  of  great  severity  in  the  region 


iNTESriNAL  TUBERCULOSIS  693 

of  the  colon,  especially  in  the  lower  portion.  In  such  cases  every  evacuation 
distresses  the  patient  for  more  or  less  time,  often  only  for  a  few  minutes, 
sometimes  for  hours,  and  then  completely  exhausts  the  sufferer. 

Pain  confined  to  definite  areas  of  the  abdomen,  persisting  for  days 
but  varying  in  intensity,  and  not  markedly  influenced  by  the  intestinal 
function,  may  be  regarded  as  of  peritoneal  origin,  especially  when  there  is 
local  tenderness  on  pressure  and  a  rise  in  temperature,  and  when  nausea 
and  a  tendency  to  vomit  are  accompaniments. 

These  peritoneal  symptoms  may  be  acute  and  of  great  severity, 
and  may  be  the  forerunners  of  the  gravest  form  of  peritonitis,  that  due  to 
pfci'foration.  But  in  intestinal  tuberculosis  an  insidious  onset  and  a  course 
showing  complications  and  frequent  relapses  is  more  common.  Often  the 
pain  and  the  local  sensitiveness  to  pressure  are  the  only  symptoms  of  the 
condition;  sometimes  a  circumscribed,  plastic,  fibrinous  exudate  is  formed, 
the  demonstration  of  which  may  be  impossible;  after  these  peritoneal 
attacks  adhesions  of  the  intestine  invariably  form,  and  not  infrequently 
cause  new  functional  disturbances  of  the  intestine.  These  are  slightest 
in  the  very  common  serous  exudates,  often  of  enormous  extent,  which 
occur  in  tuberculous  inflammations  of  the  peritoneum. 

Hemorrhage  from  the  intestine  is  the  most  positive  sign  of  ulcer.  Tuber- 
culous intestinal  ulcers,  however,  rarely  show  a  tendency  to  bleed,  for  the 
tubercle,  as  such,  is  non-vascular,  and,  furthermore,  it  is  a  peculiarity  of 
the  tubercular  toxin  speedily  to  obliterate  small  vessels.  Nevertheless,  in 
intestinal  tuberculosis  of  considerable  intensity  and  very  difficult  to  con- 
trol I  have  several  times  seen  hemorrhage,  particularly  from  the  lower 
portions  of  the  bowel.  In  such  copious  hemorrhages  mechanical  injury  to 
the  vessels  from  impacted  fecal  masses  probably  plays  a  greater  role  than 
erosion  of  the  wall  of  the  vessel — similar  to  the  condition  in  pulmonary 
cavities — by  a  rapidly  advancing  process  of  ulceration.  Yet  in  no  other 
pathologic  process  is  there  such  great  recuperative  power,  such  a  dispro- 
portion between  destruction  and  restitution,  as  is  peculiar  to  the  tubercu- 
lar; consequently  in  severe  and  repeated  hemorrhages  from  tuberculous 
intestinal  ulcers  we  must  never  give  up  hope.  I  have  seen  the  hemorrhage 
arrested,  and  even  amelioration  for  years  of  all  the  severe  anemic  conditions 
which  followed  such  hemorrhage. 

The  transformation  of  tuberculous  granulation  tissue  into  cicatricial 
connective  tissue,  connective  tissue  proliferation  in  the  surroundings  of 
tuberculous  ulcers,  and  the  formation  from  the  plastic  exudate  of  pseudo- 
membranes  and  indurations  upon  the  serosa  of  the  intestine,  corresponding 
to  the  seat  and  the  areas  surrounding  the  tuberculous  ulcers,  in  some 
cases  assist  the  conspicuous  tendency  of  the  latter  to  heal.  These  patho- 
logic processes  which  favor  the  healing  of  ulcers  may,  however,  have  a 
decidedly  injurious  effect  upon  the  permeability  of  the  intestine.  Cica- 
trization of  an  ulcer  leads  to  cicatricial  stenosis;  diffuse  infiltration  and 
45 


694        DIARRHEA,  CATARRH,   AND  INTESTINAL  TUBERCULOSIS 

thickening  of  the  walls  of  a  portion  of  the  intestine  prevent  the  propulsion 
of  the  peristaltic  wave.  Induration  of  the  serosa  of  a  section  of  the  bowel 
also  interrupts  peristalsis,  and  pseudo-membranous  adhesipns  readily  pro- 
duce traction  and  kinking  in  the  lumen  of  the  intestine,  and  consequent 
constriction  and  deformity  which  render  the  propulsion  of  the  intestinal 
contents  difficult. 

By  compensatory  hypertrophy  of  the  intestinal  musculature  above  the 
point  of  obstruction  these  conditions  may  for  a  long  time  remain  dormant 
and  disturbances  of  fecal  movement  be  compensated  for.  The  diffuse, 
rigid  infiltration  and  indurative  thickening  of  definite  sections  of  the  bowel 
first  become  noticeable  because  these  assume  the  form  of  a  cylindrical 
strand  or  of  a  tumor  of  irregular  shape  and  extent.  These  may  then  be 
palpated,  but  only  in  areas  of  the  abdomen  where  the  intestine  and  par- 
ticularly the  colon  are  readily  palpable  under  normal  circumstances,  i.  e., 
in  the  region  of  the  cecum  and  of  the  sigmoid  flexure.  Often  the  begin- 
ning of  the  colon,  the  cecum  with  the  appendix,  and  the  ascending  colon, 
are  found  to  be  the  seat  of  the  tuberculous  infection.  A  tumor-like  mass 
is  felt  in  the  right  iliac  fossa,  and  the  sigmoid  flexure  in  the  left  iliac  fossa 
is  found  to  be  thickened,  whereas,  in  many  cases,  these  pathologic  changes 
in  the  flexure  of  the  colon,  particularly  upon  the  left  side,  cannot  be  deter- 
mined during  life. 

In  the  small  intestine,  on  account  of  the  fluid  or  thin,  semi-solid  con- 
sistence of  the  intestinal  contents,  disturbances  in  compensation  appear 
only  late,  after  the  intestinal  constriction  has  reached  an  extreme  degree. 
The  same  is  true  of  the  colon,  particularly  in  the  cases  which  run  their 
course  with  chronic  diarrhea.  As,  however,  in  most  cases  only  a  portion 
of  the  ulcer  is  cicatrized,  while  another  is  still  ulcerated  and  irritated  by 
the  intestinal  contents,  every  spasm  due  to  the  irritation  of  the  ulcer,  any 
accidental  inspissation  of  the  feces,  may  disturb  compensation  in  stenosis 
of  the  colon. ^ 

Tlie  first  sign  of  a  disturbance  in  compensation  is  the  distention  of 
the  intestine  above  the  stenosis.  It  may  be  circumscribed  and  soon  dis- 
appear, or  may  rapidly  increase  in  extent  and  distribute  itself  over  the 
entire  abdomen.  Great  peristaltic  unrest  combined  with  gurgling  and 
rumbling  in  the  abdomen  then  follows.  With  the  increase  of  the  abdom- 
inal distention  the  diaphragm  is  pressed  upward,  rendering  respiration 
difficult  and  causing  great  discomfort.  The  distress  is  increased  when 
nausea,  eructations,  singultus  and  a  tendency  to  vomit  appear,  or  when 
the  accumulations  of  decomposed  chyme  from  the  small  intestine  regurgi- 

1  Til  a  tuberculous  stenosis  of  the  ileo-cecal  valve  T  saw  a  chronic  invajrination 
of  the  diseased  lower  ileum  into  the  cecum  and  ascending  colon.  The  replacement 
was  ronijtaratively  easy,  and  subsequent  invagination  was  prevented  by  a  suitable 
haiidatrc.  Doitli  finally  occurred,  not  from  intestinal  occlusion,  but  chiefly  in  conse 
iliitiicc  of  ;i  complicating  valvular  lesion. 


{ 


INTESTINAL  TUBERCULOSIS  695 

tate  into  the  stomach  and  the  eructations  of  gas  or  the  vomitus  acquire  a 
disagreeable  odor. 

From  time  to  time  marked  peristaltic  waves  occur  in  the  greatly  dis- 
tended abdomen;  and  these  may  be  due  to  extreme  medianical  distention 
of  the  intestine,  to  chemical  irritation  from  the  highly  decomposed  intes- 
tinal contents,  to  reflexes,  to  the  overloading  of  the  stomach  in  eating  or 
drinking,  to  cooling  of  the  abdominal  surface  when  the  clothes  are  re- 
moved, or  to  mechanical  irritation  by  percussion  or  palpation  during  the 
examination  of  the  abdomen,  particularly,  however,  from  friction  of  the 
belly;  these  waves  forcibly  propel  the  fluid  intestinal  contents  downward 
toward  the  obstruction,  and  so  tensely  fill  a  greater  or  less  number  of 
intestinal  coils  in  front  of  the  stenosis  that  their  contours  may  be  dis- 
tinctly seen  through  the  thin  abdominal  wall.  These  inflated  intestinal 
coils  are  stiff  upon  palpation — intestinal  rigidity — ^those  nearest  the  steno- 
sis often  being  as  hard  as  wood,  tumor-like.  With  this  violent  peristalsis 
agonizing  pain,  resembling  uterine  pain,  sets  in  and  gradually  increases  to 
the  highest  intensity.  This  intestinal  rigidity  and  pain  remain  at  their 
acme  for  a  few  seconds,  occasionally  for  a  minute,  but  rarely  longer,  and 
then  suddenly  cease,  while  the  fluid  contents,  accompanied  by  loud  rum- 
bling and  gurgling  and  apparently  under  the  contraction  of  the  over- 
distended  intestinal  coils  (therefore  antiperistaltically),  are  again  forced 
back.  Before  this  regurgitation  occurs  we  occasionally  hear  in  the  stenosed 
intestinal  area  a  murmur  of  long  or  short  duration,  a  sort  of  squirting 
sound,  which  is  due  to  the  forced  passage  of  the  fluid  and  gas-containing 
intestinal  contents  through  the  stenosis. 

During  a  peristaltic  wave  of  this  kind  the  pain  is  often  so  great  that 
the  face  of  the  patient  becomes  contorted  as  in  severe  colic;  the  eyes 
sink  in  their  orbits,  the  nose  becomes  pointed,  and  the  expression  of  anx- 
iety and  suffering  thus  presented  resembles  the  facies  hippocratica.  Cold 
sweat  often  appears,  the  pulse  becomes  small  and  weak,  even  intermittent; 
in  very  debilitated  persons  syncope  follows. 

Gradually  the  patient  becomes  so  accustomed  to  this  wave-like  peristal- 
sis that  it  no  longer  causes  pain.  This  is  not  a  good  omen,  for  in  such 
cases  it  certainly  indicates  that  the  tonus  of  the  intestine  has  been  im- 
paired, that  a  great  dilatation  of  that  portion  of  the  bowel  situated  in 
front  of  the  obstruction  has  taken  place,  or  there  is  regurgitation  into 
the  small  intestine.  Improvement  in  such  cases  is  only  apparent  and 
transitory,  and  symptoms  of  intestinal  occlusion  rapidly  appear. 

In  both  varieties  of  intestinal  tuberculosis,  primary  and  secondary, 
the  local  symptoms  which  have  been  described  are  the  same,  that  is,  they 
may  be  the  same.  The  general  clinical  picture,  however,  varies  extraordi- 
narily, and  in  secondary  intestinal  tuberculosis  is  influenced  to  a  great 
extent  by  the  tubercular  infection  of  other  organs,  particularly  of  the  lungs, 
to  which  intestinal  tuberculosis  is  superadded. 


696        DIARRHEA,  CATARRH,  AND  INTESTINAL  TUBERCULOSIS 

Clinically  the  relations  are  frequently  such  that  the  first  bowel  symp- 
toms occur  only  in  an  advanced  stage,  in  pulmonary  tuberculosis  usually 
in  the  stage  of  cavity  formation,  and  then  profuse  diarrhea,  which  is  often 
of  colliquative  type,  rapidly  exhausts  the  remaining  strength  of  the  patient, 
who  has  been  reduced  by  long-existing  cough  and  expectoration,  by  under- 
nutrition, by  hectic  fever  and  sweats.  In  such  cases  the  intestinal  symp- 
toms are  but  slightly  developed  in  proportion  to  the  pulmonary  findings. 
The  ulcerative  process  in  the  intestinal  wall  often  shows  no  correspond- 
ence with  the  severity  and  persistency  of  the  diarrhea,  for  this  is  in  part  of 
toxic  nature. 

In  other  instances,  simultaneously  or  very  shortly  afterward,  the  symp- 
toms of  tuberculosis  of  the  lungs  and  of  the  intestines  develop  conjointly, 
and  as  phthisis  pulmonum  et  enterum  progress  until  the  patient  perishes. 
Even  here  the  stubborn  diarrhea  is  the  most  prominent  of  the  intestinal 
symptoms.  In  a  third  series  of  eases,  neither  pulmonary  nor  intestinal 
symptoms  are  of  special  severity;  the  cough  may  be  slight,  expectoration 
entirely  absent,  functional  disturbance  of  the  intestine  appears,  but  rather 
as  constipation  than  as  diarrhea;  nevertheless  the  patients  suffer  from 
unconquerable  loss  of  appetite,  have  the  phthisical  habit,  and  succumb  to 
the  slow  but  progressively  fatal  disease. 

Among  the  clinical  symptoms  of  another  group  of  cases  signs  on  the 
part  of  the  tuberculous  abdominal  organs  are  prominent:  Tuberculosis 
of  the  intestine  and  of  the  mesenteric  lymph-glands,  tuberculosis  of  the 
peritoneum,  tuberculosis  of  the  retroperitoneal  lymph-glands  and  of  the 
urogenital  apparatus.  In  some  of  these  patients  the  history  points  to  a 
pulmonary  catarrh  and  influenza,  to  a  pleuritis,  or  to  scrofulous  disease 
of  tlie  tonsils  or  the  glands,  to  bone  and  joint  disease  which  may  have 
existed  previously;  briefly  to  maladies  during  the  course  of  which  tuber- 
culous poison  has  been  conveyed  to  the  abdominal  and  pelvic  organs  either 
by  means  of  the  lymph  tracts  or  by  the  circulation.  Where  there  is  no  such 
history  we  may  be  dealing  with  primary  disease,  especially  with  primary, 
intestinal,  mesenteric  and  peritoneal  tuberculosis  in  children  and  in  the 
young.  In  these  cases,  as  a  rule,  obstinately  chronic  remissions  and  im- 
provements which  simulate  recovery  are  observed  for  years  and  decades, 
after  which  those  changes  in  .the  intestine  develop  which  lead  to  constriction 
of  the  intestine  and  to  the  formation  of  inflammatory  tumors  in  the  bowel. 

These  severe  changes  in  the  intestine  and  the  peritoneum — without 
internal  and  surgical  treatment — ^may  spontaneously  ameliorate.  True, 
a  new  metastatic  affection  may  appear  in  consequence  of  a  severe  infec- 
tion from  the  intestine,  and  this  is  not  rare,  abscess  may  occur  in  the 
mesenteric  lymph-glands,  peritonitis  may  develop  from  perforation,  or 
aoute  miliary  tuberculosis  may  rapidly  bring  about  a  fatal  termination. 

Miliari/  fiihercvlosis,  under  the  guise  of  a  severe  acute  infectious  dis- 
ease, may  set  in,  in  most  cases  suddenly  and  unexpectedly,  when  from  a 


INTESTINAL  TUBERCULOSIS  697 

latent  or  manifest  pathologic  focus  the  tuberculous  poison  reaches  the  cir- 
culation and  is  disseminated  throughout  the  body.  Miliary  tuberculosis  of 
the  intestine  as  such  is  usually  masked  behind  an  affection  of  other  organs, 
for  example,  of  the  lungs,  of  the  brain,  and  of  the  meninges.  If,  how- 
ever, in  consequence  of  a  tubercular  eruption  of  the  mucous  membrane 
and  serosa  of  the  intestine,  the  symptoms  of  diarrhea  and  of  meteorism 
become  especially  marked,  they  may  often  resemble  enteric  fever. 


DIAGNOSIS 

The  diagnosis  of  intestinal  tuberculosis  is  easy  when  the  symptoms 
of  an  affection  of  the  bowel  are  added  to  demonstrable  tuberculosis  in  other 
organs ;  when,  however,  they  appear  alone  and  no  other  signs  of  tuberculo- 
sis are  present,  they  cannot  always  be  recognized  as  of  tuberculous  origin, 
for  chronic  diarrhea  and  enteritis,  ulcer  of  the  intestine  and  constriction 
of  the  intestine,  inflammatory  ulceration  of  the  bowel,  and  adhesive,  exuda- 
tive, perforative  peritonitis  develop  also  from  many  other  causes.  When, 
therefore,  the  chronic  course  of  an  intestinal  affection,  fever,  sweating,  the 
habitus,  constitutional  peculiarities,  and,  last  but  not  least,  the  personal 
or  family  history  lead  us  to  suspect  tuberculosis,  we  must  seek  to  find 
the  tubercle  bacillus  as  the  cause  of  the  disease. 

Sometimes  the  tubercle  bacilli  can  be  readily  found  by  the  ordinary 
methods,  especially  in  the  shreds  of  mucus  and  tissue  which  are  voided 
with  the  feces.  Very  often,  however,  the  most  careful  search  for  tuber- 
cle bacilli  in  the  intestinal  evacuations  reveals  nothing,  and  to  this  must 
be  added  the  fact  that  when  only  isolated  bacilli  which  are  not  adherent 
to  the  intestinal  mucus  are  found  in  the  feces  these  are  by  no  means  posi- 
tive proof  that  the  bacilli  originate  from  a  tuberculous  affection  of  the 
bowel,  for  tubercle  bacilli  which  have  been  accidentally  swallowed  may 
be  present  in  the  feces,  and  may  be  excreted  unaltered. 

If  in  such  cases  we  cannot  wait  until  the  probable  diagnosis  is  con- 
firmed by  subsequent  observation,  there  is  no  danger  in  making  an  early 
diagnosis  by  the  cautious  injection  of  tuberculin. 

Besides  the  clinical  examination  of  the  patient,  the  systematic  investi- 
gation of  the  dejecta,  especially  its  quality  and  quantity,  and  frequently 
also  the  examination  of  the  rectum  by  palpation  and  rectoscopy.  is  abso- 
lutely necessary  for  the  special  diagnosis  of  the  intestinal  affection.  The 
feces  should  be  examined  according  to  the  rules  given  in  preceding  chap- 
ters. In  addition,  if  we  suspect  the  existence  of  tuberculous  ulcers  this 
suspicion  will  be  confirmed  by  finding  an  admixture  of  blood  and  pus  with 
the  feces  and  a  bloody  discoloration  of  the  mucus  (Teichmann's  or 
Weber's  tests,  spectroscopy).  Furthermore,  the  exceedingly  offensive  odor 
of  the  flatus  and  the  feces  in  the  chronic  diarrhea  of  phthisical  patients 
is  noteworthy  and  not  without  diagnostic  importance;  it  adheres  most 


698        DIARRHEA,   CATARRH,   AND   INTESTINAL  TUBERCULOSIS 

tenaciously  to  the  bed-clothes  and  the  body  linen  of  the  patient,  and  by 
the  experienced  physician  is  easily  recognizable  upon  entering  the  sick 
room.  Besides  the  functional  weakness  of  the  digestive  juices  and  the 
limitation  of  intestinal  absorption  in  consequence  of  increased  peristalsis, 
a  cause  of  this  immoderate  intestinal  decomposition  is  the  profuse  admix- 
ture of  pathological  secretions  from  the  intestine  with  the  feces.  Fat 
absorption  suffers  early  and  most  severely  in  the  chronic  diarrhea  of  patients 
widi  intestinal  tuberculosis,  and  to  an  extraordinary  degree  in  those  cases 
of  primary  or  even  of  secondary  intestinal  tuberculosis  in  which  the  mes- 
enteric lymph-glands  are  to  a  great  extent  diseased.  Nevertheless,  there  is 
less  fat  in  diarrheic  feces  than  is  found  in  steatorrhea  with  disease  of  the 
liver  and  of  the  pancreas. 

Corresponding  to  this  excessive  intestinal  decomposition  we  frequently 
find  in  chronic  diarrhea  from  intestinal  tuberculosis  a  decided  increase  of 
indican  and  of  ethyl  sulphuric  acid  (C2H5HSO4)  in  the  urine. 

TREATMENT 

The  treatment  of  intestinal  tuberculosis  is  exceedingly  difficult,  espe- 
cially when  it  appears  as  a  complication  of  tuberculous  disease  of  other 
organs,  and  the  obstinate  diarrhea  which  accompanies  it  makes  impossible 
the  employment  of  one  of  the  most  important  remedies  in  the  treatment 
of  tuberculosis,  namely,  hypernutrition.  Recognizing  this  condition  in 
pulmonary  tuberculosis,  we  must  be  exceedingly  careful  to  see  that  the 
sputum  rich  in  bacilli  does  not  find  its  way  into  the  intestine  by  degluti- 
tion. Unfortunately,  we  cannot  prevent  small  children  from  swallowing 
sputum;  even  with  older  ones  it  is  difficult  to  enforce  this  prophylactic 
measure,  as  well  as  with  very  sensitive  patients  who  regard  the  expectoration 
of  sputum  as  a  violation  of  estheticism  which  is  more  flagrant  than  their 
violation  of  the  laws  of  hygiene-  by  swallowing  it.  The  educational  effect 
of  sanatoria  for  pulmonary  diseases  is  especially  evident  in  their  recognition 
of  the  preventability  of  autoinfection. 

In  the  prophylaxis  of  primary  intestinal  tuberculosis,  certain  sanitary 
laws  in  regard  to  the  inspection  of  meat  and  the  consumption  of  meat 
from  animals  infected  by  tuberculosis  are  operative.  But  a  greater  dan- 
ger than  confronts  adults  by  the  use  of  meat  threatens  nurslings  and 
young  children  by  the  ingestion  of  milk  from  tuberculous  cows.  Marag- 
liauo  and  other  investigators  made  an  attempt  to  immunize  these  animals 
and  to  obtain  from  them  a  curative  serum,  v.  Behring  systematically  car- 
ried out  his  immunization  theory  which  he  designates  as  Jennerization 
not  only  in  a  few  animals  but  also  in  entire  herds  of  cattle.  According 
to  his  experience,  it  seems  to  be  possible  to  introduce  antibodies  into 
nurslings  and  small  children  by  ordinary  nutrition  with  the  milk  of  cows 
tliat  have  been  rendered  immune  to  tuberculosis,  and  thus  to  tide  them 
over  the  dangerous  period  of  contamination. 


INTESTINAL  TUBERCULOSIS  699 

Many  attempts  have  been  made  to  find  a  specific  curative  serimi  for 
tuberculosis.  All  hopes  based  upon  remedies  new  or  old,  or  upon  patent 
medicines,  have  been  blasted,  and  the  enormous  amount  of  energy  and 
time  consumed  to  find  a  specifically  acting  serum  has  led  to  no  satisfac- 
tory results.  Preventive  inoculations  with  attenuated  tuberculous  virus 
and  injections  into  the  tuberculously  diseased  body  of  other  bacteria  antag- 
onistic to  tubercle  bacilli  have  not  found  their  way  into  practice. 

In  the  year  1890,  at  the  International  Medical  Congress  in  Berlin, 
the  communication  of  R.  Koch  that  he  had  obtained  a  product  from 
tubercle  bacilli  which  would  have  a  specific  effect  upon  the  tuberculously 
diseased  organism,  this  substance  being  first  designated  as  Koch's  lymph 
and  later  as  tuberculin,  made  a  great  furore,  and  awakened  intense  enthu- 
siasm; but  here  popular  enthusiasm  was  rapidly  followed  by  a  depressing 
disillusionment  which  lasted  until,  at  the  beginning  of  this  century  and 
after  years  of  critical  labor  and  study,  it  was  demonstrated  that  Robert 
Koch's  remedy  forms  the  basis  of  an  etiologic  specific  therapy  of  tuber- 
culosis, and  that  among  numerous  tuberculosis  specifics  which  had  in  the 
meantime  been  produced  his  tuberculin  deserves  preference  as  a  diagnostic 
remedy. 

From  his  researches  R.  Koch  assumed  that  incipient  phthisis  could  cer- 
tainly be  cured  by  his  remedy ;  "  this  may  still  be  true  of  the  cases  not  too 
far  advanced."  It  is  therefore  of  the  utmost  importance  for  the  success 
of  the  specific  treatment  that  we  use  Koch's  tuberculin  as  early  as  possible. 
In  doubtful  cases  which  appear  to  be  tuberculosis  we  now  employ  the 
tuberculin  injections  in  order  to  make  the  diagnosis  certain;  hence,  those 
cases  are  particularly  suitable  for  tuberculin  treatment  in  which  a  posi- 
tive reaction  follows  the  diagnostic  injection.  R.  Koch  has  produced  vari- 
ous tuberculin  substances;  but  only  two  of  these  are  employed,  the  old 
tuberculin,  the  original  Koch's  lymph,  and  the  new  tuberculin  which  is' 
an  emulsion  of  tubercle  bacilli.  For  diagnostic  purposes  the  former  is 
preferable;  but  for  therapeutic  purposes  after  the  old  tuberculin  has  given 
a  positive  reaction  in  a  diagnostic  test,  and  when  this  therapeutic  use  does 
not  produce  the  desired  effect,  the  new  tuberculin  should  also  be  tried. 

The  technic  is  simple  and  presupposes  strict  asepsis;  prior  to  the 
diagnostic  injection,  the  temperature  of  the  patient  should  be  determined 
by  a  temperature  record  taken  every  three  hours  for  two  or  three  days. 
The  Hochst  tuberculin  is  used  in  a  pipette  divided  into  a  hundred  parts; 
it  is  diluted  with  boiled  water  in  a  proportion  of  1 :  1,000  or  0.1 :  100,  so 
that  each  division  of  a  Pravaz  syringe  will  then  contain  .1  of  a  milli- 
gram of  tuberculin.  This  dose  is  injected  into  the  back  between  the 
shoulder  blade  and  the  vertebral  column,  and  the  temperature  is  taken 
earlv  in  the  morning  as  there  is  usuallv  a  reaction  after  twelve  hours. 
"  A  rise  in  temperature  of  .9°  F.  above  the  normal  temperature  is  regarded 
as  a  reaction.     If  with  .1  of  a  milligram  there  is  no  reaction  but  a  rise 


700        DIARRHEA,  CATARRH,   AND  INTESTINAL  TUBERCULOSIS 

in  temperature  of  about  ,5°  to  .7°  F.,  in  the  next  injection,  which  should 
follow  in  about  three  days,  a  dose  of  .2  of  a  milligram  will  produce  a 
distinct  reaction.  If,  after  the  first  injection,  there  is  no  rise  in  tem- 
perature, for  the  second  injection  I  give  .5  of  a  milligram,  for  the  third, 
one  milligram,  etc.,  until  in  adults  10  milligrams  at  most  are  given;  in 
children,  according  to  Koch,  5  milligrams  must  be  regarded  as  a  maximum 
dose.  If  these  doses  fail  to  produce  a  rise  in  temperature  of  at  least  .9°  F. 
the  reaction  may  be  regarded  as  negative"   (Moeller).^ 

The  therapeutic  employment  of  tuberculin  is  the  same  as  the  diag- 
nostic. The  dose  is  regulated  by  the  reaction  in  a  concrete  case,  a  marked 
individual  reaction  is  avoided,  and  the  injections  should  not  too  rapidly 
succeed  each  other,  being  usually  given  not  oftener  than  twice  a  week. 
A  decrease  in  the  intensity  of  the  reaction  after  large  individual  doses  of 
tuberculin  indicates  improvement.  Eecovery  may  be  assumed  if,  after 
months  or  years,  repeated  diagnostic  injections  of  tuberculin  no  longer 
produce  a  reaction. 

In  addition  to  the  specific  treatment  of  tuberculosis,  symptomatic  treat- 
ment of  the  bowel  disturbances  in  intestinal  tuberculosis  should  not  be  left 
out  of  consideration.  In  far  advanced  cases  which  are  unsuitable  for 
specific  treatment,  or  in  which  there  are  complications,  the  greatest  weight 
is  to  be  attached  to  the  symptomatic  treatment  of  the  intestinal  affection, 
and  this  must  be  pursued  according  to  the  plan  proposed  in  the  previous 
chapters. 

Therefore  in  the  chronic  diarrhea  of  intestinal  tuberculosis  flushing 
of  the  intestine  from  above  by  drinking  mild  mineral  waters  as  warm  as 
possible  or  infusions  of  peppermint  and  other  aromatic  drugs  early  in 
the  morning  on  an  empty  stomach,  or  the  persistent  irrigation  of  the 
intestine  from  below  with  dilute  saline  solutions,  mineral  waters  (Ems, 
'Selters,  Carlsbad,  Vichy),  or  chamomile  tea  may  be  resorted  to, 
possibly  with  disinfecting  or  deodorizing  substances,  such  as  salicylic  acid 
(1:1,000),  creosote,  and  perhaps  menthol.  When  there  is  immoderate 
intestinal  decomposition  menthol  in  the  form  of  a  coa,ted  pill  may  be  given 
frequently  and  at  regular  intervals  during  the  day  until  the  odor  is  no 
longer  perceptible.  Thymol,  which  markedly  corrodes  the  mucous  mem- 
brane of  the  mouth,  must  be  given  in  gelatin  capsules,  or,  like  salol  and 
iodoform,  in  Sahli's  glutoid  capsules.  In  conclusion,  small  doses  of  opium 
wliich  should  be  invariably  given  at  meal-time  (in  pill  form  in  combina- 
tion with  hydrochloric  acid  or  extr.  ligni  campech.)  are  worthy  of  trial, 
as  also  the  occasional  administration  of  bismuth  and  tannic  acid  prepara- 
tions and  alum  whey. 

When  there  is  constipation,  either  occasional  or  persistent,  laxatives 

1  See  chapter  by  Moeller  upon  "  The  Specific  Treatment  of  Chronic  Pulmonary 
Tuberculosis  "  in  the  "  Handbuch  der  Therapie,"  etc.,  by  Schroeder  and  Blumenfeld. 
Earth's  Verlag,  Leipzig,  1904. 


INTESTINAL  TUBERCULOSIS  701 

by  mouth  are  to  be  avoided,  as  these  are  liable  to  damage  the  general 
nutrition  by  wasting  unabsorbed  nutritive  material,  and  the  bowels  must 
be  regulated  by  systematic  oil  treatment.  Occasionally,  instead  of  pure 
poppy-seed  oil  or  sesame  oil,  the  addition  of  creosote  to  the  oil  (^  to  1  per 
cent.)  appears  to  be  beneficial.  In  inflammatory  and  ulcerative  processes 
in  the  colon  and  in  the  rectum,  oil  enemata  of  proper  proportions,  regu- 
larly given  at  a  suitable  time,  render  excellent  service.  They  exert  a 
powerful  effect  upon  the  motor  and  sensory  irritative  phenomena,  and 
favor  and  promote  the  healing  of  wounds  by  the  protection  which  they 
afford  to  the  exposed  and  granulating  tissues.  When  there  is  marked 
tenesmus,  an  addition  of  tincture  of  opium  (5  to  10  drops)  to  an  oil 
enema  is  useful,  provided  the  opium  does  not  lead  to  constipation  and 
the  inspissation  of  the  feces. 

With  the  careful  observance  of  all  the  conditions  which  may  arise, 
we  undoubtedly  have  in  the  oil  treatment  a  prophylactic  as  well  as  cura- 
tive measure  for  hemorrhages  and  intestinal  ulcers,  at  least  the  deep- 
seated  ones,  and  suited  to  the  individual  requirements.  By  the  addition 
of  bismuth  subnitrate  to  the  oil  (rubbing  the  bismuth  with  lukewarm  oil 
in  a  mortar),  I  believe  that  in  many  cases  I  have  promoted  and  hastened 
the  healing  of  ulcers  in  the  rectum  and  the  lower  colon.  The  effect  of 
the  bismuth  and  oil  upon  hemorrhages  did  not  appear  to  be  any  greater 
than  that  of  pure  oil. 

On  the  other  hand,  bismuth  is  a  valuable  remedy,  if  applied  in  sub- 
stance directly  to  the  ulcerated  granulating  surfaces  in  the  rectum.  This 
can  be  accomplished  in  the  following  manner:  After  introducing  a  cylin- 
drical intestinal  speculum  as  high  as  possible  (and  removing  the  obtura- 
tor) the  intestine  is  cleansed  by  irrigation;  then  by  means  of  an  insufflator, 
or  by  a  glass  spoon  with  a  long  handle,  or  by  an  applicator  which  can 
be  introduced  through  the  intestinal  speculum,  the  latter  being  then  slowly 
withdrawn,  bismuth  can  be  applied  to  the  diseased  intestinal  mucous  mem- 
brane. Touching  the  ulcerated  surface  with  a  1,  2  or  3  per  cent,  silver 
nitrate  solution  prior  to  the  application  of  bismuth  has  often  been  found 
beneficial,  but  the  silver  nitrate  frequently  so  stimulated  peristalsis  that 
the  bismuth  was  soon  ejected.  The  same  is  true  of  liquor  ferri  sesqui- 
chlorati  applied  to  bleeding  ulcers  and  of  tampons  in  the  rectum.  For 
this  reason  I  have,  as  a  rule,  used  locally  either  oil  or  bismuth  alone,  or 
bismuth  suspended  in  water  as  in  the  treatment  of  gastric  ulcer.  This 
was  injected  into  the  intestine,  and  if  hemorrhage  from  the  bowel  fol- 
lowed I  administered  alum  whey  to  the  patient. 

In  a  few  instances  adrenalin  was  employed  as  an  addition  to  small 
enemata  of  oil  (20  to  30  drops  of  a  1-1,000  alcoholic  solution)  or  as 
an  addition  to  injections  of  water  for  rectal  ulcers  which  showed  a  tendency 
to  hemorrhage;  I  have  as  yet  come  to  no  conclusion  regarding  the  value 
of  this  remedy. 


702        DIARRHEA,  CATARRH,   AND  INTESTINAL  TUBERCULOSIS 

In  cases  of  ulcerating  intestinal  tuberculosis  with  profuse  diarrhea 
and  an  admixture  of  blood  in  the  diarrheic  feces,  besides  such  measures 
as  are  necessary  to  arrest  the  diarrhea  I  have  administered  gelatin  by 
mouth  and  have  also  given  it  in  small  enemata.  Bismuth  continues  much 
longer  in  suspension  in  gelatin  than  in  water,  therefore  gelatin  and  bis- 
muth enemata  are  sometimes  very  effective  in  the  local  treatment  of 
ulcers.  Finally,  when  tuberculous  ulcers  in  the  rectum  may  be  reached, 
cauterization  (under  anesthesia)  with  a  Paquelin  cautery  may  be  em- 
ployed to  quiet  local  hemorrhage.  I  have  known  this  method  of  treat- 
ment for  hemorrhages  to  be  very  beneficial.  Cauterization  is  unsuitable 
for  the  general  treatment  of  rectal  ulcers  because  a  single  scarification  is 
insufficient,  and  repetitions  of  the  process,  which  are  only  possible  under 
anesthesia,  are  too  painful,  the  pain  often  lasting  for  several  days  after- 
ward. 

In  the  surgical  treatment  of  intestinal  tuberculosis  many  measures  may 
1)0  indicated,  but  these  vary  according  to  the  individual  circumstances  of 
the  ease.  In  stenosis  of  the  intestine  in  which  a  tuberculous  process  so 
lessons  its  permeability  that  a  condition  of  motor  insufficiency  develops, 
the  obstruction  must  be  relieved  by  surgical  aid  or  removed.  In  some 
cases  the  mode  of  operation  can  only  be  decided  upon  after  the  abdominal 
cavity  is  opened  and  Ave  have  recognized  the  exact  anatomical  relations 
by  palpation  with  a  finger  or  by  inspection.  If,  in  a  given  case  of  intes- 
tinal stenosis,  the  pathologic  focus  shows  local  limitation,  resection  of 
tlie  stenosed  intestinal  area  must  be  attempted,  and  if  in  another  instance 
the  pathologic  changes  show  great  local  extension,  enteroanastomosis  must 
1)6  performed  to  overcome  the  narrowed  or  occluded  intestinal  coils.  In 
cases  in  which  none  of  these  methods  of  operation  can  be  carried  out 
because  of  technical  difficulty,  or  on  account  of  advancing  debility  of  the 
patient,  we  must  be  content  with  enterostomy  at  a  suitable  point.  In 
some  cases  of  tuberculous  intestinal  occlusion  the  formation  of  such  an 
artificial  anus  is  an  indicatio  vitalis.  The  arrest  of  the  difficulties,  and  the 
marked  improvement  in  local  and  general  conditions  after  this  compara- 
tively slight  symptomatic  operation  justifies  its  performance  also  in  cases 
of  intestinal  tuberculosis  in  which  there  is  no  organic  stenosis,  but  in 
which,  however,  extensive  ulcerative  processes  in  the  colon  cause  profound 
suhjoctive  disturbances,  such  as  severe  diarrhea  which  cannot  be  controlled 
by  intoinal  remedies,  and  especially  hemorrhage.  Colostomy  above  the 
diseased  intestinal  region  excludes  the  latter  from  taking  part  in  the  labor 
of  digestion,  induces  much  better  conditions  for  the  healing  of  the  ulcer, 
renders  possible  a  more  active  local  treatment  of  the  diseased  intestinal 
mucous  membrane,  and,  what  is  more  important,  enables  us  to  give  suffi- 
cient nourishment  and  a  general  treatment.  Whether  the  artificial  anus 
must  later  be  closed  depends  upon  the  further  progress  of  the  case. 

Tuberculosis  of  the  rectum  most  frequently  necessitates  surgical  meas- 


INTESTINAL  TUBERCULOSIS  703 

ures  because  inflammatory  and  ulcerative  processes  in  this  portion  of  the 
intestine  which  is  not  covered  by  peritoneum  readily  penetrate  from  the 
intestinal  Avail  to  the  perirectal  cellular  tissue,  or  perforate  it  and  there 
form  abscesses  which  must  be  incised.  Both  incised  and  spontaneously 
perforating  perirectal  abscesses  leave  the  familiar  internal  or  external 
anal  fistula  which  may  also  be  complete,  for  the  treatment  of  which  exten- 
sive division  through  the  sphincter  is  the  best  remedy. 

The  tuberculous  patient  in  all  stages  of  his  disease  needs  every  pos- 
sible advantage  that  can  accrue  from  a  hygienic  mode  of  life  and  careful 
nursing.  Patients  with  intestinal  stenosis  do  not  reap  the  same  benefit 
from  treatment  in  sanatoria  and  large  institutions  for  the  cure  of  tuber- 
culosis as  those  suffering  from  pulmonary  tuberculosis,  since,  owing  to 
the  nature  of  the  intestinal  disturbance,  their  nutrition  necessitates  greater 
specialization  than  is  practicable  in  a  large  institution  in  which  general 
over-nutrition  is  to  be  carried  on  for  some  time.  Nor  are  they  adapted 
for  treatment  in  high  altitudes  and  at  the  seashore,  for  they  are  often 
very  susceptible  to  changes  of  temperature;  hence  bath  cures,  salt  baths, 
and  (when  intestinal  tuberculosis  is  combined  with  peritonitis)  peat  baths 
can  only  come  into  consideration  after  the  intestinal  disturbance  shows 
a  certain  degree  of  improvement  or  has  become  latent. 

Until  such  amelioration  occurs,  nutritive  therapy  must  be  one  of  the 
chief  aims  of  the  treatment,  and  for  this  the  fundamental  laws  have  been 
detailed  in  preceding  chapters.  As  soon  as  the  condition  of  the  intestine 
will  warrant  it  we  order  a  mixed  diet,  preferably  of  boiled  flour  foods, 
in  such  quantities  as  may  substitute  for  losses  which  have  taken  place 
in  consequence  of  fever,  diarrhea  and  the  under-nutrition  due  to  the  latter, 
and  will  finally  bring  about  an  increase  in  weight.  Care  and  observation 
by  coproscopy  will  determine  the  proper  additions  of  fat  to  the  nutrition, 
for  it  has  been  proven  by  experience  that  in  intestinal  dyspepsia  due  to 
tuberculosis  fat  absorption  suffers  early  and  continuously,  and  in  such  a 
way  that  even  the  most  perfect  of  foods,  milk,  is  often  not  well  borne. 


CONSTIPATION   AND   HEMORRHOIDS 

By  J.  BOAS,  Berun 

Constipation  and  hemorrhoids,  as  is  well  known,  belong  to  the  most 
common  affections  of  the  intestinal  canal.  Perhaps  because  scientifically 
resultless,  some  physicians  regard  these  conditions  as  a  quantite  negligeable 
— for  there  is  in  medicine  a  certain  unmistakable  timocratic  principle. 
Possibly,  even  to-day,  the  opinion  is  extant  that  constipation  and  hemor- 
rhoids are  slight,  though  troublesome,  evils,  and,  here  and  there,  an  im- 
pression exists  that  internal  medicine  taken  altogether  is  powerless  per- 
manently to  relieve  this  condition. 

I  hope  to  convince  all  that  neither  of  these  views  is  correct.  Above 
all,  1  wish  to  state  explicitly  that  the  treatment  of  constipation  and  hemor- 
rhoids is  one  of  the  most  fruitful  fields  of  internal  medicine,  and  that  it 
is  our  imperative  duty  as  physicians  thoroughly  to  acquaint  ourselves  with 
this  condition  since  it  represents  the  principal  branch  of  the  so-called 
"  Nature  Cure."  It  would  be  actually  derogatory  to  our  science  if  we 
were  unable  to  obtain  similar,  if  not  better  results  than  these  empirics. 

But,  before  proceeding  to  the  treatment  of  habitual  constipation  and 
hemorrhoids,  I  shall  first  define  and  portray  our  conception  of  the  first 
mentioned  symptom-complex. 

CONSTIPATION 

We  may  differentiate  between  physiologic  and  pathologic  constipa- 
tion. Constipation  is  physiologic  so  long  as  the  delay  in  the  evacuation 
of  feces  produces  no  disturbance,  not  even  slight,  in  the  intestinal  tract 
or  in  remote  organs.  These  physiologic  effects  we  have  learned  to 
recognize  in  other  organs,  for  example,  in  the  heart  (physiologic  brady- 
cardia), in  the  female  genitalia  (appearance  of  menstruation  every  two 
or  three  months),  etc. 

Within  these  limits  the  degree  of  diminished  activity  may  vary  widely. 
Much  found  in  earlier  literature,  for  example,  the  report  that  patients 
have  had  only  one  or  two  evacuations  in  a  year,  may  be  referred  to  the 
domain  of  legend.  But  I  have  certainly  seen  a  patient  who  had  a  fecal 
evacuation  only  once  in  four  weeks,  and  then  it  had  to  be  each  time 
extracted  digitally  by  a  nurse. 

This  patient,  on  account  of  some  gynecologic  affection,  had  undergone 
several  laparotomies ;  probably  adhesions  had  formed  between  different  por- 
704 


ETIOLOGY  705 

tions  of  the  intestines.  In  every  other  respect,  however,  her  condition  left 
nothing  to  be  desired.  Her  appearance  was  robust,  the  urine  was  normal, 
and  the  amount  of  indican,  in  particular,  was  not  increased. 

In  another  ease,  that  of  a  lady,  aged  69,  I  obtained  the  history  that 
the  patient  had  been  small  and  weak  from  her  youth.  Only  once  a  week 
was  there  any  desire  to  have  a  fecal  evacuation.  She  had  experienced  no 
discomfort  from  this  throughout  her  entire  life,  but  she  later  succumbed 
to  carcinoma  of  the  esophagus. 

^Nevertheless,  such  diminished  physiologic  activity  must,  at  least,  be 
looked  upon  as  a  chronic  anomaly  and  is  certainly  rare.  Usually  this 
results  in  a  slow  or  rapid  systemic  disturbance,  and  physiologic  constipa- 
tion leads  to  true  pathologic  habitual  constipation. 

But  we  must  be  even  more  precise  than  this : 

Not  every  case  of  chronic  constipation  can  be  designated  as  habitual. 
On  the  contrary,  by  custom  this  nomenclature  has  been  applied  only  to 
those  anomalies  in  which,  in  the  first  place,  there  are  no  other  primary 
disturbances;  and  secondly,  to  the  cases  in  which  the  intestinal  evacua- 
tion as  such  is  nowise  due  to  mechanical  or  toxic  effects  (for  example, 
lead  colic).  It  is  readily  seen  that  such  a  limitation  cannot  possibly  be 
absolute,  that  under  the  picture  of  simple  habitual  constipation  all  sorts 
of  pathologic  pictures,  occasionally  serious  and  prognostically  unfavorable 
ones,  may  be  masked.  Nevertheless,  we  must  be  content,  as  elsewhere  in 
the  practice  of  medicine,  with  a  symptomatic  diagnosis  so  long  as  we  have 
no  deeper  insight,  so  long  as  other  decisive  factors  have  not  been  added, 
or,  finally,  while  the  entire  course  of  the  disease  receives  another  inter- 
pretation. 

Here,  at  the  beginning  of  our  description,  we  must  necessarily  be  sus- 
picious of  the  diagnosis  of  habitual  constipation  in  those  eases  in  which 
the  facts  are  not  absolutely  uniform  and  clear.  In  the  chapter  devoted 
to  diagnosis  we  shall  have  an  opportunity  to  justify  this  position  in  extenso. 


ETIOLOGY 

ETIOLOGY   OF  HABITUAL  CONSTIPATION 

In  consonance  with  the  above  definition  we  can  only  enumerate  those 
causes  of  habitual  constipation  in  which  organic  changes,  no  matter  of 
what  nature,  are  absent.  The  number  of  secondary  factors  which  induce 
habitual  constipation  is  so  great  that  an  exhaustive  compilation  is  impos- 
sible. 

The  causal  factors  of  idiopathic  constipation  are  practically  important 
because  with  their  removal  the  affection  is  Occasionally  cured. 

In  imbiased  judgment,  we  must  exclude  a  large  group  in  which  a  dis- 
tinct, causal  etiology  cannot  be  recognized.     The  affection  is  mild  at  the 


706  CONSTIPATION  AND  HEMORRHOIDS 

onset,  but  the  intestine  becomes  sluggish,  although  the  patient  attaches 
but  little  importance  to  this  until  gradually  the  necessity  for  relief  causes 
a  resort,  usually  to  purgatives,  more  rarely  to  injections.  As  the  former 
gradually  lose  their  effect,  more  active  purgatives  are  employed,  and  the 
condition  is  thus  carelessly  allowed  to  continue  year  in,  year  out,  until, 
finally,  all  remedies  are  inactive,  or  pain  and  catarrhal  phenomena  neces- 
sitate rational  and  comprehensive  interference. 

Habitual  constipation  may  frequently  be  referred  to  hereditary  influr 
ences.  Constipation  to  a  greater  or  less  extent  prevails  in  entire  families. 
Occasionally  the  condition  has  its  beginning,  as  I  have  repeatedly  observed, 
in  the  first  days  or  weeks  after  birth,  and  even  in  this  early  stage  it  is 
sometimes  very  difficult  to  combat. 

This  hereditary  predisposition  is  often  combined  with  a  lack  of  true 
"  hoirel  training."  The  children  are  not  taught  to  observe  regularity  in 
regard  to  their  bowel  movements  or — and  this  is  particularly  the  case  with 
young  girls — false  modesty  leads  the  children  to  artificial  suppression. 
This  sin  is  most  frequently  committed  in  schools,  while  upon  visits,  and  in 
summer  resorts. 

In  rare  cases  this  form  of  constipation  may  be  due  to  a  dilatation  of  the 
colon  (probabl}^  congenital),  the  so-called  Hirschsprung's  disease,  the 
prognosis  of  which,  even  under  the  operation  recently  proposed,  is  very 
unfavorable. 

A  frequent  cause  of  habitual  constipation,  which  I  have  called  alimen- 
tary constipation,  is  due  to  improper  nutrition;  in -particular,  the  immod- 
erate ingestion  of  meat  and  the  avoidance  of  vegetables  leaving  a  residue, 
as  well  as  the  use  of  rye  bread  and  varieties  of  sugar. 

The  physician  himself  is  responsible  for  alimentary  constipation  more 
frequently  than  is  generally  supposed.  As  an  example,  I  may  mention 
tlie  diet  prescribed  for  diabetes,  which,  as  employed  in  most  cases,  neces- 
sarily produces  constipation.  A  milk  diet,  too,  as  ordered  in  anemia,  chlo- 
rosis, and  nephritis,  frequently  has  an  unfavorable  effect,  or,  at  least,  it 
does  not  produce  the  desired  result  because  the  constipation  which  usually 
follows  the  use  of  a  milk  diet  is  too  little  considered. 

To  this  must  be  added  another  common  form  of  constipation  which 
is  not  sufficiently  borne  in  mind,  and,  indeed,  is  not  generally  recognized : 
Thai  due  to  the  employment  of  drugs.  In  acute  intestinal  disturbances  and 
in  cholera  nostras,  but  particularly  in  appendicitis,  and  probably  also  in 
other  forms  of  peritonitis,  in  occlusion  of  the  bowel  or  in  pseudo-ileus,  large 
doses  of  opiates  or  the  belladonna  preparations  are  frequently  used  or, 
more  correctly,  wasted,  and  this  is  followed,  as  I  have  seen  in  innumerable 
instances,  by  severe  and  most  unyielding  intestinal  paresis.  Besides 
opiates,  substances  containing  tannic  acid  are  often  too  long  employed 
for  diarrhea,  and.  occasionally  even  after  a  short  time,  produce  constipa- 
tion :  in  the  course  of  years  I  have  seen  several  well  developed  cases  of  this 


ETIOLOGY  707 

kind.  We  can  scarcely  be  wrong  in  assuming  that  extremely  severe  changes 
in  function  are  du6  to  an  abnormal  tannic  acid  effect. 

As  a  curious  abnormality,  I  shall  here  call  attention  to  a  natural  in- 
crease of  habitual  constipation  which  I  have  repeatedly  observed  in  my 
practice :  The  purposely  limited  ingestion  of  food.  While  it  does  not 
seem  plausible,  many  individuals,  mostly  neurasthenics,  have  an  idea  that 
by  a  natural  limitation  of  the  ingestion  of  food  they  may  relieve  their 
difficulties  due  to  constipation. 

A  much  more  frequent  cause,  and  one  which  requires  less  considera- 
tion than  the  foregoing,  is  the  familiar  one,  lack  of  exercise,  which  has  been 
much  discussed,  and  which  also  plays  an  important  role  in  the  etiology  of 
hemorrhoids,  as  we  shall  later  have  occasion  to  note.  The  influence  of 
active  exercise  and,  where  this  is  impossible,  of  passive  exercise  cannot  be 
doubted,  yet  we  must  be  careful  not  to  exaggerate  the  importance  of  this 
as  a  causative  factor.  For  example,  it  is  generally  known  that  extreme 
habitual  constipation  is  found  in  persons  whose  occupations  certainly  indi- 
cate no  want  of  exercise,  for  example,  in  farmers,  army  officers,  gymnasts, 
bicyclists  and  others.  On  the  other  hand,  I  have  several  times  called  atten- 
tion to  the  fact  that  in  certain  forms  of  habitual  constipation  which  will 
shortly  be  described  bodily  rest  is  much  more  likely  to  relieve  the  affection 
than  forced  exercise. 

One  of  the  chief  causes  of  habitual  constipation  is  neurogenous,  or 
psychogenous,  which  is  a  better  term.  It  is  an  almost  constant  accom- 
paniment of  general  neurasthenia,  but  may  occasionally  present  itself  as 
a  substantive  intestinal  neurosis. 

A  widely  distributed  type  of  neurogenous  constipation  is  found  in 
enteroptosis,  the  relation  of  which  to  neurasthenia  cannot  to-day  be  doubted 
even  tliough  their  intimate  connection  is  still  a  mooted  question.  As 
acute  psychical  factors  may  generate  a  state  of  anxiety,  an  irritation  of 
peristalsis  from  nerve  tracts  which  we  refer  to  the  splanchnic  area,  so  by 
chronic  irritation  there  may  be  a  permanent  diminution  of  the  energy  of 
innervation. 

I  recently  treated  Miss  D.,  a  teacher,  aged  34,  who,  since  Whitsuntide,  1901,  had 
suffered  from  occasional  diarrhea,  swelling  of  the  feet,  pain  in  the  left  hypochondrium, 
insomnia  and  great  lassitude.  During  her  holidays  there  was  marked  improvement, 
but  soon  after  resuming  teaching  marked  nervousness  and  constipation  simultaneously 
appeared.  Purgatives,  to  which  the  patient,  however,  had  never  accustomed  herself, 
were  without  effect.  In  the  beginning  simple  enemata,  and,  later,  even  enemata  of 
oil,  were  ineffectual.  She  ceased  to  teach,  and  the  condition  of  the  bowels  steadily 
improved  until  gradually  there  was  a  profuse  and  spontaneous  evacuation  daily. 
Constipation  reappeared  only  after  excitement,  even  though  of  a  pleasant  nature. 

In  other  cases  of  psycliogenous  constipation,  the  greatest  variations 
between  constipation  and  diarrhea  may  be  observed. 

[As  an  additional  cause  of  chronic  constipation,  one  finds  in  America 


708  CONSTIPATION   AND  HEMORRHOIDS 

the  habit  of  irregularity  and  postponement  of  defecation  because  of  the 
discomfort  of  the  American  outdoor  privy,  especially  in  the  winter  months. 

It  is  to  be  noted,  too,  that  child-bearing  women  who  suffer  from  dias- 
tasis of  the  recti  abdominalis  muscles  and  consequent  weakness  of  the 
abdominal  walls  suffer  more  or  less  from  ptosis  of  the  intestines.  The 
weakened  abdominal  walls  prevent,  too,  the  abdominal  press,  which  is  so 
necessary  in  the  act  of  defecation. 

Anal  fissure  and  other  painful  conditions  of  the  fundament  with  result- 
ing spasm  of  the  external  sphincter  result  in  constipation,  chiefly  because 
of  the  fear  of  pain  which  a  bowel  movement  produces.  Sphincter  spasm 
is  also  a  direct  cause  of  constipation. — Ed.] 


ETIOLOGY   OF   HEMORRHOIDS 

Any  of  the  causes  which  lead  to  habitual  constipation  will  soon  or  late 
cause  a  more  or  less  marked  development  of  hemorrhoids.  Stasis  of  the 
intestinal  contents  in  the  lowest  portions  of  the  intestine  from  the  sigmoid 
flexure  downward  is  a  particularly  active  factor;  there  is  congestion  of 
the  hemorrhoidal  veins  which  no  longer  have  power  to  empty  their  blood 
normally  into  the  inferior  vena  cava.  Other  causative  factors  are  also 
operative,  1)ut  they  are  alike  in  the  fact  that,  externally  or  internally,  they 
inhibit  propulsion  to  the  great  reservoirs  of  the  abdomen.  The  most 
important  are :  Tumors  of  the  rectum,  hypertrophy  of  the  prostate  glands, 
uterine  retroflexion,  ovarian  tumors,  hematocele  retrauterina,  myomata 
and  fibromata  of  the  uterus,  various  affections  of  the  bladder,  and  also 
large  tumors  of  the  pelvis,  etc. 

Hemorrhoids  form  a  very  frequent  and  distressing  complication  in 
pregnancy.  As  a  rare  etiologic  factor,  cholelithiasis  has  been  mentioned; 
this,  however,  has  little  in  common  with  hemorrhoids  except  that,  in 
this  condition,  habitual  constipation  is  exceedingly  common.  A  hereditary 
])redis])osition  to  hemorrhoids  has  already  been  spoken  of,  but  here,  prob- 
ably, the  factor  of  hereditary  constipation  which  so  invariably  occurs  must 
\)Q  taken  into  consideration. 

Although  constipation  and  hemorrhoids  show  an  unmistakable  sym- 
l)iosis,  other  less  frequent  causes  must  not  be  undervalued.  Thus,  the 
decided  formation  of  varices  unquestionably  occurs  also  in  chronic  diar- 
rhea, as  may  be  readily  understood  when  their  seat  and  cause  are  in  the 
lower  portions  of  the  intestine.  In  the  course  of  years  I  have  observed 
quite  a  number  of  such  postdiarrheic  hemorrhoidal  formations. 

Tn  recent  text-books  circulatory  disturbances  are  frequently  cited  as 
the  cause  of  varices.     As,  however,  Esmarch  *  and  Nothnagel  -  quite  prop- 

1  Esmarch,  "  Krankheiten  des  Mastdarnis,"  p.  168. 

2  Nothnagel,  "  Darmkrankheiten,"  2   Aufl.,  p.   469. 


SYMPTOMATOLOGY  709 

erly  maintain,  the  pathologic  increase  in  pressure,  even  with  severe  cardiac 
insufficiency,  distributes  itself  over  such  an  extensive  vascular  area  that  it 
can  scarcely  be  operative  in  the  hemorrhoidal  plexus  in  the  manner  sup- 
posed. 

In  conclusion,  age  and  sex  must  be  enumerated  among  the  causal  fac- 
tors. Varices  in  earliest  childhood  are  extremely  rare;  their  occurrence 
in  later  years  reveals  a  marked  difference  in  regard  to  sex,  inasmuch  as 
the  male  sex  shows  proportionately  a  much  greater  liability  than  the  female 
sex,  while  the  inverse  is  true  of  habitual  constipation.  In  my  opinion,  the 
explanation  of  this  can  only  be  found  in  the  more  numerous  venus  plexuses 
of  the  female  genitalia,  the  collateral  circulation  of  which  furnishes  an 
outlet  for  the  stasis  of  blood. 

SYMPTOMATOLOGY 
SYMPTOMS  OF  HABITUAL   CONSTIPATION 

In  the  simplest  and  mildest  form  of  habitual  constipation  the  symp- 
toms consist  in  the  incapacity  of  the  intestine  to  expel  the  intestinal  con- 
tents within  twenty-four  or  forty-eight  hours.  But,  with  accurate  obser- 
vation, we  may  discuss  somewhat  more  minutely  the  degree  and  nature 
of  diminished  intestinal  peristalsis. 

(a)  In  the  large  intestine,  in  toto,  particularly,  however,  in  its  upper 
portion,  muscular  activity  is  lessened. 

(b)  The  intestinal  contents  cannot  be  propelled  normally  to  the  lower 
portions  of  the  intestine,  congestion  occurring  in  the  sigmoid  flexure  and 
in  the  rectum.  These  portions  then  become  the  seat  of  a  deficient  power 
of  expulsion. 

In  both  cases  the  ultimate  effect  is  the  same,  but  scientifically,  and,  as 
we  shall  see  later,  also  therapeutically,  the  point  at  which  the  deficient 
power  of  expulsion  exists  is  more  or  less  essential. 

According  to  recent  experiences  (Fleiner,  Westphalen  and  others)  and 
clinical  observation,  we  may  differentiate  four  varieties  of  habitual  con- 
stipation :  First,  the  atonic  spastic  form.  It  must  be  expressly  stated  that 
the  differentiation  between  atonic  and  spastic  constipation  is  somewhat 
artificial.  In  the  former,  according  to  Fleiner,  the  bowel  contents  are  said 
to  be  more  compact  and  drier  than  usual ;  they  consist  of  clumps  closely  • 
adherent  or  of  cylindrical  masses  of  large  caliber,  sometimes  even  of  indi- 
vidual particles  or  scybalae  bearing  a  visible  impression  made  by  the  haustra 
of  the  intestine.  Secondly,  the  spastic  form  is  said  to  consist  of  small, 
friable,  pediculated  cylinders,  usually  of  about  the  thickness  of  a  lead- 
pencil,  or  of  globular  fecal  masses  the  size  of  a  hazelnut.  Since,  however, 
as  Fleiner  has  shown,  numerous  transformations  and  combinations  of  these 
forms  take  place — any  one  can  observe  thia  personally  at  any  time — 
Fleiner's  classification  is  of  little  consequence.  More  distinctive  than  the 
46 


710  CONSTIPATION   AND  HEMORRHOIDS 

formation  of  the  stool  is  the  proof  of  spastically  contracting  intestinal 
coils,  which  we  shall  consider  later.  In  my  experience  these  conditions 
vary  greatly  in  the  same  individual.  Nevertheless,  continuous  and  exten- 
sive spastic  contractions  are  frequently  found  associated  with  a  spastically 
formed  bowel  movement.^ 

As  a  third  form  of  habitual  constipation  that  variety  characterized  by 
me  as  a  fragmentary  bowel  movement  must  be  differentiated.  In  this  con- 
dition, as  in  the  case  of  hemorrhoids,  proctitis,  or  rectal  carcinoma,  there 
is  marked  tenesmus  which  compels  the  patient  to  seek  the  toilet  every  few 
hours,  yet  the  abdominal  pressure  brings  forth  only  a  few  particles  of 
feces.  I  have  usually  observed  this  condition  in  patients  suffering  from 
intestinal  neurasthenia. 

Finally,  we  must  mention  a  fourth  form  which  is  distinctly  charac- 
terized and  very  frequent :  Stercoral  diarrhea.  In  this  affection  there  is 
at  first  constipation  which  lasts  from  one  to  three  days,  sometimes  even 
longer,  and  is  accompanied  or  followed  by  severe  colicky  intestinal  pain 
and  rumbling,  and  by  one  or  several  copious  diarrheic  discharges;  these 
are  at  first  firm,  then  fluid,  but  may  be  diarrheic  from  the  start.  The  same 
typical  symptom-complex  then  reappears,  varying  only  in  severity,  fre- 
quency and  duration,  both  in  the  attacks  and  the  intervals. 

These  are  the  most  common  and  comparatively  the  most  typical  forms 
of  liabitual  constipation.  Besides  those  mentioned  there  are  undoubtedly 
other  modifications  which  cannot  be  described. 

]\Iore  necessary  is  the  description  of  two  important  and,  occasionally, 
very  distressing  and  painful  symptoms  of  constipation :  Flatulency  and 
infest inal  colic.  The  former  is  either  due  to  abnormal  filling  of  the  intes- 
tine with  putrid  gases  which  the  intestinal  musculature  is  powerless  to 
expel,  or  it  may  be  attributed  to  an  abnormal  and  excessive  production  of 
gaseous  products  while  the  intestinal  motility  is  good.  In  the  former 
case,  therefore,  gas  production  is  normal  but  there  is  diminished  intes- 
tinal peristalsis;  in  the  latter  case  there  is  an  abnormal  and  copious  gas 
formation  with  sufficient  intestinal  motility.  In  the  last,  the  bowel  move- 
ments may  be  sufficient  and  regular. 

Without  doubt  the  first  mentioned  form  is  by  far  the  most  unpleasant, 
and  is  intimately  connected  with  the  colic  now  to  be  described.  But  the 
second  form,  also,  is  no  less  unpleasant  to  the  patient  than  to  those  about 
him.  Intestinal  colic,  as  mentioned,  may  be  due  either  to  abnormal  reten- 
tion of  gas  (flatulent  colic)  or  to  other  non-gaseous  products  of  decom- 
position   (stercoral  colic).     In  the  former  case  the  attack  of  pain  after 


1  However,  spastic  intestinal  contractions  are  by  no  means  always  pathologic. 
I  have  seen  them  also  when  the  composition  of  the  feces  was  quite  normal.  In 
chronic  diarrhea  (not  stercoral  diarrhea)  I  also  demonstrated  well-developed,  con- 
tracted, intestinal  coils. 


SYMPTOMATOLOGY  711 

more  or  less  time  ceases  with  the  passage  of  gas;  in  the  latter,  euphoria 
only  follows  a  copious  fecal  discharge. 

From  this  true  intestinal  colic  we  must  carefully  differentiate  certain 
gastric  difficulties  to  which  Knud  Faber  ^  has  recently  called  attention, 
and  whose  experiences  we  can  absolutely  confirm. 

Another  condition  which  belongs  to  the  symptom  picture  of  habitual 
constipation  has,  since  Bouchard's  celebrated  researches,  been  designated 
as  autointoxication.  Headache,  sometimes  appearing  as  pressure  in  the 
cranium  and  sometimes  as  migraine,  also  dizziness  and  lassitude  here  play 
an  important  role.  In  fact,  we  cannot  at  once  reject  the  theory  of  a  causal 
connection  here,  and  every  physician  of  experience  will  recall  many  cases 
in  which  the  above  mentioned  symptoms,  particularly  if  not  well  devel- 
oped,  permanently  disappeared  on  regulating   the  bowels. 

On  the  other  hand,  it  would  be  a  manifest  exaggeration  to  attribute 
to  migraine  all  attacks  resembling  migraine  and  running  their  course  with 
habitual  constipation.  Only  too  frequently  it  becomes  my  duty  to  dispel 
the  illusions  of  my  patients  who  suffer  from  migraine  and  refer  their  con- 
dition to  faulty  gastrointestinal  digestion,  and  the  fruitlessness  of  treatment 
directed  to  this  condition  has  almost  invariably  shown  me  to  be  correct. 

Finally,  the  well-marked  picture  of  neurasthenia  is  frequently  com- 
bined with  habitual  constipation,  as  has  already  been  mentioned,  and  in 
these  cases,  objectively  speaking,  the  neurasthenia  cannot  be  regarded  as 
the  consequence  but  the  cause  of  chronic  intestinal  inactivity. 

Habitual  constipation  may  also  exert  an  influence  upon  the  kidneys; 
thus,  as  Kobler  ^  and  Ebstein  ^  have  observed,  and  as  I  may  confirm,  occa- 
sionally slight  albuminuria  and  cylindruria  are  met  with.  In  how  far  we 
are  here  dealing  with  a  mild  grade  of  nephritis  or  a  true  coprogenous 
albuminuria  cannot  at  present  be  determined.  Kobler's  investigations 
favor  the  view  of  coprogenous  albuminuria.  According  to  my  own  expe- 
rience, albuminuria  and  cylindruria  undoubtedly  form  the  rarest  compli- 
cations of  habitual  constipation. 


SYMPTOMS  OF  HEMORRHOIDS 

Hemorrhoids,  on  account  of  their  intimate  connection  with  habitual 
constipation,  naturally  present  many  of  the  same  symptoms.  But  the 
localization  of  the  affection  and  the  formation  of  varices  add  to  the  pre- 
viously described  picture  a  few  peculiarities. 

The  explanation  of  these  is  found  in  the  mechanical  effect  which  they 
produce.     As  such,  the  atony  in  the  lowest  portion  of  the  large  intestine 

1  Knud  Faber,  Arch.  f.  Verdauungskrankheiten,  1902,  Bd.  VIII,  Heft  1. 

2  Kobler,  Wiener  klin.  Wochenschrift,  1898,  Nr.  20. 

3  Ebstein,  "  Die  chronische  Stuhlverstopfung  in  der  Theorie  und  Praxis."  Stutt- 
gart, 1901,  p.  86. 


712  CONSTIPATION  AND  HEMORRHOIDS 

and  in  the  rectum  must  be  first  mentioned.  This  causes  stagnation  of 
the  intestinal  contents  in  the  sigmoid  flexure  and  in  the  ampulla  recti, 
and  also  the  development  of  a  catarrh  of  the  rectum,  occasionally  even  of 
the  sigmoid  flexure.  Tenesmus,  which  is  very  frequent,  is  also  due  to 
stagnation  of  the  intestinal  contents  in  the  rectum  and  in  the  sigmoid 
flexure. 

Occasionally  the  propulsion  of  the  contents  becomes  difficult  from  a 
purely  mechanical  cause,  namely,  the  extension  of  the  varices  and  nodules. 
Thus  a  vicious  circle  is  formed,  for  the  varices  increase  the  constipation 
and,  vice  versa,  the  latter  condition  aggravates  the  hemorrhoidal  affection. 

Another  source  of  difficulty  is  the  ready  tendency  to  inflammation  or 
even  ulceration  of  the  nodules  (which  have  extraordinarily  thin  walls) 
from  tlie  continuous  mechanical  irritation  to  which  they  are  exposed,  this 
being  favored  by  a  lack  of  cleanliness.  This  gives  rise  to  the  itching  and 
burning  of  which  the  patients  so  frequently  complain,  and  occasionally 
also  to  severe,  boring,  unbearable  pain  combined  with  the  most  distress- 
ing tenesmus.  Xot  infrequently  the  pain  and  burning  sensation  are  felt 
not  at  the  point  of  affection  but  higher  up,  in  the  lumbar  region  or  in 
the  shoulders,  and  quite  typical  attacks  of  sciatica  may  occur — I  have 
seen  several  undoubted  cases  of  this  kind — which,  if  the  origin  of  the 
trouble  is  not  located,  may  lead  to  various  therapeutic  errors. 

The  most  common  manifestation  of  hemorrhoids,  as  is  known  to  every 
layman,  is  the  periodically  appearing  hemorrhages.  These  may  vary  in 
degree  and  frequency.  It  was  formerly  assumed  that  the  hemorrhage  from 
hemorrhoids  was  beneficial,  and  to  some  extent  a  self -regulation  of  the 
condition  of  stasis  in  the  portal  vein  circulation. 

Upon  unprejudiced  testing  we  must  admit  that  there  is  at  least  a  grain 
of  truth  in  this  view,  inasmuch  as,  after  diffuse  depletion,  there  is  a 
transitory  decrease  in  the  varices  distended  with  blood  and,  hand  in  hand 
with  this,  euphoria  of  shorter  or  longer  duration  may  appear.  Beyond 
this  there  is  no  salutary  influence  from  the  bleeding  of  hemorrhoids;  for, 
in  the  first  place,  the  expected  amelioration  from  loss  of  blood  does  not 
always  follow,  and,  moreover,  from  their  duration  and  intensity,  the  latter 
may  produce  severe  anemia  without  in  the  slightest  degree  diminishing  the 
local  affection.  The  proverb,  "  All  that  glitters  is  not  gold,"  is  also  true 
of  ''  the  golden  vein."  The  formation  of  hemorrhoids  is  intimately  con- 
nected with  enlargement  of  the  liver.  I  cannot  express  this  relation  in 
figures,  but  all  who  are  accustomed  carefully  to  percuss  and  palpate  the 
liver  of  patients  with  hemorrhoids  must  have  noted  the  frequency  of  hepatic 
congestion. 

One  of  the  most  positive  and  interesting  cases  of  this  combination  is 
the  following:  A  hotel  proprietor,  aged  40,  but  an  exceptional  example 
of  temperance  in  regard  to  alcohol,  for  many  years  had  been  suffering 
from   hal)itual  constipation   and   highly  developed   external  and   internal 


I 


DIAGNOSIS  713 

hemorrhoids.  The  liver  was  four  fingerbreadths  below  the  margin  of  the 
ribs;  there  was  no  enlargement  of  the  spleen.  The  appetite  was  good, 
the  patient  digested  all  food  without  difficulty.  From  time  to  time  the  en- 
largement of  the  liver  increased  decidedly,  and  caused  a  feeling  of  pressure 
and  tension  in  the  abdomen.  Whenever  hemorrhage  from  the  hemorrhoids 
appeared,  the  liver  decreased  in  size,  and  the  symptoms  disappeared.  In- 
stead of  bleeding  from  the  hemorrhoids  sometimes  there  was  very  copious 
hematemesis;  no  symptoms  of  ulcer  or  gastritis  were  ever  observed,  but 
in  the  course  of  time  there  were  six  severe  attacks  of  hematemesis.  With- 
out forcing  scepticism  too  far,  we  are  here  actually  dealing  with  a  case  of 
vicarious  gastric  hemorrhage.  .  This,  therefore,  is  not,  as  v.  Schrotter  *  has 
recently  maintained,  a  canard  (Raubergeschichte). 

Earlier  literature,  which  found  fanatic  expression  chiefly  in  the  teach- 
ings of  Georg  Ernst  Stahl,  ascribed  to  hemorrhoids  a  far  greater  impor- 
tance than  that  just  alluded  to.  According  to  this,  the  stoppage  of  hem- 
orrhoidal bleeding  was  said  to  produce  all  sorts  of  internal  diseases  (gout, 
diseases  of  the  liver,  the  heart,  the  lungs,  and  others).  There  can  be  no 
doubt  that  this  teaching  over-reached  its  mark,  and  was  justified  only  in 
so  far  as  congestion  in  the  deeper  areas,  occasionally  also  in  organs  situ- 
ated higher  up,  was  affected  by  the  portal  vein  circulation. 

DIAGNOSIS 

DIAGNOSIS   OF   HABITUAL   CONSTIPATION 

In  turning  to  the  diagnosis  of  habitual  constipation  and  hemorrhoids, 
the  recognition  of  these  affections  at  first  sight  appears  very  simple,  and 
to  require  no  special  elucidation.  In  fact,  this  is  true  in  the  overwhelming 
majority  of  cases.  But  even  this  apparently  simple  clinical  picture  may 
cause  perplexity  in  diagnosis,  and  it  is  therefore  absolutely  necessary  that 
patients  complaining  of  habitual  constipation  be  examined  just  as  thor- 
oughly as  those  suffering  from  any  other  affection. 

The  important  question  to  be  decided  in  every  case  is  this:  Is  the 
constipation  habitual,  viz.,  primary,  like  that  previously  described,  or  is 
another  causal  factor  present?  At  the  beginning  of  this  article  we  called 
attention  to  the  numerous  causes  which  may  produce  this  condition ;  possi- 
bly their  role  is  not  always  important,  but  a  thorough  diagnostic  insight 
is  also  a  valuable  aid  in  the  treatment. 

At  this  point  we  shall  busy  ourselves  especially  with  the  various  diag- 
nostic difficulties  which  are  referable  to  the  digestive  apparatus  itself. 

It  is  a  common  experience  to  find  that  patients  with  various  disturb- 
ances of  digestion  regard  habitual  constipation  as  the  most  prominent  and 

1  V.  Schrotter,  Verhandl.  des  Congresses  fiir  innere  Mcdicin,  1902.  "  Discussion 
zu  dem  Vortrage  von  Ewald,  Ueber  die  Diagnose  des  MagengeschwQrs." 


714  CONSTIPATION   AND   HEMORRHOIDS 

frequent  cause  of  these,  which  occasionally,  however,  masks  other  impor- 
tant symptoms.  Thus,  I  have  frequently  noted  that  patients  with  steno- 
sis of  the  pylorus,  even  with  gastric  carcinoma,  complain  merely  of  habit- 
ual constipation,  while  the  serious  underlying  gastric  affection  is  revealed 
only  by  a  careful  examination. 

The  possibility  of  deeply  situated  intestinal  disease  is  more  significant. 
First  in  importance  is  carcinoma  of  the  intestine,  especially  that  involv- 
ing the  colon,  not  on  account  of  its  frequency,  but  because  it  may  lead 
to  grave  errors.  Of  the  entire  structure  of  the  symptom-complex  only 
constipation  can  be  discerned  upon  careful,  and  especially  upon  super- 
ficial, examination.  What  is  true  of  carcinoma  is  also  true  of  benign 
stenosis.  A  less  serious  error,  but  nevertheless  not  without  interest,  con- 
sists in  the  non-recognition  of  the  combination  of  habitual  constipation 
with  colitis,  to  which  we  shall  refer  later. 

These  considerations,  which  by  no  means  exhaust  the  differential  diag- 
nosis, sufficiently  indicate  that  the  diagnosis  of  habitual  constipation  must, 
under  all  circumstances,  be  preceded  by  a  thorough  local  and  general 
examination. 

The  special  diagnosis  which  then  follows  must  comprehend  the  physical 
investigation  of  the  intestines  and  the  feces. 

In  the  former,  the  recognition  of  intestinal  atony  by  filling  the  bowel 
with  water  or  gas  is  easy.  The  same  condition  is  pointed  out  by  the 
finding  of  contracted  intestinal  coils,  especially  of  the  transverse  colon, 
the  cecum  and  the  sigmoid  flexure,  which  also  indicate  the  spastic  char- 
acter of  the  chronic  constipation.  Extreme  meteorism  favors  stagnation 
of  the  contents;  on  the  other  hand,  sensitiveness  to  pressure  in  the  region 
of  the  colon  is  not  common  in  simple,  habitual  constipation,  but  indicates 
colitis. 

The  examination  of  the  rectum  is  an  integral  part  of  an  examination 
of  the  intestinal  canal.  Aside  from  the  discovery  of  hemorrhoids,  which 
will  1)6  fully  described  later,  ampullar  bulgings  will  probably  be  observed 
which  indicate  stagnation  of  the  dejecta  in  the  lower  portion  of  the  bowel. 
If  large  scybala  are  recognized  in  the  rectum,  the  correct  remedy  may  be 
at  once  employed. 

In  conclusion,  observation  of  the  howel  movement  itself  is  a  valuable 
aid  in  the  recognition  of  the  nature  and  the  extent  of  the  constipation. 
Particles  of  mucus  should  be  examined,  provided  a  so-called  exploratory 
irrigation  of  the  intestine  is  not  undertaken;  these  I  always  advise,  particu- 
larly if  the  patient  reports  the  appearance  of  mucus,  or  if  there  is  sensi- 
tiveness to  pressure  over  the  colon. 

For  the  physician  not  familiar  with  intestinal  diseases  it  may  here 
lie  remarked  that  irrigation  of  the  intestine  is  carried  out  in  a  manner 
similar  to  gastric  lavage.  For  this  purpose  a  soft  rectal  tube  is  attached 
hy  means  of  a  small  glass  tube  to  a  rubber  tube  about  a  yard  and  a  half 


I 


DIAGNOSIS  715 

long  which  has  inserted,  at  its  upper  end,  a  glass  funnel.  The  funnel 
is  elevated  and  water  at  a  temperature  of  about  30°  C.  is  permitted  to 
flow  into  the  intestine;  upon  lowering  the  funnel  the  fluid  is  returned 
and  received  in  a  vessel  held  for  this  purpose.  This  fluid  may  then  be 
readily  examined  for  mucus  and  other  pathologic  constituents. 


DIAGNOSIS  OF  HEMORRHOIDS 

The  diagnosis  of  hemorrhoids  necessitates  a  local  inspection  of  the 
anus,  and  a  digital  examination  of  the  rectum.  This  examination,  which 
is  really  self-evident,  is  unfortunately,  notwithstanding  the  urgent  advice 
given  in  text-books  and  medical  Journals,  not  sufficiently  often  made.  The 
operative  treatment  of  rectal  carcinoma,  which  is  too  often  unrecognized 
and  sails  under  the  flag  of  hemorrhoids,  would  then  give  us  much  more 
favorable  results. 

In  every  case  of  hemorrhoids  it  must  also  be  determined  whether  we 
are  dealing  with  external,  internal,  or  mixed  hemorrhoids.  While  the  first 
are  readily  recognizable,  the  diagnosis  of  internal  hemorrhoids  may  occa- 
sion great  perplexity.  Internal  hemorrhoids  are  most  readily  revealed  by 
strong  pressure,  and  best  after  injections  of  a  hot  saline  solution  or 
glycerin. 

Where  nodules  do  not  thus  appear,  and  the  bleeding  from  the  anus 
indicates  a  hemorrhoidal  origin,  it  is  possible,  as  J.  Schreiber  ^  has  lately 
shown,  to  determine  the  source  of  the  hemorrhage  by  the  rectoscope,  and 
to  control  and  treat  it  surgically.  Similar  cases  have  been  described  by 
Xothnagel "  and  Ewald.^  According  to  Schreiber,  hemorrhoidal  venous 
dilatation  is  observed  much  higher  in  the  intestine  than  was  previously 
thought  possible,  even  as  high  as  the  sigmoid  flexure. 

The  differential  diagnosis  and  the  complications  of  hemorrhoids  require 
a  few  brief  remarks.  In  regard  to  the  former,  it  must  be  emphasized  that 
the  confusion  of  hemorrhoids  with  other  diseases  of  the  rectum,  provided 
the  rectum  is  carefully  palpated,  is  very  rare.  At  most  small  polypi  or 
angiomata  may  cause  perplexity.  The  differentiation  of  a  beginning  car- 
cinoma from  ulcerating  hemorrhoids  is  sometimes  difficult,  all  the  more 
so  since  from  these  cancroids  may  develop  in  the  course  of  time.  Suc- 
cessive palpations  and  rectoscopic  examinations,  perhaps  the  excision  of 
a  portion  under  narcosis  or  local  anesthesia,  will  in  most  cases  clear  the 
situation. 

The  complications  of  hemorrhoids  are  numerous.  Catarrh  of  the  rec- 
tum   (proctitis   haemorrhoidalis)   has  already  been  mentioned;  this  fre- 

1  J.  Schreiber,  "  Die  Rectoromanoskopie."     Berlin,  1903,  p.  73  et  seq. 

2  Sothnagel,  "  Zur  Klinik  der  Darmkrankheiten."  Festschrift  z.  Feier  d.  60.  Oe- 
hurtstages  von  Max  Jaffe.     Braunschweig,  1901. 

8  Ewald,  "  Klinik  der  Verdauungskrankheiten,"  1902,  III,  pp.  425  u.  426. 


716  CONSTIPATION  AND  HEMORRHOIDS 

quenlly  runs  its  course  with  tenesmus.  On  strong  pressure  we  observe, 
as  a  rule,  the  discharge  of  a  gelatinous  yellowish-white  mucus. 

In  the  course  of  hemorrhoids  more  or  less  deep  ulceration  often 
occurs,  and  causes  severe  burning  or  pain.  Careful  examination  with  the 
speculum  will  usually  enable  us  to  recognize  this  complication. 

Occasionally  there  is  incontinence  of  the  sphincters  of  the  rectum,  which, 
even  without  the  prolapse  of  nodules,  leads  to  familiar  disturbances,  par- 
ticularly to  the  discharge  of  thin,  fluid  feces.  Inspection  and  digital 
examination  will  readily  reveal  this  condition. 

When  hemorrhoids  have  persisted  for  a  long  time,  hemorrhoidal  pro- 
lapse frequently  develops  and  may  vary  greatly  in  severity.  In  the  milder 
cases  prolapse  only  occurs  upon  defecation.  In  more  advanced  cases  it 
may  follow  any  movement,  for  instance,  sneezing,  the  passage  of  flatus,  etc. 


TREATMENT 

TREATMENT  OF  HABITUAL   CONSTIPATION 

Where  physico-dietetics  have  been  added  to  true  drug  treatment,  vari- 
ous methods  for  relieving  habitual  constipation  are  to-day  resorted  to  by 
physician^;.  The  decision  as  to  the  efficacy  of  the  different  measures  is 
made  extremely  difficult  from  the  fact  that  the  various  curative  agents 
employed  in  practice  arc  so  numerous,  and  are  even  multiplied  in  spas  and 
sanatoriums.  This  perplexity  in  judging  as  to  the  effectiveness  of  indi- 
vidual drugs  and  metliods  is  still  further  enhanced  inasmuch  as  they  are 
sometimes  employed  in  mild,  at  other  times  in  severe  cases.  Upon  accu- 
rate investigation  the  usual  criteria  for  this  are  not  positive;  therefore, 
at  the  beginning  of  this  section,  a  brief  outline  of  the  degrees  of  consti- 
pation is  not  out  of  place. 

Upon  superficial  judgment,  the  best  standard  appears  to  be  the  dura- 
tion of  chronic  constipation.  This  will  often,  but  by  no  means  invariably, 
be  found  a  true  measure.  I  hav6  had  under  observation  many  patients 
who,  for  twenty  or  thirty  years,  had  been  able  to  regulate  their  intestinal 
functions  only  by  drugs,  and,  by  the  institution  of  a  proper  diet,  they  were 
at  once  completely  and  permanently  relieved.  Inversely,  we  sometimes  see 
patients  in  whom  constipation  has  existed  but  a  short  time,  that  is,  for  one 
or  two  years,  yet,  contrary  to  all  expectation,  curative  measures  are  abso- 
lutely ineffectual. 

Afore  exact  tests,  but  by  no  means  always  decisive  of  the  degree  of 
habitual  constipation,  are  the  effect  and  the  dose  of  the  remedies  or  cura- 
tive measures  which  have  been  employed.  Here  we  may  differentiate 
between  laxatives,  purgatives,  and  drastics,  and  between  these  are  the 
so-eallod  neutral  salts.  In  some  cases  mere  laxatives — and  among  these 
]    (ount    rhubarb,  preparations  of  frangula,   cascara  sagrada,   tamarinds. 


TREATMENT  717 

compound  licorice  powder,  flowers  of  sulphur  and  the  like— in  small  doses 
are  sufficient,  sometimes  for  years;  these  cases  are,  therefore,  unquestion- 
ably mild.  In  others  these  remedies  are  without  result  or  are  effective 
only  in  very  large  doses.  Such  cases  may  be  designated  as  moderately 
severe.  The  most  extreme  degree  of  chronic  constipation  is  represented 
by  the  patients  in  whom  the  neutral  salts,  and  even  drastics  in  large  doses, 
either  fail  to  bring  relief  or  act  insufficiently.  But  another  group  is  also 
to  be  differentiated,  and  in  these  neither  mild  nor  drastic  purgatives  pro- 
duce free  action,  while  the  simple  injection  of  water  at  once  gives  relief. 
These,  apparently,  are  the  cases  in  which  the  lower  portion  of  the  intes- 
tine is  the  seat  of  intestinal  atony,  and  here  we  must  bear  in  mind 
the  psychogenous  or  neurogenous  group  in  which  purgatives,  injections, 
and  massage,  etc.,  are  without  effect  unless  supplemented  by  the  com- 
plete removal  of  the  patient  from  his  former  surroundings  and  the  cares 
of  his  occupation. 

Only  by  such  a  separation  can  we  decide  as  to  the  nature  and  degree 
of  the  affection,  and  only  thus  can  we  correctly  estimate  the  value  of 
the  many  remedies  and  methods  employed  to  relieve  the  condition. 

Before  proceeding  with  our  discussion  it  is  by  no  means  superfluous 
for  us  to  ask:  What  is  meant  by  the  cure  of  habitual  constipation?  In 
my  opinion  we  can  only  speak  of  habitual  constipation  as  cured  if,  a  year 
after  the  termination  of  the  treatment,  there  is  a  spontaneous  and  ample 
evacuation  every  twenty-four  to  forty-eight  hours. 

If  all  physicians  were  to  accept  this  as  a  standard,  our  confidence  in 
the  efficacy  of  measures  which  have  apparently  been  very  successful  would 
soon  be  shattered. 

As  soon  as  we  lower  our  standard,  and  regard  temporary  improve- 
ments as  cures,  the  number  of  successful  remedies  is,  of  course,  very  con- 
siderable. 

In  the  following,  the  treatment  of  habitual  constipation  will  be  con- 
sidered only  from  that  standpoint  which  we  have  established  as  indicating 
a  cure. 

As  everywhere  in  medicine,  prophylaxis  plays  the  leading  and  most 
important  role.  It  begins  in  childhood  with  the  consideration  of  the  pre- 
viously mentioned  congenital  predisposition  to  constipation.  In  addition 
to  this,  it  must  be  the  object  of  home  training  and  of  our  professional 
endeavors  to  instruct  children  as  to  the  importance  of  regulating  their 
intestinal  functions.  To  attain  this  end  a  thorough  understanding  of  the 
process  of  nutrition  is,  above  all,  necessary. 

We  know  that,  especially  in  the  better  classes,  the  desire  for  a  strength- 
ening diet  takes  precedence  of  all  other  considerations,  and  the  mistaken 
parents  regard  expensive  meat  and  the  nutritious  egg  as  the  only  nour- 
ishing, or,  at  least,  the  best  food. 

Aside  from  the  fact  that  a  too  stereotyped  diet  fails  to  produce  the 


718  CONSTIPATION  AND  HEMORRHOIDS 

nutritive  effect  expected  (to  the  astonishment  of  those  who  institute  it), 
another  undesirable  factor  is  added — habitual  constipation.  It  is  there- 
fore the  duty  of  the  physician  to  regulate  the  nutrition  of  children,  and 
from  time  to  time  to  add  to  the  uniform,  constipating  diet  food  which 
favors  the  regular  action  of  the  bowels. 

What  is  true  of  children  also  applies  to  the  condition  in  adults  desig- 
nated by  me  as  alimentary  constipation.  In  particular,  the  table  d'hote 
with  its  abundance  of  meat  and  fish  in  contrast  with  its  usually  small 
amount  of  vegetables  is  a  frequent  cause  of  constipation  in  young 
persons. 

Here,  in  a  restricted  sense,  the  same  laws  of  treatment  are.  operative 
which,  in  Germany  at  least,  Albin  Hoffmann  first  utilized  with  such 
marked  success  in  therapy:  exercise  and  abstinence.  In  alimentary  consti- 
pation exercise  is  the  more  necessary;  upon  this,  in  fact,  are  based  our  most 
important  methods  of  treatment,  which  range  from  ordinary  walks  to 
Swedish  movements  and  massage.  A  practical  and  even  a  decided  influ- 
ence is  to  be  ascribed  to  the  diet  inasmuch  as  here  thermic,  chemical  and 
mechanical  stimulation,  occasionally  all  combined,  stimulate  peristalsis  to 
an  increased  activity.  As  a  practical,  pioneer  factor,  the  diet,  therefore, 
occupies  a  hading  place  among  the  curative  agents. 

In  tlie  first  place,  the  diet  of  chronic  constipation,  like  the  diet  in 
other  affections,  is  based  upon  the  law  of  experience.  To  the  present 
time  the  sanction  of  inductive  science  is  lacking.  Nevertheless,  we  may 
picture  to  ourselves  more  or  less  completely  the  effect  upon  the  in- 
testinal function  of  an  increase  in  diet  (I  designate  this  as  constipa- 
tion diet). 

It  is  generally  known  that  certain  foods  stimulate  and  others  inhibit 
intestinal  activity  just  as  do  certain  drugs,  and  upon  exact  investigation 
the  line  of  demarcation  between  the  effect  of  a  drug  and  that  of  the  food 
is  almost  obliterated.  Whether  I  administer  tannic  acid  in  the  form  of 
acidum  tannicum  or  as  acorn  coffee,  whether  bilberry  wine  or  red  wine 
containing  a  large  amount  of  tannin,  whether  rhubarb  compote  or  an 
infusion  of  the  root  of  rhubarb,  whether  I  give  fig  syrup  or  half  a  dozen 
fresh  figs  certainly  makes  no  fundamental  difference;  at  most,  in  the  one 
case  we  are  employing  the  raw  substance,  and  in  the  other  we  are  admin- 
istering the  active  principle  in  as  pure  a  form  as  possible. 

The  physiology  of  food  gives  us  a  large  number  of  such  remedies 
which  stimulate  the  intestine.  We  may  divide  them  into  the  following 
groups : 

1.  Substances  containing  sugar. — In  this  group  belong  common  cane 
sugar,  milk  sugar,  honey,  manna,  levulose,  dextrose,  sweet  whipped  cream, 
fruits  containing  large  quantities  of  sugar  (plums,  grapes,  figs,  oranges, 
dates,  etc.).  The  effect  of  sugar  is  probably  manifold.  In  the  first  place, 
sohitions  of  sugar  in  the  stomach  produce  active  secretion  (dilution  secre- 


TREATMENT  719 

tion,  Strauss),  and  in  the  sugar  not  at  once  absorbed  acids  of  fermentation 
develop. 

2.  Foods  containing  organic  acids. — Among  these  are:  Buttermilk, 
sour  milk,  kefyr,  kumiss,  sour  whey ;  also  fruit  wines,  for  example,  cider  or 
Moselle  wine,  currant  wine,  gooseberry  wine  and,  in  Kussia,  the  so-called 
"kwass";  sour  lemonade  (made  from  lemons),  acid  fruits  (apples,  sour 
cherries,  gooseberries  and  currants,  etc.) ;  rye  bread,  characterized  by  its 
amount  of  sour  dough,  belongs  to  this  category. 

3.  Salty  substances. — As  the  commonest  remedy,  ordinary  table  salt  in 
its  various  combinations  (salt  water,  salt  herring,  caviar,  sardellen,  etc.). 
Smoked  and  pickled  foods  also  belong  to  this  category. 

4.  Substances  containing  carbonic  acid  or  those  which  form  carbonic 
acid. — In  this  group  belong  the  natural  or  artificial  waters  which  contain 
carbonic  acid,  also  the  simple  alkaline  waters,  and  the  above  mentioned 
kefyr,  kumiss,  kwass,  matzoon,  etc.  Yeast  and  yeast  bread  may  also  be 
included  in  this  category.  Finally  a  number  of  so-called  gas-forming 
vegetables;  these  produce  CO,  as  well  as  other  varieties  of  gas. 

5.  Substances  which  contain  fat,  and  in  which  the  amount  of  fatty 
acid  assists  the  action. — The  most  common  remedies  here  are  butter,  olive 
oil,  sesame  oil,  or  linseed  oil,  which  is  generally  and  quite  properly,  I 
think,  regarded  as  difficult  of  digestion.  Perhaps  the  value  of  linseed  (see 
later)  depends  upon  the  large  amount  of  fat  it  contains.  Here,  on  ac- 
count of  its  contents  of  fat,  the  so-called  mayonnaise  is  to  be  included,  as 
well  as  Italian  salad  and,  perhaps,  all  salads  prepared  with  oil. 

These  are  the  main  chemical  stimulants  to  the  intestine,  and  to  these 
must  be  added  the  thermic  and  mechanical  ones. 

6.  On  account  of  its  thermic  effect  only  cold,  naturally,  must  be  con- 
sidered. This  is  best  employed  as  a  drink  in  the  form  of  cold  water, 
cold  milk,  either  sweet  or  sour,  cold  lemonade.  Cold  soups  (such  as  fruit 
soups,  and  the  like)  have,  in  addition  to  other  effects,  also  a  certain  ther- 
mic influence.  On  the  other  hand,  cold  or  frozen  fruits,  because  usually 
introduced  into  a  full  stomach  where  equalization  of  temperature  soon 
occurs,  are  less  beneficial.  The  action  of  these  substances  depends  mainly 
upon  the  state  of  the  stomach,  whether  full  or  empty,  and  the  optimum 
of  the  thermic  effect  is  consequently  found  in  an  empty  stomach,  a  fact 
daily  demonstrated  in  practice. 

7.  The  mechanical  effects  of  food  are  manifold.  The  more  the  indi- 
gestible residue  from  a  food,  cceteris  paribus,  the  more  it  promotes  the 
passage  of  the  intestinal  contents. 

The  greater  the  proportion  of  food  absorbed  in  the  intestinal  canal, 
the  less  suitable  is  it  in  the  treatment  of  habitual  constipation. 

We  are  indebted  to  the  researches  of  Eubner  for  our  knowledge  of  the 
absorption  of  food ;  if  not  of  all  at  least  of  the  most  common  ones.  Ac- 
cording to  these  the  percentage  of  non-absorption  is  as  follows: 


720 


CONSTIPATION   AND  HEMORRHOIDS 


Of  the  dbied 
substance 

Of 

ALBUMIN 

Of  carbo- 
rtdrates 

In  broiled  and  fried  meat 

4.9-5.3 

4.3 

5.2 

8.8 

4.2 

5.6 
13.1 
20.9 
19.3 

4.1 

9.1 
15.0 
18.3 

9.4 
14.4 
20.7 

2.0-3.6 

2.5 

2.6 

7.8 
21.8 
22.2 
36.7 
46.6 
43.0 
20.4 
17.5 

36!  2 
30.5 
18.5 
39.0 

In  shell  fish 

Hard  boiled  eggs 

Milk 

Wheat  bread  from  fine  flour 

1.1 

Rolls 

2.9 

Rye  bread  from  coarse  ground  corn 

2.9 

Rye  bread  from  the  whole  corn 

Pumpernickel 

.  14.3 

13.8 

Rice 

0.9 

Peas  

3.6 

Green  beans 

Beans 

Mashed  potatoes 

7.4 

Savoy 

15.4 

Yellow  turnips 

18.2 

This  Table  is  very  instructive  for  our  purpose.  It  shows  the  almost 
complete  absorption  of  animal  substances.  The  digestibility  of  milk  in 
adults  is  only  slightly  less  than  in  infants,  which  would  scarcely  be  sup- 
posed from  its  composition,  but  there  are  probably  individual  differences. 

The  absorbability  of  vegetable  substances  is  far  less  than  that  of 
animal  substances.  As  is  shown  by  the  Table,  much  of  this  depends  upon 
the  mode  of  preparation.  In  materials  which  are  baked  the  addition  of 
coarse  bran  lessens  absorption;  finely  ground,  however,  it  increases  ab- 
sorption. Cellulose  in  the  potato  is  readily  digested,  and  best  the  cellulose 
of  young  leaf  vegetables.  In  all  of  these  carbohydrates  the  absorbability 
is  largely  dependent  upon  the  manner  of  preparation. 

As  is  also  evident  from  the  Table,  bread  made  of  rye,  ground  from  the 
whole  grain  and  baked  with  yeast,  and  pumpernickel  show  the  lowest 
degree  of  absorbability.  Among  vegetables,  the  same  is  true  of  beans. 
Savoy  cabbage,  yellow  turnips.  It  is  to  be  regretted  that  the  degree  of 
absorbability  of  other  vegetables  and  other  varieties  of  cabbage  is  not  given 
in  Rubner's  Tables.  The  latter,  however,  may  generally  be  reckoned 
among  the  carbohydrates  that  are  only  slightly  absorbed. 

Among  substances  which  exert  a  mechanical  action  belong  all  products 
with  skins,  membranes  which  are  usually  eaten  raw,  but  sometimes  also 
cooked,  and  which  are  very  imperfectly  digested.  Among  these  are  all 
the  different  fruits,  in  so  far  as  they  are  unpeeled,  among  the  legumes 
peas  and  beans,  and  among  other  vegetables  asparagus  in  particular. 
Mushrooms  are  not  at  all  digested;  probably  to  the  same  category  belongs 
the  radish.  Complete  absence  of  digestion  also  characterizes  mustard  seed 
and  linseed.  These,  therefore,  are  occasionally  employed  with  success  as 
coarse,  mechanical,  euperistaltic  remedies.  However,  the  possibility  of  the 
entrance  of  mustard  seed  or  linseed  into  the  appendix  may  be  regarded 
as  a  source  of  danger. 


TREATMENT  721 

We  note,  therefore,  from  this  description  that,  in  a  broad  sense,  the 
diet  contains  all  the  potentials  which  are  necessary  to  affect  a  sluggish 
intestine,  and  that  these  are  occasionally  combined  with  one  another  in  a 
most  remarkable  manner.  For  example,  in  fruit  we  find  sugar,  acid, 
cellulose  and  pectin.  The  methods  of  serving  these  also  produce  combina- 
tions which  assist  intestinal  activity;  for  example,  sour  milk  with  sugar 
and  rye  bread,  cold  cereals,  sugar,  currants  and  hyperfermented  beer. 

We  are  thus  enabled  to  find  a  number  of  laxative  remedies  from  which 
we  must  select  the  best  and  most  effective,  and  combine  them. 

It  must  be  primarily  emphasized  that  in  cases  of  advanced  habitual 
constipation  that  are  at  all  stubborn,  any  single  remedy  to  stimulate  in- 
testinal activity  will  usually  be  without  effect.  If,  however,  we  combine 
several  of  these,  for  example,  by  administering  sugar,  acids,  table  salt, 
oil,  material  rich  in  residue,  in  proportions  adjusted  to  the  mode  of  life 
and  the  habits  of  the  patient,  the  total  effect  equals  that  of  a  powerful 
purgative. 

It  is  obvious  that  in  the  choice  of  these  natural  purgatives  we  must 
individualize  very  strictly.  In  addition  to  certain  idiosyncrasies  or  bad 
habits  which  must  be  reckoned  with  in  practice,  the  state  of  the  gastro- 
intestinal canal  comes  into  question.  Acid  and  fatty  substances  are  fre- 
quently not  well  borne;  they  may  produce  pyrosis  and  a  sense  of  gastric 
oppression.  In  other  cases  coarse  bread  and  pumpernickel  generate  gas, 
and  other  products  must  occasionally  substitute  for  the  varieties  of  sugar 
and  fruit.  Certain  disturbances  in  metabolism,  for  example,  gout,  obes- 
ity and  diabetes,  may  necessitate  a  reduction  in  amount. 

This  apparent  or  actual  intolerance  should  by  no  means  force  us  to 
abandon  the  treatment,  for  the  dietetic  laxatives  which  remain  may  be 
given  in  increased  quantity.  On  the  other  hand,  inversely,  the  diet  must 
be  so  regulated  that  secondary  disturbances,  for  instance,  anemia,  chlorosis, 
under-nutrition,  and  enteroptosis  may  be  favorably  influenced  by  it.  In 
such  cases  the  proteids,  sugar,  and  fat  should  be  particularly  prominent 
in  the  diet. 

A  significant  point  in  the  treatment  of  habitual  constipation  is  the 
strict  avoidance  of  astringent  substances  which  inhibit  peristalsis.  Self- 
evident  as  this  appears  to  be,  in  my  experience  such  errors  are  frequently 
committed.  Thus,  for  example,  a  patient  with  constipation  is  placed  upon 
a  very  suitable  diet,  but,  at  the  same  time,  is  permitted  to  take  cocoa, 
red  wine,  rice  or  fine  wheat  bread,  or,  what  is  equivalent,  these  foods  are 
not  strictly  prohibited.  Attention  need  scarcely  be  called  to  the  fact  that 
a  diet  for  constipation  is  thus  made  absolutely  of  no  effect. 

Concerning  this  somewhat  complicated  system  the  question  may  be  and 
has  been  asked:  Why  institute  such  a  tedious  treatment  when  we  may 
more  quickly  attain  the  same  results  with  other  curative  remedies? 

Were  this  actually  the  case,  the  dietetic  treatment  of  habitual  consti- 


722  CONSTIPATION   AND  HEMORRHOIDS 

pation  would,  in  truth,  be  an  unnecessary  hardship.  Later  on  we  shall 
discuss  other  valuable  remedies  which  increase  intestinal  activity.  But, 
in  considering  the  results  of  dietetic  treatment,  and  out  of  a  rich  experi- 
ence, 1  deduce  the  following: 

The  effect  of  the  constipation  diet  is,  in  the  overwhelming  majority 
of  cases,  very  rapid,  and  appears,  as  a  rule,  even  within  the  first  few 
days.  In  most  cases  this  result  is  permanent,  and  the  patient  gradually 
resumes  his  normal  diet.  We  then  consider  this  an  actual  cure.  In  the 
minority,  however,  after  weeks  or  months  the  effect  apparently  ceases;  the 
patients  respond  imperfectly,  or  not  at  all,  to  the  diet.  We  see,  therefore, 
the  same  necessity  of  adapting  the  stimulation  to  the  case  as  in  a  treatment 
by  purgatives.  Occasionally,  however,  this  diminution  of  stimulation  is 
not  due  to  the  cumulative  effect  of  the  diet,  but  to  the  fact  that  in  the 
course  of  time  the  patients  fail  to  adhere  to  it.  Occasionally  the  treatment 
is  interrupted  by  prolonged  traveling,  by  improper  food  in  hotels,  by 
psychical  emotion  or  other  unfavorable  circumstances,  and  it  then  becomes 
exceedingly  difficult  to  stimulate  afresh  the  impaired  intestinal  function. 
In  conclusion,  there  are  patients  in  whom  a  regulated  diet  acts  only  so 
long  as  they  adhere  rigidly  to  all  of  its  details;  even  slight  modifications 
produce  disturbances.  In  these  cases  a  cure  such  as  I  mean  is  out  of 
the  question. 

These  exceptions,  however,  cannot  alter  the  fact  that  the  effect  is 
permanent  in  a  large  number  of  cases.  To  say  nothing  of  purgatives, 
such  a  permanent  cure  never  tahes  place  otherwise  nor  hy  any  other 
remedy. 

For  this  reason  dietetic  treatment  of  the  mild  as  well  as  of  the  severe 
forms  of  habitual  constipation  must  form  the  normal  process.  When  this 
is  not  effective,  other  remedies  are  to  supplement  it,  but  by  no  means  to 
substitute  for  it.  Following  this  is  a  diet  list  for  an  ordinary  case  of 
habitual  constipation,  the  condition  of  the  stomach  being  considered 
normal : 

In  the  morning  upon  an  empty  stomach :  A  glass  of  salt  water  or  sugar 
water. 

8  o'clock :  Coffee  with  milk,  one  tablespoonful  of  milk  sugar  (or  manna 
or  levulose),  50  grams  of  Graham  bread,  or  D.K.  bread,  or  Simon's  bread, 
10  grams  of  butter,  20  grams  of  honey  or  sweet  marmalade. 

11  o'clock:  250  grams  of  sour  milk,  or  buttermilk,  or  kefyr  2  days 
old;  50  grams  of  Graham  bread,  or  D.K.  bread,  or  Simon's  bread;  10 
grams  of  butter  (1  egg^). 

2  o'clock:  50  grams  of  potatoes  (mashed  potato  or  with  the  skin), 
200  grams  of  vegetables,^  150  grams  of  meat  or  fish,  50  grams  of  salad 

1  With  a  good  constitution  this  may  be  omitted. 

-  With  a  weak  stomach  as  pur6e;  with  a  good  stomach,  in  the  natural  form. 


TREATMENT 


723 


(with  lemon  and  oil) ;  about  100  grams  of  stewed  fruit  (sweet  or  sour), 
150  to  200  grams  of  cider.  Moselle  wine,  or  lemonade;  raw  fruit. 

4  o'clock :  Coffee  with  milk  or  whipped  cream,  50  grams  of  marmalade, 
25  grams  of  Graham  bread  or  Graham  biscuit. 

8  o'clock:  100  to  150  grams  of  meat  or  fish  (cold  or  warm);  salad 
(see  above) ;  50  grams  of  stewed  fruit;  soft  cheese;  50  grams  of  G'raham 
or  rye  bread,  or  pumpernickel  with  butter;  100  to  150  grams  of  cider 
or  Moselle  wine. 

Before  going  to  bed :  Eaw  fruit  of  various  kinds  (according  to  season) 
and  in  desirable  quantity. 

We  add  here,  as  an  example  of  a  variation  in  the  diet,  the  following 
which  may  be  given  in  a  mild  case  of  diabetes: 

Upon  an  empty  stomach :  A  glass  of  salt  water. 

8  o'clock:  Coffee  (black);  30  grams  of  manna,  20  grams  of  Graham 
bread,  30  grams  of  butter. 

11  o'clock:  250  grams  of  sour  milk  (buttermilk,  kefyr) ;  eggs  (1  to  3), 
also  scrambled  eggs  with  considerable  butter  or  bacon. 

2  o'clock:  About  200  grams  of  vegetables  (spinach,  string  beans,  cauli- 
flower, Brussels  sprouts,  asparagus,  artichokes,  sweet  potatoes) ;  about  50 
grams  of  salad  (with  lemon  and  oil),  about  100  grams  of  diabetic  stewed 
fruit;  200  grams  of  cider  or  Moselle  wine;  radishes;  butter  and  cheese 
according  to  desire,  25  grams  of  Graham  bread,  and  two  apples. 

4  o'clock :  Coffee  without  milk,  50  grams  of  manna,  50  grams  of  hitter 
marmalade. 

8  o'clock :  100  to  200  grams  of  meat  or  fish  (even  fat  varieties,  warm  or 
cold)  ;  salad  (as  above)  or  mayonnaise;  diabetic  stewed  fruit;  50  grams 
of  pumpernickel;  30  to  50  grams  of  butter;  cheese  (as  desired);  Moselle 
wine;  radishes. 

Before  going  to  bed:  Two  apples. 

In  this  diet  the  amount  of  carbohydrates  is  not  very  considerable,  but 
it  may  be  even  further  reduced.  Manna,  which  acts  as  a  stimulant  even 
in  the  severest  forms  of  diabetes,  undergoes  complete  combustion.  Atten- 
tion is  called  to  the  large  amount  of  fat  in  the  food  which  serves  the 
purpose  of  stimulating  intestinal  activity. 

If  there  be  a  predisposition  to  obesity,  the  fat  should  be  omitted 
from  the  diet,  and  this,  as  a  rule,  will  produce  a  sufficient  reduction. 

In  the  given  case  other  curative  methods  may  be  added  to  these 
dietetic  rules,  and  this  will  ensure  a  gratifying  result.  Although  there 
can  certainly  be  no  objection  to  this,  yet,  from  a  critical  standpoint,  it 
is  advisable  first  to  test  the  effect  of  one  method,  and  to  employ  a  second 
only  when  the  first  has  failed. 

With  this  constipation  diet  marked  flatulency  is  frequently  observed, 
even  when  its  effect  is  otherwise  very  good.  By  a  suitable  change  in  the 
details  this  may  be  avoided  without  decidedly  lessening  the  effect.     Occa- 


724  CONSTIPATION   AND  HEMORRHOIDS 

sionally,  however,  as  I  have  observed,  a  certain  self-adaptation  of  the  in- 
testine is  noted.  The  fermentation,  previously  marked,  gradually  ceases, 
and  occasionally  this  cessation  appears  to  be  sudden. 

As  further  aids,  we  most  frequently  resort  to  the  following:  Abdom- 
inal massage,  gymnastic  exercises,  and  electricity.^ 

In  regard  to  the  first  of  these  we  must  discriminate  accurately,  as  in 
tlie  results  of  the  diet,  between  temporary  success  and  permanent  cure. 
That  the  former  is  often  attained,  even  with  surprising  rapidity,  there 
cannot  be  the  slightest  doubt.  But,  in  my  experience,  a  permanent  cure, 
even  in  cases  not  too  far  advanced,  i.  e.,  those  which  promptly  respond 
to  dietetic  treatment,  does  not  so  frequently  occur.  At  all  events,  the 
cases  of  cure  of  severe  habitual  constipation  exclusively  by  massage  are 
certainly  rare.  It  might  be  urged  in  opposition  to  this  that  massage  was 
inisui  table  in  these  cases,  or,  perhaps,  that  it  was  not  long  enough  con- 
tinued. This  is,  however,  not  the  case.  I  have  seen  striking  failures 
after  very  thorougli  and  long-continued  massage. 

The  results  of  electric  {usually  faradic)  treatment  are,  in  my  experi- 
ence, more  favorable.  For  tliis  purpose  we  employ  only  faradization  of 
the  abdominal  walls  by  means  of  broad,  flat  electrodes,  or,  even  better, 
l)y  means  of  massage  rolls,  or,  what  is  perhaps  best,  intrarectal  faradiza- 
tion by  means  of  soft  rectal  sounds  composed  of  Nelaton  rubber.^  The 
treatment,  at  first,  should  be  for  about  ten  minutes  daily,  and  with  in- 
creasing improvement  may  be  only  every  second  or  third  day.  In  the 
course  of  time  the  patients  frequently  learn  to  apply  the  current  them- 
selves, or  with  the  aid  of  some  one  at  home;  a  factor  which  is  not  to  be 
undervalued  in  comparison  with  massage. 

Whether  severe  cases  of  habitual  constipation  can  be  cured  either  by 
faradization  of  the  abdominal  walls  or  by  intrarectal  application  appears 
to  me  to  be  doubtful.  But  I  can  positively  assert  that  the  combination 
of  faradization  with  the  diet  elaborated  above  will  generally  bring  about 
a  permanent  recovery.  Unquestionably  relapses  will  occur  and — although 
rarely — failures.  In  my  experience  a  point  of  practical  importance  is  that, 
if  no  results  are  obtained  by  rectal  faradization  within  the  first  two  weeks, 
they  do  not  follow  even  with  continued  treatment. 

As  massage  and  electrotherapy  have  found  numerous  adherents,  so  also 
have  gymnastic  exercises,  indoor  gymnastic  exercises  (Schreber's  curative 
gymnastics)  as  well  as  mechanical  gymnastics  (Swedish  curative  gynl- 
nasties).  In  how  far  these  methods  are  permanently  effective  without 
the  aid  of  others  I  cannot  state,  as  I  have  no  personal  experience.  That 
they  assist  in  a  greater  or  less  degree  cannot  be  doubted. 

1  It  is  not  our  object  to  enter  here  upon  the  technic  of  these  methods,  and  we 
limit  ourselves  to  a  critical  analysis  of  their  curative  value. 

-  lioas,  "  Diagnostik  und  Therapie  der  Darmkrankheiten."  Leipzig,  1901,  2.  Aufl., 
page  178. 


TREATMENT  725 

Among  the  methods  of  treatment  most  frequently  employed,  and  also 
misemployed,  is  hydrotherapy  in  its  various  modes  of  application.  In 
the  atonic  forms  of  habitual  constipation,  cold  Sitz  baths,  or  half  baths 
(22°  to  20°  R.)  with  high  affusions  over  the  abdomen,  as  well  as  rain 
baths  with  a  movable  stream  upon  the  abdomen,  are  of  use.  In  the  spastic 
form  protracted  full  baths  of  warm  water  (30°  to  32°  R.)  or  warm  Sitz 
baths  are  advised.  The  warm  douche,  the  Scotch  douche,  warm  com- 
presses to  the  abdomen,  application  of  hot  tubes,  steam  compresses,  and 
thermophores  are  all  beneficial.  In  obstinate  atonic  constipation  I  have 
occasionally  seen  remarkably  good  results  from  the  application  of  an  ice- 
bag  to  the  abdomen. 

In  one  case,  which  was  extraordinarily  tenacious,  there  was  a  profuse 
evacuation,  contrary  to  all  expectation,  when  the  patient  (who  was  suf- 
fering from  purulent  cholecystitis)  had  an  ice-bag  applied  over  the  hepatic 
region.  After  the  cessation  of  the  attack  constipation  reappeared.  On  the 
repetition  of  the  attack  of  cholecystitis,  an  ice-bag  was  again  applied,  and 
normal  bowel  movements  again  took  place. 

Such  hydropathic  treatment  is  generally  indicated  in  cases  of  intes- 
tinal neurasthenia;  but,  on  careful  observation,  we  must  admit  that  fail- 
ures under  this  form  of  treatment  are  by  no  means  so  rare  as  some  enthu- 
siastic hydrotherapeutists  report. 

Up  to  a  certain  degree,  some  varieties  of  sport  are  included  among 
the  physical  methods:  Bicycling,  rowing,  tennis,  golf  and  others.  They 
may  also  assist  the  curative  action  of  other  remedies. 

We  now  come  to  the  important,  and  most  popular,  form  of  treatment: 
treatment  by  purgatives. 

The  value  of  purgatives — of  this  there  is  no  doubt — is,  according  to 
the  nature  of  the  case,  chiefly  symptomatic.  Nevertheless,  we  note  in 
some  cases  that  mild  or  strong  purgatives  are  taken  for  years,  and  even 
decades,  without  injury  to  the  patient  and — what  is  more  important — 
they  do  not  lose  their  effect.  As  a  rule,  however,  such  a  permanent  effect 
is  not  often  seen. 

Usually  the  condition  is  such  that  patients  rapidly  exhaust  the  entire 
range  of  purgatives,  from  the  mildest  to  the  most  drastic;  and  it  not 
rarely  happens  that  even  these  are  ineffectual  unless  taken  in  dangerously 
large  doses,  when,  accompanied  by  severe  pain,  they  produce  the  desired 
result. 

These  experiences  which  are  constantly  repeated  in  tiresome  monotony 
give  to  the  true  purgatives  a  merely  secondary  position  in  the  treatment 
of  habitual  constipation.  I  employ  them  only  under  two  circumstances: 
In  cases  of  constipation  so  obstinate  that  dietetic  or  physical  remedies  have 
no,  or  but  verv  slight,  result.  But  in  such  cases  I  also  utilize  the  powerful 
effect  of  the  'constipation  diet,  and  supplement  it  by  the  administration 
of  a  mild  laxative  in  the  smallest  doses,  or  by  suitable  injections.  I  use 
47 


726  CONSTIPATION   AND  HEMORRHOIDS 

purgatives  extensively  in  the  constipation  of  the  aged,  i.  e.,  in  persons 
beyond  sixty  years  of  age.  At  this  age  we  may  expect  to  use  moderately 
strong  purgatives  for  years  without  experiencing  difficulty.  In  the  last, 
or  prior  to  the  last,  decade  of  life  I  also  prefer  purgatives  to  injections  as 
being  more  simple.  It  is  presupposed  in  this  that  the  patients  have  not 
as  yet  exhausted  the  whole  armamentarium  of  purgatives. 

In  regard  to  the  choice  of  purgatives  in  the  individual  case,  mild  purga- 
tives have  for  a  long  time  been  distinctly  separated  from  true  drastic 
agents.  The  latter  are  never  employed  in  the  treatment  of  habitual  con- 
stipation unless  complications  occur  in  the  course  of  the  disease.  A  great 
number  of  mild  remedies  are  at  our  disposal,  so  great  that  the  physician, 
no  matter  how  numerous  his  patients,  will  scarcely  ever  be  in  a  position 
to  utilize  all  the  drugs. 

In  my  experience  the  following  remedies  are  quite  sufficient:  Rhubarb 
in  its  various  forms,  magnesia,  effervescent  magnesium'  citrate,  Carlsbad 
salt,  flowers  of  sulphur,  compound  licorice  powder,  extract  of  cascara 
sagrada  (in  the  form  of  the  fluid  extract  or  in  pill),  the  preparations  of 
tamarind  and,  finally,  among  the  newer  remedies,  purgen  (0.5  three  to 
four  times  daily).  Preparations  of  aloes,  podophyllin,  colocynth,  hitter 
waters  and  hitter  salts,  castor  oil,  and  many  others  should  be  relegated  to 
oblivion  in  the  treatment  of  habitual  constipation:  They  do  more  harm 
than  most  physicians  believe. 

The  different  laxative  teas  commonly  used  by  the  laity  (Gastein  tea, 
Hamburg  tea,  Hartz  Mountain  tea)  and  similar  compositions  are  merely 
arbitrary  and  wholly  superfluous  combinations  of  various  active  laxatives, 
the  effect  of  which  must,  naturally,  vary  according  to  the  dose  and  prep- 
aration. 

More  suitable  and  simple  laxative  teas  for  domestic  use  are,  for  exam- 
ple, alder  or  senna  tea  (and  also  cassia) ;  the  herbs  are  placed  in  cold  water 
and  then  allowed  to  boil.  I  occasionally  employ  the  latter  in  this  form, 
and  it  acts  very  profusely  and  without  causing  griping. 

In  employing  either  of  these  remedies  it  is  well,  as  Einhom  advises, 
gradually  to  decrease  the  dose;  this  may  be  done  in  many,  but  not  all 
cases.  In  any  event,  it  should  be  our  object  not  to  use  laxatives  unneces- 
sarily, and  it  is  wise  to  continue  to  use  the  same  remedy,  even  though  in 
increased  doses,  as  long  as  possible. 

Combined  with  a  laxative  therapy  is  the  emplojnnent  of  mineral  waters. 
Among  these  sodium  chlorid  and  Glauber  salt,  occasionally  also  Epsom 
salt,  play  the  main  role.  Possibly  the  action  of  these  spring  waters  is 
more  or  less  increased  by  the  amount  of  carbonic  acid  which  they  contain. 
As  representatives  of  the  first  group  we  have  the  so-called  sodium  chlorid 
waters  (Kissingen,  Homburg,  Wiesbaden,  Mergentheim,  Soden).  Glauber 
salt  is  represented  by  the  hot  springs  of  Carlsbad,  the  cold  springs  of 
Marienbad,  Tarasp,  Elster,  and  Franzensbad.    Epsom  salt  springs  umy  he 


TREATMENT  727 

employed  in  stubborn  cases,  such  as  those  of  Kissingen,  Friedrichshall, 
Hunyadi-Janos,  Saidschiitz,  Montmirail,  Apenta,  etc. 

It  is  evident  that  mineral  water  cures  are  nothing  more  than  purga- 
tive cures,  and  that  from  these  alone  permanent  relief  (in  our  sense)  is 
not  to  be  expected.  Therefore,  cases  of  habitual  constipation  should  not 
be  sent  to  such  spas  with  the  idea  that  the  treatment  there  forms  the  main 
indication.  In  such  cases,  the  patients  return  from  the  fatiguing  and 
expensive  journey  much  disappointed;  a  condition  which  I  see  every  sea- 
son. On  the  other  hand,  mineral  water  cures,  like  laxatives,  may  heighten 
the  effect  of  proper  dietetic  treatment  or  may  lessen  and  even  remove 
some  of  the  complications  of  habitual  constipation,  for  example,  chole- 
lithiasis, hemorrhoids,  and  the  symptoms  of  so-called  autointoxication. 

Unfortunately,  in  the  realization  of  this  hope  the  diagrammatic  effect 
of  the  spa  treatment  with  its  monotonous,  bland  diet  is  rather  inhibitive 
than  effective.  In  this  respect,  the  spa  physician  should  try  to  modify  the 
traditional  and  uniform  dietary  in  force  at  the  different  resorts. 

Injections  form  a  valuable  auxiliary  in  the  treatment  of  habitual  con- 
stipation. It  is  well  to  differentiate  between  occasional  enemata  and  re- 
tained enemata;  both  have  their  distinct  indications  and  proper  places. 
The  first  serve  to  dislodge  by  a  single,  quick  stimulation  masses  of  feces 
impacted  in  the  lower  portion  of  the  bowel.  For  this  purpose  we  may 
combine  chemical  or  thermic  stimulants  with  the  fluid  used  for  injection. 

Since,  however,  in  these  cases,  as  the  name  indicates,  the  action  is  to 
be  rapid,  medicaments  are  of  little  importance.  We  may  rather  look  for 
an  effect  from  thermic  agents.  For  this  the  rule  is  to  employ  occasional 
injections,  preferably  without  additions,  about  one-half  to  one  liter  of  cool 
or  cold  water.  The  smaller  the  quantity  used  the  better  the  result,  as, 
otherwise,  an  immoderate  distention  of  the  already  paretic  musculature 
may  easily  be  produced. 

Much  more  suitable,  and  probably  more  efficacious,  are  retained 
enemata.  They  are  indicated  in  atony  of  the  entire  colon,  and,  inversely, 
chemical  additions  are  very  suitable,  particularly  such  as  have  a  tendency 
gradually  to  soften  the  fecal  masses,  while  the  low  temperature  may  read- 
ily cause  an  abnormally  rapid  peristalsis,  and,  consequently,  only  partial 
evacuation. 

Among  valuable  retained  enemata  we  must  first  mention  those  of  oil 
which  have  been  much  employed  by  Fleiner's  advice.  The  action  of  these  oil 
enemata  is  not,  as  might  be  supposed,  coprolytic  but  antispasmodic.  They 
quiet  the  abnormally  excited  muscular  action  of  the  intestines,  and  thus 
produce  normal  peristalsis.  The  chief  indication  for  oil  enemata  is,  there- 
fore, in  spastic  constipation,  although  satisfactory  results  are  now  and 
then  attained  also  in  the  atonic  form. 

The  oil  enema  should  consist  of  not  more  than  200  to  300  grams,  and 
this  should  remain  in  the  large  intestine  about  ten  hours.     Larger  quan- 


728  CONSTIPATION  AND  HEMOHHHOIDS 

tities  are  superfluous,  and  are  expelled  more  rapidly  than  is  desired.  In- 
versely, we  may  also  obtain  results  with  smaller  quantities,  and  it  is 
therefore  advisable  gradually  to  decrease  the  quantity  of  oil.  Occasion- 
ally, from  the  beginning,  smaller  quantities  of  oil  (50  to  100  grams)  will 
suffice. 

Floiner  attaches  great  value  to  a  neutral  oil,  and  for  this  reason  advises 
the  purest  olive  oil.  In  my  extensive  experience  other  less  refined  oils  are 
just  as  useful,  for  example,  poppy-seed  oil,  palm  oil,  linseed  oil,  rape  oil, 
and  others.  Sesame  oil  is  less  costly  than  olive  oil,  and  just  as  free  from 
fatty  acid,  while  peanut  oil,  lately  introduced  into  commerce,  is  good  and 
cheap. 

One  disadvantage  of  the  treatment  by  oil  enemata  is  the  soiling  of  the 
body  and  bed  linen,  which  cannot  be  prevented  even  by  the  greatest  care. 
An  attempt  has  therefore  been  made  to  substitute  other  active  agents  for 
oil  enemata.  Among  these  I  have  advised  emulsions  of  soda,  castor  oil  and 
cod-liver  oil.  Soap  water  may  also  be  emulsified  with  oil  and  glycerin, 
and  various  additions  may  be  made  to  these  emulsions  (castor  oil,  gum 
arable,  honey,  etc.). 

In  my  opinion  it  is  best  to  give  the  retained  enema  late  at  night  when 
absolutely  at  rest,  i.  e.,  while  the  patient  is  in  bed.  The  injection  should 
be  given  by  means  of  a  simple  irrigator  and  a  soft  rectal  tube.  When 
experience  has  shown  that  the  oil  is  not  retained,  the  irrigation  tube  may 
be  placed  in  a  glass  or  porcelain  vessel  so  that  the  escaping  oil  may  flow 
out  without  soiling  the  bed-linen.     I  have  rarely  made  use  of  this  method. 

Instead  of  an  irrigator,  large  glass  syringes,  or  even  more  complicated 
apparatus  may  be  used,  but  in  none  of  these  instruments  do  I  see  any 
particular  advantage. 

Although  the  treatment  of  intestinal  peristalsis  by  oil  and  emulsion 
enemata  gives  excellent  results,  yet  this  by  no  means  effects  a  cure  of 
liahitual  constipation.  The  method  is  only  palliative.  If  the  treatment 
is  suspended  after  a  short  time,  intestinal  activity  also  ceases,  but  unques- 
tionably, as  a  palliative  method,  the  treatment  by  oil,  although  not  con- 
venient, is  certainly  the  most  effective  method.  It  has  the  additional  advan- 
tage that  it  does  not  lose  its  effect  by  long-continued  use,  and  in  this  re- 
spect is  superior  to  internal  laxatives. 

Instead  of  large  injections,  so-called  minimal  enemata  may  be  used, 
Formerly  Oidtmann's  purgative,  which  consisted  chiefly  of  glycerin,  was 
considered  very  useful.  In  fact,  glycerin  in  small  doses  (2  to  5  grams) 
will  liquefy  fecal  masses  in  the  lower  portion  of  the  intestine.  In  1887, 
instead  of  glycerin  enemata,  I  employed  glycerin  suppositories,  i.  e.,  hollow 
cones  made  of  cacao  butter  and  filled  with  glycerin,  which  since  then  have 
been  much  used,  and  are,  unfortunately,  often  found  in  commerce  in  im- 
proper form. 

Glycerin  and  glycerin  suppositories  may  have  an  irritating  effect;  in 


TREATMENT  729 

hemorrhoids  they  sometimes  increase  the  tendency  to  bleeding,  and,  under 
these  circumstances,  are  contraindicated.  When  there  is  fecal  accumula- 
tion in  the  rectum,  however,  they  are  valuable. 

Hiller^  and,  lately,  Kohlstock  =  have  advised  for  rectal  injection  the 
addition  of  active  principles  of  other  laxatives.  According  to  Kohlstock, 
alpin  and  cathartic  acid,  and,  in  particularly  stubborn  cases,  colocynthin 
and  citrullin  should  be  employed.  These  minimal  enemata  are  said  by 
Kohlstock  to  have  a  prompt  and  painless  effect.  But  the  high  price  of 
the  remedies  unfortunately  prohibits  their  general  employment. 

The  treatment  of  constipation  by  means  of  subcutaneous  injections  has 
found  little  favor,  but  some  of  the  above  named  remedies  and  some  of 
the  neutral  salts  (magnesium  sulphate)  have  been  employed  with  more 
or  less  success.  The  same  is  true  of  endermatic  treatment  of  constipation 
by  means  of  croton  oil  (6  to  10  drops  in  15  to  20  grams  of  olive,  oil)  as 
advised  by  Scarbinato. 

Furthermore,  I  must  call  attention  to  a  mode  of  treatment  of  habitual 
constipation  which  is  apparently  paradoxical,  nevertheless,  in  the  severest 
forms,  it  has  produced  some  surprising  results.  This  is  the  rest  cure.  I 
employ  this  in  cases  accompanied"  by  general  nervous  weakness,  in  which 
the  patient  is  under-nourished,  and  in  which  habitual  constipation  is  the 
main  symptom.  In  cases  which  for  years  had  resisted  the  strongest  purga- 
tives, I  have  seen  results  in  a  very  short  time,  usually  after  even  a  few  days. 

The  diet  is  that  formerly  described.  The  rest  treatment  is  preferably 
carried  out  in  a  sanatorium,  and  should  be  continued  for  from  four  to 
six  weeks.  Under  this  treatment  the  patients  usually  increase  decidedly 
in  weight,  which  favorably  influences  the  general  neurasthenia.  By  this 
method,  or  at  least  after  a  very  few  days,  the  patient  must  do  without 
laxatives  or  enemata,  if  possible. 

Another  method  of  treatment  in  the  neurogenous  form  of  constipa- 
tion consists  in  hypnosis,  which,  so  far  as  I  know,  was  first  successfully 
employed  by  Forel.  Lately  H.  Delius '  has  called  attention  to  the  good 
effects  of  hypnotism  in  functional  constipation. 

From  this  it  is  evident  that  the  number  of  remedies  and  methods  of 
treatment  for  habitual  constipation  is  very  great,  and  the  list  of  laxative 
drugs  increases  from  year  to  year.  In  addition,  some  or  even  most  of  these 
curative  methods  are  used  in  combination,  which  makes  it  difficult  to  esti- 
mate their  value. 

In  my  experience  the  most  effectual  remedy  we  possess  is  a  proper  diet 
rigidly  adhered  to  in  the  manner  previously  detailed.  Occasionally  it  may 
be  without  result,  but,  in  such  cases,  other  curative  measures  are  also 


iHiller,  Zeitschr.  f.  klin.  Medicin,   1882,  IV,  p.  481. 

2  Kohlstock,  Charite-Annalen,  1893,  XVII. 

3  H.  Delius,  Berliner  klin.  Wochenschr.,  1903,  Nr.  38. 


730  CONSTIPATION   AND  HEMORRHOIDS 

fruitless.  In  addition  to  the  diet  for  constipation,  intrarectal  faradiza- 
tion of  the  intestine  alone  can  be  considered  a  permanently  useful  remedy, 
and  this  is,  at  the  same  time,  one  that  can  be  readily  used  by  the  patient. 
Treatment  by  enemata  and  suppositories,  as  a  palliative  method,  and  cor- 
rectly used,  is  harmless  in  uncomplicated  habitual  constipation,  and,  if  the 
other  curative  measures  mentioned  fail,  this  should  first  be  tried.  But 
the  other  remedies,  whether  of  chemical  or  physical  nature,  can  be  dis- 
pensed with  to-day  to  a  much  greater  extent  than  is  generally  supposed. 
Treatment  by  purgatives,  now  so  popular,  is,  except  for  a  few  previously 
mentioned  indications,  the  survival  of  a  medieval,  humoral  pathology 
which  we  should  forever  discard. 


TREATMENT  OF   HEMORRHOIDS 

The  treatment  of  hemorrhoids,  as  is  well  known,  forms  one  of  the 
many  boundary  lines  between  internal  medicine  and  surgery.  Therefore, 
from  my  internal  standpoint,  I  limit  myself  chiefly  to  the  conservative 
treatment  of  hemorrhoids,  and,  in  so  far  as  operative  treatment  comes 
into  question,  I  shall  describe  the  principal  indications. 

As  we  have  previously  seen,  hemorrhoids  are  largely  due  to  local  in- 
hibitive  causes  which  prevent  the  flow  of  blood  into  the  great  reservoirs  of 
the  liver  (the  portal  vein  and  vena  cava),  and  therefore,  broadly  viewed, 
the  primary  object  of  treatment  is  the  removal  of  these  factors  which 
inhibit  the  circulation  of  the  blood. 

In  many  cases  the  carrying  out  of  an  etiologic  treatment  is  simply 
impossible;  for  example,  in  hemorrhoids  due  to  pregnancy,  in  inoperable 
tumors  of  the  bladder,  of  the  colon,  and  of  the  rectum,  in  marked  enlarge- 
ments of  the  prostate  gland. 

Nevertheless,  these  conditions  are  decidedly  subordinate  compared  with 
the  most  frequent  form  of  hemorrhoids  which  chiefly  owe  their  develop- 
ment to  fecal  masses  impacted  in  the  lower  part  of  the  intestine.  More- 
over, hemorrhoids  are  not  infrequently  accompanying  symptoms  of  catarrh 
of  the  colon,  even  when  this  latter  affection  leads  to  diarrhea. 

In  delineating  the  treatment  we  shall  consider  first  the  common  form 
of  hemorrhoids,  that  due  to  habitual  constipation,  and  here  the  relations 
arc  easily  traced.  Our  first  object  must  be  the  removal  of  the  cause  of 
the  hemorrhoids,  i.  e.,  the  constipation,  and  especially  the  accumulation  of 
feces  in  the  lowest  portion  of  the  intestine.  There  are  many  remedies  and 
methods  for  this  purpose,  but  all  are  not  practicable,  some  are  even  dan- 
gerous. In  general,  we  may  state  that  all  treatment  by  laxatives,  not 
merely  by  drastics,  is  inadvisable. 

Laxatives,  which  are  at  first  given  in  very  small  doses,  soon  lose  their 
effect ;  or,  if  given  in  large  doses,  their  action  is  too  powerful  and  pro- 
duces unpleasant  secondary  symptoms.    The  patient  is  then  in  a  constant 


TREATMENT  73I 

struggle  between  incomplete  or  immoderate  evacuations,  both  unfavorable 
conditions  for  hemorrhoids. 

The  same  may  be  said  of  the  treatment  of  hemorrhoids  by  enemata. 
Frequently  the  varices  become  inflamed  by  mechanical  or  chemical  irri- 
tation, and  this  increases  the  sufferings  of  the  patient.  At  most,  mild 
enemata  of  oil  by  means  of  a  soft  rectal  tube  which  should  be  cleansed 
each  time  before  use  may  prevent  these  disagreeable  consequences. 

In  hemorrhoids  combined  with  constipation  the  rational  method  con- 
sists in  producing  sufficient  and  properly  formed,  i.  e.,  pappy,  evacuations 
by  a  continuous  dietetic  treatment,  and  to  prevent  fecal  impaction  in  the 
region  of  the  ampulla  recti.  As  this  is  made  possible  in  the  overwhelm- 
ing majority  of  cases,  even  the  very  chronic  ones,  by  the  previously  de- 
scribed diet  for  constipation,  there  is,  as  a  rule,  no  indication  for  treat- 
ment by  laxatives.  Exceptionally  this  must  be  considered,  either  when 
rigid  adherence  to  these  dietetic  rules  is  impossible  or  when,  in  fact,  even 
with  careful  employment,  it  produces  no  result.  But  in  these  cases,  as 
already  stated,  small  doses  of  the  mildest  laxatives  will  be  sufficient— I 
allude  to  the  old  and  reliable  compound  licorice  powder,  flowers  of  sulphur, 
rhubarb,  cascara  sagrada,  and  the  like. 

Besides  the  special  diet,  general  hygienic  laws,  so  far  as  practicable 
considering  the  occupation  of  the  patient,  must  be  observed:  As  much 
exercise  as  possible,  gymnastics,  swimming,  rowing,  billiards  and  bowl- 
ing, lawn  tennis  and  football.  On  the  other  hand,  it  is  frequently  main- 
tained that  horseback  riding  and  bicycling  increase  the  distress  from 
hemorrhoids. 

The  value  of  these  exercises  must  not  be  undervalued,  but  neither  must 
it  be  exaggerated ;  in  my  experience  the  latter  is  most  often  the  case. 

According  to  Oeder,^  a  valuable  aid  in  the  treatment  of  hemorrhoids 
consists  in  elevating  the  buttocks;  this  may  best  be  accomplished  by  using 
a  wedge-shaped  pillow  or  by  the  elevation  of  the  foot  of  the  bed,  thus  caus- 
ing a  better  circulation  of  the  blood  from  the  nodule.  This  is  said  to  be 
more  beneficial  than  any  form  of  bodily  exercise. 

Mineral  water  cures  take  a  prominent  place  to-day  in  the  treatment  of 
hemorrhoids  and  are  carried  out  either  at  home  or  at  the  springs.  Here, 
too.  the  springs  which  contain  sodium  chlorid  or  Glauber  salt  are  the  best. 
As  to  the  results  of  this  treatment  we  may  refer  to  what  has  been  pre- 
viously said,  in  which  perhaps  the  effect  of  these  cures  may  be  estimated 
somewliat  more  highly  than  in  the  case  of  uncomplicated  constipation, 
since  here  simultaneously  the  favorable  influence  of  the  baths  is  added. 
But  just  as  habitual  constipation  is  never  cured  by  mineral  water  treat- 
ment or  even  relieved  for  any  length  of  time,  neither  is  there  any  perma- 
nent effect  upon  the  hemorrhoids.    It  is  therefore  the  duty  of  the  family 

1  Oeder,  Zeitschr.  f.  didtet.  u.  physikal.  Therapie,  1900-1901,  IV,  Heft  8. 


732  CONSTIPATION  AND  HEMORRHOIDS 

physician,  if  such  a  treatment  is  under  consideration,  expressly  to  warn 
the  patient  not  to  entertain  exaggerated  hopes. 

In  the  same  category  as  mineral  spring  treatment  is  the  grape  cure, 
which  also  tends  to  regulate  the  intestinal  function,  and  in  this  manner 
has  an  immediately  favorable  effect  upon  the  hemorrhoids.  But,  like 
the  treatment  with  mineral  waters  containing  sodium  chlorid  and  Glauber 
salt,  there  is  no  permanent  result. 

Another  part  of  the  treatment  of  hemorrhoids  consists  in  the  observa- 
tion and  the  proper  treatment  of  the  nodules  themselves. 

Observation  should  begin  in  the  earliest  stage  of  hemorrhoids.  Cold 
applications  to  the  hemorrhoids,  solutions  of  tannin,  iodin,  potassium 
iodid  or  alum  are  advisable,  preferably  after  a  fecal  evacuation  for  the 
nodules  are  then  most  prominent.  By  this  treatment  the  vascular  wall 
becomes  somewhat  leathery,  and  the  tendency  to  hemorrhage  and  ulcer- 
ation is  lessened.  With  so-called  internal  hemorrhoids,  the  same  effect 
may  be  produced  by  injections  into  the  rectum  of  the  previously  mentioned 
solutions. 

The  etiologic  treatment  of  hemorrhoids  is  valuable,  and  chiefly  indi- 
cated in  those  cases  of  hemorrhoids  not  yet  far  advanced.  It  fails  of 
success,  however,  where  the  affection  has  become  severe,  or  where  there 
are  complications. 

Even  in  such  cases  symptomatic  treatment  is  often  useful,  and  may 
produce  permanent,  sometimes  only  temporary,  amelioration. 

Except  for  some  rare  sequels,  the  complications  to  be  chiefly  considered 
are  the  following:  Ulceration,  hemorrhage,  incarceration,  and  prolapse. 

Mild  cases  of  ulceration  may  be  cured  by  suitable  astringent  suppos- 
itories consisting  of  tannin  or  aloin,  or,  quite  properly,  anusol  supposi- 
tories (bismuth  with  iodin,  resorcin,  and  sulphurous  acid)  or  by  injections 
of  solutions  of  silver  or  protargol. 

According  to  Kossobudskj,  suppositories  consisting  of  chrysarobin,  iodo- 
form and  belladonna  are  much  employed  in  about  the  following  formula: 

1^   Chrysarobin 0.08 

Iodoform    0.02 

Extr.  Belladonnae 0.01 

Butyr.   Cacao    2.0 

M.  D.     S. :  Suppository  introduced  two  or  three  times  daily. 

In  external  ulceration  an  ointment  of  the  following  composition  is 
advised,  and  is  to  be  used  in  the  same  way : 

^   Chrysarobin 0.8 

Iodoform   0.3 

Extr.    Belladonnae 0.6 

Vaselin 15.0 

M.  D.     S. :  Applied  several  times  daily. 


TREATMENT  >  733 

In  severe  cases  it  is  well  not  to  spend  too  much  time  on  palliative  meth- 
ods, but  to  advise  the  operative  removal  of  the  nodules. 

Bleeding  from  hemorrhoids,  if  only  slight  or  infrequent,  requires  no 
special  treatment.  When  it  occurs  regularly  and  debilitates  the  patient,  it 
must  be  checked. 

In  such  cases  we  must  first  attempt  to  control  the  hemorrhages  by 
proper  regiilation  of  the  bowels,  i.  e.,  as  far  as  possible  to  combat  the 
condition  by  diet.  This  is  by  no  means  always  practicable,  and  therefore 
to  control  the  hemorrhages,  or,  at  least,  to  limit  them,  we  must  resort  to 
suitable  internal  or  external  remedies.  For  this  purpose,  styptics  have 
been  advised  and  employed,  naturally  in  the  form  of  anal  injections.  It  is 
obvious  that  these  remedies  (iron  chlorid,  tannin,  alum,  lead  acetate,  ferro- 
pyrin,  iodoform,  etc.)  have  very  little  value,  inasmuch  as  they  control  only 
a  momentary  hemorrhage  but  by  no  means  prevent  its  repetition.  As  a 
matter  of  fact,  I  have  never  seen  success  from  these  styptic  remedies  in 
cases  of  obstinate  hemorrhage.  On  the  other  hand,  excellent  results  are 
attained  by  injections  of  calcium  chlorid  into  the  rectum.  I  order  these 
in  a  solution  of  10  to  100,  of  which  10  c.c.  are  injected  once  or  twice 
daily  by  means  of  a  small  rectal  syringe.  I  am  unable  to  say  from  my 
own  experience  whether  the  same  results  may  be  attained  by  gelatin  injec- 
tions, but  it  is  quite  likely,  since  the  action  of  gelatin  is  due  to  the  amount 
of  calcium  salt  which  it  contains.  At  all  events,  the  injection  of  solutions 
of  calcium  chlorid  has  the  advantage  of  greater  simplicity.  Even  with  this 
method  I  have  occasionally  seen  failures  or  imperfect  results;  but  this  is 
exceptional. 

Styptics  have  also  been  employed  internally,  and  I  must  mention  par- 
ticularly the  extract  of  hamamelis  which  is  praised  by  some  as  almost  a 
specific  in  the  bleeding  of  hemorrhoids.  I  have  employed  the  fluid  ex- 
tract of  hamamelis  in  doses  of  a  teaspoonf  ul  three  times  daily,  and  in  some 
cases  unquestionably  with  good  results.  To  effect  a  permanent  cure,  how- 
ever, it  must  be  continued  for  many  months.  Besides  the  internal  use 
of  hamamelis,  suppositories  of  hamamelis  (0.25  per  dose)  may  be  em- 
ployed, but  I  believe  that  better  results  are  obtained  by  its  internal  admin- 
istration. 

In  a  serious,  acute  hemorrhage  we  should  not  spend  much  time  on 
uncertain  remedies.  The  most  effective  is  careful  tamponing  of  the  rec- 
tum with  ferropyrin,  iron  cUorid,  or  iodoform  gauze.  Tamponing  with 
gauze  dipped  in  a  30  per  cent,  solution  of  hydrogen  peroxid  is,  perhaps, 
advisable,  for  HoOo,  as  I  have  long  known,  has  an  excellent  styptic  action. 
With  this  treatment,  however,  we  must  be  careful  to  see  that  the  tampon 
actually  reaches  the  bleeding  point,  for,  otherwise,  the  hemorrhage  will 
continue  in  spite  of  the  tampon.  At  the  same  time  a  decided  dose  of 
opium  should  be  given  internally  to  arrest  intestinal  peristalsis.  After 
the  hemorrhage  has  ceased  the  tampon  may  be  removed,  and  the  intestine 


734  CONSTIPATION  AND  HEMORRHOIDS 

may  be  emptied  by  oil  enemata  or  the  internal  administration  of  castor 
oil. 

Another  and  very  serious  complication  is  incarceration  of  the  nodules. 
TTsually  the  physician  is  called  in  after  many  improper  methods  to  pro- 
duce taxis  have  increased  the  incarceration  to  the  utmost.  It  is  danger- 
ous then  to  continue  efforts  to  replace  these  nodules,  particularly  if  they 
are  swollen,  of  an  intense  blue  color,  the  surroundings  edematous,  and 
the  patient  moaning  with  pain.  Here  quiet  waiting  is  preferable  to  any 
active  measures.  We  must  be  content  with  elevating  the  buttocks  in  the 
manner  described  by  Oeder,  the  application  of  ice  to  the  hemorrhoids,  and 
the  employment  of  opium  and  belladonna  by  suppository.  If  the  physician 
is  called  to  the  patient  during  the  daytime,  depletion  by  the  application 
of  leeches  to  the  areas  surrounding  the  varices  (not  these  themselves) 
may  rapidly  produce  amelioration  and  the  desired  reposition.  If  gan- 
grene has  already  set  in,  we  make  no  attempt  to  replace  the  hemorrhoids, 
but  treat  the  gangrenous  nodules  with  antiseptic  powders  (xeroform,  airol, 
vioform  and  others). 

In  conclusion,  we  must  mention  one  of  the  most  disagreeable,  although 
not  very  painful,  complications,  prolapse  of  the  hemorrhoids.  In  milder 
cases,  i.  e.,  those  in  which  prolapse  occurs  only  upon  defecation,  the  patients 
soon  learn  to  aid  themselves  and  readily  return  the  prolapse  to  the  rectum. 
In  advanced  cases,  prolapse  follows  any  exertion,  or,  at  least,  any  that  is 
considerable,  and  then  it  becomes  desirable  and  necessary  to  resort  to  pre- 
ventive measures.  Simple  remedies,  and  also  occasionally  very  useful,  are 
the  so-called  liemorrJioidal  pessaries  (first  advised  by  Dr.  Liitje).  But 
these  often  fail  in  their  action,  causing  pressure  and  pain,  and  are  more 
often  carried  in  the  pocket  of  the  patient  than  in  the  rectum. 

In  severe  cases  of  hemorrhoidal  prolapse,  a  so-called  rectal  support 
has  been  advised  by  Esmarch,  i.  e.,  a  sort  of  plate  which  is  placed  over 
the  anus  to  prevent  the  prolapse.  I  do  not  know  whether  or  not  this 
apparatus  has  proven  useful.  I  tried  it  in  a  few  cases  of  severe  prolapse, 
and  it  was  unsuccessful. 

As  is  shown  by  the  preceding,  internal  and  conservative  therapy  has  a 
wide  field  in  the  treatment  of  hemorrhoids,  particularly  if  the  affection 
is  not  too  far  advanced,  and  if  there  are  no  serious  complications;  but 
it  also  has  its  limits,  when  the  only  relief  is  by  operation.  This  method 
will  be  employed  more  rarely,  the  earlier  and  more  carefully  we  institute 
trt'atment  by  the  methods  above  described. 


^MUCOUS  COLIC  AND   MEMBRANOUS. 
INTESTINAL   CATARRH 

By  G.  HOPPE-SEYLER,  Kiel 

The  appearance  of  membranous,  tape-like  or  circular,  even  net-like 
masses  in  the  feces  has  frequently  interested  the  laity  and  physicians.  The 
occurrence  makes  the  patient  anxious,  and  gives  him  an  idea  that  these 
are  parasites,  tape-worms  or  the  like,  or  even  that  portions  of  the  intes- 
tine, particles  of  its  mucous  membrane  covering,  are  desquamated.  If,  as 
frequently  happens,  there  are  severe  symptoms,  attacks  of  colic  or  tenes- 
mus, and  only  very  scant,  hard  masses  are  voided,  among  which  are  pro- 
fuse amounts  of  the  abnormal  particles,  it  is  not  necessary  that  the  patient 
be  of  a  nervous  disposition,  as  most  of  these  patients  are,  to  make  him  fear 
that  he  is  suffering  from  a  severe  disease.  Neither  does  the  physician 
regard  this  clinical  picture  with  the  easy  assurance  which  he  feels,  for 
instance,  in  the  case  of  an  ordinary  chronic  catarrh  of  the  large  intestine 
which,  in  consequence  of  an  improper  mode  of  life,  has  developed  into  an 
acute  catarrh  with  frequent  relapses.  We  are  not  yet  certain  of  the  nature 
of  the  affection;  a  positive  etiologic  and  anatomic  foundation  is  lacking, 
and  curative  treatment  proves  to  be  difficult,  tedious  and  elusive.  Scarcely 
do  we  think  we  have  mastered  the  disease  when  an  error  in  diet,  a  psychical 
climax,  any  irregularity  restores  it  in  all  its  severity.  Nevertheless,  the 
medical  world  has  frequently  and  very  actively  busied  itself  with  this  dis- 
ease in  the  last  few  decades,  and  the  interest  which  it  has  awakened  finds 
expression  in  the  great  number  of  designations  which  have  been  proposed 
for  it,  and  which  now  abound  in  literature.  According  to  the  special 
view  of  its  nomenclator,  the  greatest  stress  is  laid  either  upon  the  intes- 
tinal lesion  or  upon  the  nervous  disturbances.  We  find  the  following  terms 
employed  as  synonyms:  Enteritis  s.  colitis  membranacea,  pseudo-mem- 
branacea,  pellicularis,  tubularis,  mucomembranosa,  crouposa,  fibrinosa, 
etc.,  pseudoenteritis,  catarrhus  desquamativus,  diarrhoea  membranacea, 
tubularis,  etc.,  finally,  colica  mucosa,  mucous  colic,  as  Nothnagel  ^  desig- 
nates at  least  some  of  the  cases.  Some  of  these  designations  apply  only 
to  a  few  of  the  cases ;  the  designation  "  crouposa "  or  "  fibrinosa "  does 
not  coincide  with  what  we  know  to-day  of  the  composition  of  the  charac- 
teristic membranous  masses.     As  they  are  principally  composed  of  mucus, 

1  Nothnagel,  "  Beitrage  zur  Physiologie  und  Pathologie  des  Darms,"  Berlin,  1884; 
"  Erkrankungen  des  Darms  und  Peritoneums,"  Wien,  1895,  p.  144. 

735 


736      MUCOUS  COLIC  AND  MEMBRANOUS   INTESTINAL  CATARRH 

the  designation  "  mucosa  "  is  more  fitting.  Lately,  an  endeavor  has  been 
made  to  discriminate,  and  to  designate  by  the  terms  enteritis  or  colitis 
memhranacea,  etc.,  only  those  cases  which  present  definite  symptoms  of 
intestinal  catarrh,  and  particularly  of  chronic  intestinal  catarrh.  The 
formation  of  compact  membranous  mucus  masses  is  characteristic  of  this 
form  in  contrast  to  other  catarrhs  of  the  large  intestine.  By  colica  mucosa 
or  mucous  colic,  however,  we  mean  cases  which  are  characterized  by  the 
passage  of  firm  membranous  masses  of  mucus  in  connection  with  severe 
attacks  of  colic.  In  these  we  do  not  assume  a  catarrhal  condition  of  the 
intestinal  mucous  membrane,  but  believe  the  condition  to  be  due  to  a 
so-called  neurosis  of  secretion.  This  is  favored  by  the  fact  that  the  affec- 
tion is  usually  observed  in  persons  who  present  other  distinct  symptoms 
of  nervous  disturbance. 

In  the  conception  of  mucous  colic  as  a  purely  nervous,  intestinal  dis- 
ease, we  find  that  it  is  clinically  difficult  to  exclude  a  catarrhal  condition 
of  the  intestine,  and  that  all  possible  transitional  stages  are  known,  ranging 
from  an  apparently  chronic  catarrh  of  the  large  intestine  with  the  occa- 
sional passage  of  membranous  mucus  masses  to  a  well-developed  mucous 
colic  without  distinctly  prominent  processes  of  inflammation  of  the  mucous 
membrane.  In  describing  the  clinical  and  the  anatomical  picture  we  shall 
have  to  consider  this  condition  somewhat  more  in  detail. 


ETIOLOGY  AND   PATHOGENESIS 

Inquiry  into  the  caw.se  and  mode  of  development  of  the  disease  pri- 
marily reveals  the  conspicuous  fact  that  the  condition  usually  occurs  in 
"  nervous "  individuals.  The  patients  invariably  show  distinct  signs  of 
functional  nervous  disturbance;  they  are  hysterical,  neurasthenic,  hypo- 
chondriac, and  often  decidedly  disturbed  mentally;  persons  with  melan- 
cholia are  especially  prone  to  the  attack.  These  alterations  of  the  nerv- 
ous system  have  usually  existed  prior  to  the  development  of  the  intestinal 
disease,  the  certain  relation  of  which  to  alterations  of  the  nerves  cannot 
be  denied.  Further,  the  decided  preponderance  of  females  affected  is  dis- 
tinctly noticeable.  In  about  90  per  cent,  the  cases  occur  in  women,  the 
remainder  being  divided  between  men  and  children.  Definite  relations  of 
the  affection  in  women  to  diseases  of  the  genital  organs  have  been  consid- 
ered. It  is  true  these  very  often  occur  simultaneously  with  enteritis  mem- 
hranacea; yet  a  positive  connection  cannot  be  determined.  If  we  consider, 
however,  that  in  consequence  of  disturbances  in  the  uterus  and  its  adnexa, 
disorders  of  the  digestive  organs  frequently  occur,  particularly  constipa- 
tion, chronic  irritative  conditions,  catarrh  of  the  mucous  membrane,  me- 
chanical obstruction  to  the  discharge  of  the  feces  in  consequence  of  adhe- 
sions, displacements,  etc.,  such  a  condition  does  not  appear  remarkable.  We 
must,  therefore,  assume  the  predisposition  of  women  with  genital  affections 


ETIOLOGY  AND  PATHOGENESIS  737 

to  the  disease  we  are  describing.  It  appears,  also,  that  other  factors  which 
limit  the  motility  of  the  intestine,  which  by  torsion  or  pressure  irritate 
or  narrow  it,  may  assist  in  the  development  of  the  disease;  thus  perito- 
neal adhesions,  bands  which  constrict  the  intestine,  compressing  it  and 
producing  traction  upon  it,  must  be  considered.  In  cholecystitis,  particu- 
larly that  in  consequence  of  gall-stones,  adhesions  may  readily  form  which 
implicate  the  adjacent  intestines.  After  operations  in  such  persons,  we  not 
infrequently  note  serious  disturbances  which  may  be  referred  to  adhesions 
that  have  previously  arisen.  These  manifest  themselves  as  disturbances  of 
intestinal  activity,  particularly  by  colicky  pains,  which  are  frequently  be- 
lieved to  be  gall-stone  colic.  Upon  daily  and  close  investigation  of  the 
discharges,  the  characteristic  mucous  pseudo-membranes  are  either  found 
alone  or  admixed  with  hard  fecal  masses.  In  connection  with  an  inflam- 
mation of  the  cecum  and  of  the  vermiform  appendix,  perityphlitic  adhe- 
sions very  frequently  develop  which  lead  to  similar  disturbances.  Not 
rarely  we  find  gastroptosis,  enteroptosis,  nephroptosis,  and  splenoptosis, 
etc. ;  as  consequences  of  lacing,  flaccidity  of  the  abdominal  walls  and  ema- 
ciation. In  some  cases  the  structure  of  the  body  has  a  certain  predispos- 
ing effect ;  usually  we  see  this  "  enteroptosis  "  develop  after  moderate  pres- 
sure by  tight  clothes  and  corset  has  been  exerted  upon  the  hypochondrium 
and  epigastrium,  or  where  a  ventral  hernia  has  been  produced  in  preg- 
nancy by  the  over-distention  of  the  abdominal  muscles,  and  this  proper 
support  for  the  organs  is  absent  in  an  erect  position.  These  processes 
are  often  combined  with  marked  loss  of  fat,  loosening  of  the  suspensory 
ligaments,  of  the  surrounding  connective  tissue,  disappearance  of  the  mesen- 
teric and  omental  fat,  and  this  loss  greatly  facilitates  displacement  of  the 
abdominal  organs.  This  brings  the  pressure  of  the  displaced  kidneys,  of 
the  spleen,  etc.,  upon  the  intestines,  particularly  upon  the  large  intes- 
tine, and,  on  the  other  hand,  leads  to  torsion  and  marked  volvulus  of  the 
same,  which  becomes  especially  operative  in  the  natural  bends  and  flexures 
of  the  body.  Thus  I  frequently  determined  decided  displacements  and 
changes  in  the  abdominal  organs  in  women  with  membranous  enteritis, 
and  the  difficulties  were  most  pronounced  in  the  region  of  the  ascending 
and  descending  colon,  particularly  in  the  right  and  left  flexures. 

The  mode  of  life  appears  to  have  some  influence  upon  the  development 
of  the  disease.  Frequently  the  regular  action  of  the  bowels  has  been  en- 
tirely neglected.  On  account  of  convenience  or  social  considerations  the 
inclination  to  stool  is  disregarded;  the  intestines  become  accustomed  to 
the  accumulation  of  feces,  and  evacuations  occur  only  at  intervals  of  sev- 
eral days.  Many  women  are  uninjured  by  this,  and  it  produces  no  dis- 
turbance of  health;  in  not  a  few,  however,  catarrh  of  the  large  intestine 
and  a  permanent  weakness  in  defecation  results.  Then,  when  disagreeable 
sensations  develop,  purgatives  are  taken,  without  any  change  in  the  mode 
of  life,  or  any  attempt  to  regulate  the  intestinal  activity  by  exercise,  gym- 


738      MUCOUS  COLIC   AND   MEMBRANOUS   INTESTINAL  CATARRH 

nasties  or  massage.  Preferably,  laxatives  and  drastics  are  taken  which 
powerfully  irritate  the  mucous  membrane,  and  stimulate  the  muscularis 
to  severe,  often  spasmodic,  contractions.  Thus  an  irritative  condition  of 
the  mucous  membrane  develops,  which  does  not  go  beyond  the  stage  of 
an  ordinary  catarrh,  but  which  is  combined  with  a  tendency  on  the  part 
of  the  intestine  to  irregular,  strong  contractions,  and  upon  this  founda- 
tion of  abnormal  processes,  membranous  enteritis  readily  develops. 

The  disease  usually  is  found  in  persons  of  middle  life.  In  advanced 
age  it  is  rare,  and  is  then  the  result  of  a  pathologic  habit  acquired  in 
former  years.  Not  rarely  we  hear  of  aged  women  who  had  suffered  years 
previously  from  the  passage  of  membranous  masses,  and  had  gradually 
recovered  in  later  life.  In  children  the  affection  is  rare,  yet  some  un- 
doubted cases  are  found  in  literature. 


PATHOLOGIC   ANATOMY 

The  anatomical  lesions  in  mucous  colic  and  in  membranous  intestinal 
catarrh  are  not  yet  quite  known  to  us.  But  few  autopsies  have  been  held, 
and  in  many  of  these  the  question  has  arisen,  in  how  far  the  changes  found 
are  in  actual  relation  with  the  affection,  and  whether  they  are  not  to  a 
great  extent  accidental  secondary  findings.  The  disease  in  itself  is  not 
one  that  endangers  life,  and  therefore  is  rarely  observed  at  the  necropsy; 
furthermore,  we  then  usually  find  manifold  alterations  due  to  the  affec- 
tion which  has  caused  death.  If  we  omit  from  consideration  the  cases 
not  observed  during  life,  the  autopsy  reports  are  reduced  to  merely  the 
eases  of  0.  Rothmann  ^  and  M.  Rothmann.'^  In  the  patient  of  the  first 
author,  who  suffered  from  typical  mucous  colic  and  who  succumbed  to  a  per- 
forating ulcer  of  the  duodenum,  nothing  was  found  in  the  intestine.  The 
report  states :  "  Although  the  entire  intestinal  tract  was  investigated,  the 
remaining  organs  showed  nothing  abnormal."  This  does  not  indicate 
whether  or  not  a  histologic  examination  of  the  intestinal  canal  was  made, 
ill  M.  Rothmann's  case  the  cause  of  death  was  a  carcinoma  at  the  base 
of  the  skull.  During  life  there  was  obstinate  constipation;  after  intes- 
tinal wasliings  numerous  strand-like  masses  of  a  whitish  mucus  without 
fecal  admixture  were  several  times  discharged.  Pain  was  not  present. 
In  this  case  distinct  changes  were  found  in  the  mucous  membrane,  par- 
ticularly in  the  descending  colon.  In  the  transverse  colon  were  some 
fecal  masses.  Where  these  were  absent,  the  mucous  membrane  was  injected 
and  formed  in  folds,  and  this  was  particularly  the  case  in  the  narrow, 
contracted  descending  colon.  The  narrowed  lumen  was  entirely  filled  by 
whitish,  partly  membranous,  partly  ribbon-like  masses  without  fecal  ad- 

1  Deutsche  med.   Wochenschr.,   1887,  p.  602. 

2  Deutsche  med.  Wochenschr.,   1893,  Nr.  41. 


SYMPTOMS  AND  COURSE  739 

mixture.  The  ascending  colon  was  entirely  filled  with  feces  without  mem- 
branes, but  showed  reddening  of  the  mucous  membrane.  The  membranes 
present  in  the  lower  portions  of  the  colon  and  rectum  could  be  detached 
from  the  hyperemic  mucous  membranes  without  loss  of  substance.  The 
small  intestine  was  reddened  and  contained  feces.  Upon  microscopic  ex- 
amination the  epithelial  coat  of  the  mucous  membrane  was  entirely  dis- 
placed by  the  mucus  masses;  they  penetrated  to  the  fundus  of  the  glan- 
dular ducts,  and  even  gave  off  lateral  branches  to  the  individual  beaker 
cells.  Nowhere  could  fibrin  be  found;  the  stained  preparations  gave  only 
the  signs  of  mucin.  Between  the  glandular  tubules  there  was  cell  infiltra- 
tion and  dissemination  of  the  mucosa. 

Here  we  have,  therefore,  the  characteristic  features  of  an  intense 
catarrh.  In  other  cases  in  which  the  condition  was  not  observed  intra  vitam 
the  mucous  membrane  is  described  as  normal,  as  in  the  case  first  men- 
tioned. 

It  is  evident  that  in  the  mucous  membrane  of  the  large  intestines  no 
gross  changes  need  be  present  to  produce  this  disease.  In  very  many 
cases  this  coincides  with  clinical  observation,  for  frequently  all  inflamma- 
tory symptoms  are  absent.  When  the  attack  has  run  its  course,  no  symp- 
toms can  be  noted.  Similar  conditions  are  apparently  present  in  so-called 
fibrinous  bronchitis,  as  was,  for  example,  mentioned  by  Litten.  But,  as  in 
these  cases,  accurate  anatomical  data  are  not  at  hand. 

It  is  to  be  hoped  that  we  shall,  in  the  future,  secure  positive  post  mor- 
tem findings  from  cases  that  have  suffered  from  the  disease,  and  thus 
obtain  a  clearer  idea  of  the  probable  alterations  of  the  mucous  membrane 
than  is  at  present  the  case. 

It  should  be  borne  in  mind  that  definite  conclusions  as  to  the  nature 
of  the  affection  are  not  to  be  reached  in  every  case  in  which  compact  mem- 
branes, or  strand-like  mucous  membranes,  have  once  been  passed.  Only 
when  the  characteristic  passage  of  such  masses  has  been  observed  during 
life  and,  as  in  the  case  of  M.  Rothmann,  these  are  still  present  in  the  intes- 
tine after  death,  will  it  be  possible  to  determine  the  causative  anatomical 
lesion  of  the  affection,  and,  by  the  aid  of  histologic  examination,  obtain 
any  light  as  to  its  origin. 

For  the  present,  we  must  content  ourselves  with  obtaining  grounds 
of  support  for  its  characterization  and  pathogenesis  principally  from  the 
examination  of  the  dejecta  and  from  the  clinical  picture,  and  this,  as  we 
shall  see,  is  possible  to  quite  a  decided  extent. 

SYMPTOMS  AND   COURSE 

The  most  important  feature  of  the  clinical  picture,  and  in  the  course 
of  ill  e  disease,  is  the  passage  at  irregular  intervals  of  compact  mucus  masses 
with  or  without  attacks  of  colic. 


740      MUCOUS  COLIC  AND  MEMBRANOUS  INTESTINAL  CATARRH 

The  course  varies  greatly.  In  some  eases  the  disease  appears  suddenly 
with  a  severe  attack  of  colic,  and  terminates  with  the  discharge  of  the 
characteristic  masses.  These  attacks  are  repeated  after  days,  weeks  or 
months;  or  it  may  be  that  one  attack  only  takes  place.  In  other  cases 
there  is  at  first  constipation,  sometimes  alternating  with  diarrhea,  and  this 
is  followed  by  decided  symptoms  of  tormina,  tenesmus,  and  the  passage 
of  membranous  masses  with  or  without  particles  of  feces.  Simultaneously 
there  is  usually  anorexia,  often  a  sense  of  pressure  in  the  head,  a  sensa- 
tion of  fulness  in  the  abdomen,  perhaps  even  some  pain  in  this  region, 
which,  however,  is  not  definitely  localized,  and  does  not  assume  a  colicky 
character.  The  patients  are  feeble,  are  incapable  of  mental  or  bodily  ex- 
ertion, and,  therefore,  readily  become  irritable  and  morbid.  Evacuation 
of  the  bowels,  particularly  by  enemata,  brings  relief.  Laxatives  and  dras- 
tics which  they  frequently  employ,  and  often  to  an  excess,  usually  are 
without  effect.  On  the  contrary,  these  drugs  cause  decided  pain  which 
sometimes  resembles  colic;  tenesmus  is  increased.  The  patient's  frequent 
attempts  to  evacuate  the  bowels  result  in  the  passage  of  only  small  quan- 
tities of  compact  or  fluid  feces,  with  or  without  membranes.  They  become 
exhausted,  and  are  more  miserable  than  prior  to  the  taking  of  the  purga- 
tives. Rectal  injections,  provided  irritating  substances  are  used,  also  pro- 
duce unpleasant  sensations  and  increased  tenesmus,  and  sometimes  also 
tormina.  A  one  per  cent,  salt  solution  or  Ems  water  is  more  grateful  to 
the  patient,  lessens  the  tenesmus,  and  renders  easy  the  expulsion  of  the 
mucus  masses  as  well  as  of  the  feces  that  may  be  present.  Frequently  the 
patients  take  enemata  in  rapid  succession  until  the  abnormal  masses  and 
the  fecal  contents  of  the  lower  intestinal  areas  have  been  discharged.  At 
first  fecal  particles  are  usually  passed,  then  mucus  masses  with  or  without 
feces,  finally,  often,  fecal  masses.  In  many  cases  the  patients  anxiously 
note  their  fecal  discharges.  If  delayed,  or  apparently  insufficient,  enemata 
are  at  once  resorted  to,  and  if  these  do  not  soon  produce  the  desired  results, 
laxatives  are  employed. 

The  characteristic  mucus  masses  which  are  voided  in  this  affection 
assume  various  shapes.  Sometimes  they  are  distinctly  membranous  and 
shreddy,  at  other  times  they  represent  solid  columns  which  have,  occasion- 
ally, a  net-like  arrangement.  The  ribbon-shaped,  vermiform,  or  clumpy 
masses  dissolve  in  water  or  float,  often  in  numerous,  thin,  membranous 
lamella.  In  entwining  the  mass  in  which  they  are  rolled  together,  they 
tear  at  many  points  and  are  broken  up.  Upon  being  shaken  in  water  they 
separate  into  numerous  flocculent  masses.  Desquamated  intestinal  mucous 
membrane  does  not  have  this  appearance,  nor  do  parasites,  nor  connective 
tissue  masses  originating  from  food,  or  the  like. 

The  mucus  masses  are  usually  whitish  or  grayish-white ;  sometimes  they 
are  stained  brownish  by  the  feces,  and,  according  to  Nothnagel,  in  rare 
cases  they  are  slightly  tinged  with  blood.     They  are  translucent,  but  not 


SYMPTOMS  AND  COURSE  741 

transparent,  as  is  commonly  the  ease  with  intestinal  mucus.  When  placed 
in  alcohol  the  gelatinous  masses  change  to  a  porcelain  white,  and  become 
quite  tough.  They  shrink,  and  do  not  so  readily  entwine  and  dissolve  into 
lamellae.  They  may  then  resemble  connective  tissue  masses  originating 
from  food,  or  fibrinous  pseudo-membranes  such  as  are  formed  in  diph- 
theria. 

Upon  microscopic  examination  a  light,  basic  substance  is  first  noted. 
This  shows  manifold  fine  streaks  so  arranged  that  they  resemble  very  thin 
fibers  of  connective  tissue.  On  the  addition  of  acetic  acid  the  connective 
tissue  fibrillae  should  swell  and  become  indistinct.  On  the  contrary,  the 
striation  becomes  more  distinct  and  profuse.  The  striae  form  a  delicate 
network,  the  meshes  of  which  have  very  sharp  contours  and  are  glistening, 
and  include  epithelia  and  round  cells.  Alcoholic  preparations  also  dis- 
close a  coarse,  fibrinous  basic  substance  with  a  deposition  of  cells,  and  thus 
is  explained  the  view  of  the  first  investigator  of  these  masses,  that  they 
consist  of  fibrin. 

The  epithelia  which  are  included  are  usually  changed  in  various  ways. 
Only  rarely  do  they  retain  their  ciliary  border;  sometimes  they  are  still 
arranged  in  rows,  therefore  detached  at  one  time  in  large  amounts.  Some 
of  them  still  have  their  normal,  cylindrical  form;  many,  however,  have 
enlarged  by  swelling,  and  are  misshapen,  becoming  round  or  more  closely 
resembling  pavement  epithelium.  Others  again  are  elongated  and  spindle- 
shaped,  so  that  they  resemble  smooth  muscular  fibers,  and  their  termina- 
tions are  not  pointed  but  rounded  off.  Fatty  degeneration  of  the  pro- 
toplasm, the  splitting  of  the  cells,  as  described  by  Nothnagel,  and 
disintegration  up  to  granular  decomposition  may  be  frequently  noted;  the 
disintegration  of  the  cells  causes  them  to  become  friable,  and  upon  pressure 
on  the  cover-glass  they  split  up  into  hard,  feebly-glistening,  irregular  striae ; 
this  process  has  been  referred  by  Nothnagel  to  drying,  by  Kitagawa  *  to 
hyaline  degeneration  or  coagulation  necrosis.  Adolf  Schmidt,^  on  the 
contrary,  has  proved  it  to  be  due  to  imbibition  with  soaps.  Upon  addition 
of  caustic  potash  the  cells  clear  up  and  the  nuclei  become  more  distinct, 
while  an  addition  of  acids  does  not  have  this  effect.  If  a  particle  of  the 
mucus  mass  is  thoroughly  admixed  with  acetic  acid  or  hydrochloric  acid, 
and  the  preparation  is  carefully  wanned  upon  an  object  carrier  over  a  flame, 
from  the  cells  fine  fat  globules  are  apparent  which  finally  collect  in  large 
drops  under  the  cover-glass.  The  cell  at  the  same  time  clears  up,  the 
nucleus  becomes  distinct ;  the  solubility  in  ether,  and  a  black  staining  with 
hyperosmic  acid  confirm  the  fatty  nature  of  the  drops  which  have  developed. 
The  cells,  in  spite  of  imbibition,  are  still  well  retained,  for  their  nuclei 

1  "  Beitrage  zur  Kenntniss  der  Enteritis  membranacea."  Zeitschr.  f.  klin.  Medi- 
cin,  1890,  XVIII,  p.  9. 

2  "  Ueber  Schleim  im  Stuhlgang."  Zeitschr.  f.  klin.  Medicin,  1897,  XXXII,  Heft 
3  und  4. 

48 


742       MUCOUS  COLIC   AND  MEMBRANOUS   INTESTINAL  CATARRH 

stain  readily  with  aniline  colors.  The  epithelia  are  probably  attacked  only 
after  desquamation  of  the  fatty  infiltration.  As  the  mucous  membrane 
of  the  large  intestine,  according  to  Robert,  secretes  fatty  acids  and  calcium 
salts,  and  imbibition  with  calcium  soaps,  intra  vitam,  would  not  be  impos- 
sible, therefore,  from  what  we  know  of  cell  alterations  of  this  kind,  we 
can  the  more  readily  assume  that  this  process  occurs  only  in  the  contents 
of  the  intestine.  The  great  number  of  epithelia  are  indicated  by  the  num- 
bers of  those  which  have  a  more  lamellar  character.  On  the  other  hand, 
the  solid  columnar  mucous  membrane  structures  are  decidedly  deficient 
in  these.  The  former,  to  a  great  extent,  are  said  to  be  composed  of  cells, 
so  that  intense  desquamation  of  the  mucous  membrane  is  to  be  assumed 
in  their  production. 

Bound  cells,  in  comparison  with  epithelial,  are  usually  less  marked; 
sometimes  they  can  scarcely  be  found.  A.  Schmidt  ^  showed  them  to  be 
more  profuse  in  stained  cut  sections,  and  believes  they  are  usually  present 
in  larger  numl)ers  than  is  believed,  as  they  frequently  disintegrate  and  in 
the  fresh  preparation  may  therefore  be  confounded  with  epithelium, 
l^josinophiles  may  also  be  found  among  them,  with  or  without  the  simul- 
taneous appearance  of  Charcot-Leyden  crystals.  Plentiful  numbers  of 
leukocytes  always  favor  a  decided  catarrhal  or  inflammatory  process. 
Masses  which  consist  almost  exclusively  of  pus  corpuscles  favor  ulcerative 
processes,  and  in  these  the  mucus  intermediary  substance  is  often  absent. 

Bacteria,  which  are  frequently  very  numerous  in  the  masses,  are  of 
various  kinds,  and  among  them  are  many  rods  of  different  shapes,  cocci, 
etc.  In  many  cases  hyphomycetes  with  distinct  naked  threads  are  seen. 
In  how  far  bacteria  are  the  cause  of  the  pathologic  process  cannot  be 
stated ;  some  authors  naturally  attribute  the  disease  solely  to  their  presence. 

The  preparation  of  dried  specimens  is  not  easy,  as  the  smallest  parti- 
cles are  difficult  to  break  up;  they  are  not  very  adherent  and  constantly 
slide  away;  this  is  probably  due  to  the  fat. 

Among  crystals  described  by  Nothnagel  are  cholesterin  plates  and  those 
of  ammonia-magnesia  phosphate.  These,  as  well  as  the  Charcot-Leyden 
crystals  and  the  fatty  acid  needles,  are  present  in  the  mucus  masses  in 
very  varying  amounts  and  are  by  no  means  constant.  Eemains  of  food, 
vegetable  as  well  as  animal,  are  not  rarely  embedded  in  the  masses. 

We  arrive  at  important  conclusions  by  the  chemical  examination  of 
the  membranous  structures.  Naturally  this  is  somewhat  difficult,  for  the 
masses  are  but  slightly  soluble  in  the  mediums  ordinarily  used  for  the 
solution  of  albumin  and  mucus  products.  Cold  water  will  extract  some 
mucin  and  albuminous  products  which  appear  to  consist  of  nucleo-albumin 
and  globulin;  these,  however,  are  but  small  amounts.  Weak  alkaline  so- 
lutions extract  but  little   of  mucin   and  albuminates   from   the   masses; 

1  Loo.  eit. 


SYMPTOMS  AND  COURSE  743 

stronger  solutions  will  dissolve  them,  particularly  upon  heating,  but  they 
destroy  the  mucin,  and,  therefore,  no  longer  convey  a  clear  picture.  As 
A.  Schmidt  declared,  the  difficulty  of  dissolving  the  masses  which,  other- 
wise, are  not  present  in  mucus  products,  depends  upon  their  very  inti- 
mate infiltration  with  fat.  If  the  masses  are  dissolved  by  remaining  for 
days  in  a  pepsin  solution  which  contains  hydrochloric  acid,  the  fluid 
becomes  turbid,  particularly  near  the  surface,  and  fat  globules  and  fat 
layers  are  deposited.  If  these  are  shaken  up  with  ether  the  fluid  clears, 
and  upon  evaporation  of  the  ethereal  solution  quantities  of  fat  remain. 
Schmidt  has  made  some  fat  estimations.  In  two  cases  of  membranous 
enteritis  he  obtained  respectively  19.7  per  cent,  and  9.5  per  cent,  of  fat 
from  the  dried  substance.  More  than  one-half  of  the  fat  consisted  of 
soap,  or  fatty  acids  and  soap.  In  a  case  of  true  mucous  colic,  only  2  per 
cent,  of  fat  was  present.  Microscopically,  the  fat  cannot  be  recognized; 
no  needles  of  fatty  acids  or  soap  are  to  be  seen.  Unfortunately,  the  fat 
is  so  difficult  to  extract  from  the  masses  that  a  solution  and  investigation 
of  the  unchanged  mucin  is  impossible ;  this  is  usually  altered  by  extraction. 
The  behavior  of  the  masses  in  a  so-called  triaeid  solution  after  Ehrlich 
favors  the  presence  of  mucin  in  abundance.  They  are  stained  green,  as 
mucus  assumes  this  color.  Fibrin  or  connective  tissue,  on  the  contrary, 
stains  red  when  brought  into  contact  with  this  mixture.  By  the  red  stain- 
ing of  connective  tissue  masses  originating  from  the  food,  of  desquamated 
intestinal  mucous  membrane,  and  of  fibrinous  membranes  it  is  possible  to 
differentiate  them  macroscopically  from  mucus  masses.  Schmidt  micro- 
scopically determined  this  in  sections  of  stained  and  embedded  mucous 
membrane  masses,  and  furnished  the  proof  that  fibrin  was  absent.  Only 
connective  tissue  remains  of  the  food,  which  are  often  intimately  admixed 
with  mucus,  alone  show  the  stains  which  have  been  described.  Elastic 
fibers  and  the  remains  of  vessels  are  proof,  and  will  protect  us  from  errors. 
Acetic  acid,  as  already  mentioned,  produces  in  the  mucus  masses  a  net- 
work of  strongly  refractive  threads,  which  also  is  in  favor  of  decided 
amounts  of  mucin.  Only  when  the  membranes  contain  much  cellular 
material,  and,  in  consequence,  become  non-transparent,  do  they  clear  upon 
the  introduction  of  acetic  acid,  in  consequence  of  swelling  of  the  cell  pro- 
toplasm. In  these  cases  a  larger  amount  of  albumin  will  be  found  in  the 
masses,  and,  upon  staining  with  triaeid  solution,  a  more  pronounced  red 
color  will  be  produced.  In  spite  of  the  apparently  great  masses  of  mucus 
which  some  persons  with  this  affection  evacuate  daily,  they  lose  compara- 
tively little  body-substance.  A  patient  of  Schmidt's  lost  only  0.18  grams 
of  nitrogen  in  the  large  quantities  of  mucus  which  he  voided  every  two 
or  three  days.  We  cannot,  therefore,  regard  these  mucus  dejecta  as  re- 
ducing the  strength  of  the  patient  or  as  producing  any  marked  change  in 
the  organism. 

Of  other  symptoms,  the  attacks  of  colic  are  the  most  important;  these 


744      MUCOUS  COLIC  AND  MEMBRANOUS  INTESTINAL  CATARRH 

frequently  dominate  the  entire  clinical  picture,  while  the  catarrhal  symp- 
toms on  the  part  of  the  intestine  are  quite  secondary.  These  are  the 
eases  in  which,  according  to  Nothnagel,  the  disease  should  be  looked  upon 
as  a  nervous  affection,  and  be  designated  by  the  term  mucous  colic.  The 
attacks  of  colic  often  come  on  quite  suddenly  with  severe  pain  in  the  gas- 
tric region  (transverse  colon)  or  in  the  left  side  of  the  abdomen  (descend- 
ing colon).  The  patients  give  us  the  impression  that  they  are  suffering 
from  a  very  serious  disease;  they  are  often  feeble,  pale,  are  very  anxious, 
and  we  might  readily  think  that  peritonitis,  intestinal  obstruction  or  the 
like  was  beginning.  But,  after  a  short  or  longer  time,  these  symptoms 
disappear,  and  usually  after  the  discharge  of  the  characteristic  mucus 
masses,  often  in  enormous  amounts.  The  patients  rapidly  recuperate  and 
no  longer  complain  of  anything  serious.  Obstinate  constipation,  however, 
continues,  and  sooner  or  later,  often  even  the  next  day,  a  renewed  par- 
oxysm occurs  followed  by  the  same  results.  Sometimes  the  attacks  of 
colic  occur  only  once  in  a  few  weeks  or  months,  and  the  affection  may 
consist  of  only  a  single  attack.  If  the  disease  causes  only  occasional  symp- 
toms, the  patient  in  the  interval,  apart  from  nervous  disturbances  which 
are  chiefly  hysterical  and  a  tendency  to  constipation,  are  in  their  usual 
health,  and  we  are  justified  in  designating  this  affection,  after  Nothnagel, 
as  miicous  colic  or  colica  mucosa. 

In  other  cases  there  is  a  very  profuse  discharge  of  characteristic  mem- 
branous and  ribbon-like  masses,  hut  the  attacks  of  colic  are  absent.  There 
is  a  tendency  to  constipation,  for  the  relief  of  which  purgatives  a-e  often 
taken,  as  the  patients,  usually  women,  feel  better  after  a  thorough  evacua- 
tion. The  use  of  purgatives,  however,  appears  to  aggravate  the  disease,  and 
to  increase  the  irritability  of  the  wall  of  the  intestine.  The  constipation  in 
these  cases  shows  the  peculiarity  that  it  apparently  runs  its  course  with 
narrowing  of  the  intestine.  This  narrowing  is  usually  not  organic  and 
due  to  cicatrices  or  the  like,  but  probably  originates  in  a  firm  contraction 
of  the  musculature  of  the  intestine;  to  this  marked  contraction  of  the 
intestine  we  may  also  ascribe  the  sensation  which  the  patients  have  of 
tenesmus  and  fulness  in  the  abdomen.  They  usually  declare  that  they 
liave  the  distinct  sensation  of  feces  being  present  in  the  intestine,  which 
thoy  cannot  expel.  This  irritative  condition  frequently  manifests  itself 
liy  Inniger,  which,  however,  is  usually  soon  satisfied.  The  intake  of  nour- 
isliment  is  often  scanty,  as  it  reflexly  produces  more  decided  irritation  of 
tlie  musculature  of  the  intestine  and  aggravates  the  discomfort.  Eructa- 
tions are  frequent  in  consequence  of  involuntary  swallowing  of  air.  Many 
patients  resort  to  purgatives,  others  administer  one  enema  after  another. 
After  the  latter,  as  a  rule,  nothing  is  voided  immediately;  the  water  is 
(liscliarged  unchanged.  Then  hard  particles  of  feces  appear  which  in  form 
usually  resemble  the  feces  of  sheep.  Between  these  masses,  or  discharged 
in  separate  movements,  are  the  characteristic  stools.     When  a  large  quan- 


SYMPTOMS   AND  COURSE  .  745 

tity  is  voided,  this  often  terminates  the  attack;  the  patients  have  a  feel- 
ing of  satisfaction  and  relief  after  such  purgings,  but  they  are  usually 
weak  and  debilitated.  In  these  cases  of  enteritis  membranacea  which  run 
their  course  without  colicky  pains,  a  more  or  less  decided  contraction  of 
the  large  intestine  appears  to  be  present.  Sometimes  with  a  very  flaccid 
abdominal  wall,  particularly  upon  the  left  side,  the  organ  may  be  felt  as 
a  firm  column.  But  the  contraction  is  not  so  spasmodic  or  so  excessive 
as  in  those  cases  which  are  designated  mucous  colic,  and  are  often  attrib- 
uted to  a  neurosis  of  secretion.  There  are,  however,  all  possible  transi- 
tional stages  from  a  dull  sense  of  fulness  and  pressure  with  a  feeling  of 
severe  tenesmus  and  contraction  up  to  sharp  and  colicky  pains.  The  same 
conditions  are  observed  in  the  common  diseases  of  the  large  intestine,  and 
also  after  the  administration  of  laxatives.  It  must  be  borne  in  mind  that 
nervous  and  hysterical  patients  offer  but  very  slight  resistance  to  such  sen- 
sations, that  their  reaction  to  the  irritation  of  pain  is  much  more  ready ^ 
and  much  stronger  than  in  normal  persons,  and  we  are  almost  invariably 
dealing  with  neuropathic  individuals. 

If  we  compare  the  sensations  in  the  intestine  with  those  which  are 
produced  in  severe  contractions  of  the  muscles  of  the  extremity,  where  also 
painful  spasms  occur  (for  example,  in  the  muscles  of  the  calves  in  conse- 
quence of  over-exertion,  circulatory  disturbances,  etc.),  we  note  that  the 
same  causes  often  produce  only  a  contraction  of  the  muscles  without  pain. 
One  patient  will  describe  these  spasms  as  very  painful,  while  another  re- 
ports them  as  only  slight.  Therefore,  a  strict  differentiation  of  the  forms 
of  colica  mucosa  and  enteritis  membranacea  cannot  be  made,  even  though 
we  recognize  the  causal  influence  of  the  nervous  temperament  in  the  well- 
developed  cases  of  mucous  colic,  as  was  flrst  done  by  Nothnagel.  It  does 
not  appear  likely  that  the  mucus  gives  rise  to  the  colic.  The  view  appears 
to  me  more  reasonable  that  the  mucus  is  profusely  permeated  with  epi- 
thelium, and  often  coats  the  scybala  in  a  characteristic,  firm,  membranous 
mass,  and  that  the  irritation  of  the  mucous  membrane  is  due  to  a  catarrh, 
to  irritative  contents,  and  more  or  less  severe  contractions  of  the  muscu- 
laris,  which  compress  the  mucus  produced  by  the  epithelial  cells,  and 
form  it  into  columns  and  bands,  as  has  been  accurately  described  by  Mar- 
chand.^  At  the  same  time  the  mucus  becomes  deficient  in  water,  more 
compact,  and  infiltrated  with  fat  which  probably  originates  from  the  intes- 
tinal contents  adherent  to  the  surface  of  the  mucous  membrane.  These 
masses  of  feces  discharged  show  the  effects  of  this  compression  and  de- 
ficiency of  water;  they  are  friable,  and  in  the  haustra  of  the  colon  are 
formed  into  small  or  large  balls.  Although  other  symptoms  of  catarrh 
of  the  large  intestine  are  lacking,  nevertheless,  the  presence  of  numerous 
epithelial  cells,  sometimes  also  of  round  cells  in  the  mucus,  is  in  favor  of 

1  Berliner  klin.  Wochenschr.,  1875. 


740       MUCOUS  COLIC  AND  MEMBRANOUS   INTESTINAL  CATARRH 

catarrh,  and  the  production  of  mucus  is  explained,  as  well  as  the  irrita- 
tion of  the  intestinal  wall  which  leads  to  colic  and  to  spastic  constipation; 
and  these  are  much  more  fully  and  more  naturally  explained  than  by 
the  very  problematic  hypothesis  of  a  mucus  neurosis  of  secretion.  That  the 
affection  generally  occurs  in  nervous,  hysterical  women  naturally  favors  the 
view  that  abnormalities  of  innervation  here  play  a  part.  If,  however,  there 
is  a  more  decided  irritation  of  the  intestinal  nerves,  this  generally  ex- 
presses itself  in  the  muscular  functions  of  the  intestinal  wall.  In  excite- 
ment, in  fright,  under  psychical  emotion,  as  is  well  known,  spastic  contrac- 
tion of  the  intestine  or  increased  peristalsis  readily  occurs,  and  this  is 
particularly  marked  in  chronic  catarrh,  flere,  in  excitable  persons,  spas- 
tic contraction  of  the  large  intestine  and  ensuing  constipation  arise,  which 
are  readily  relieved  by  the  administration  of  preparations  of  belladonna, 
etc.  In  the  disease  under  consideration  we  are  dealing  usually  with  easily 
excited,  sensitive  persons,  in  whom  an  irritative  condition  of  the  intestine 
very  readily  expresses  itself  by  spasm.  If  this  occur  in  the  intestine,  it  is 
followed  by  a  narrow  constriction  and  very  decided  pressure  of  the  mucous 
membrane  which  is  now  stimulated  to  a  profuse  secretion  of  mucus.  On 
account  of  a  lack  of  reliable  reports  of  anatomical  investigations,  and  the 
difhculty  involved  in  the  observation  of  the  intestine  during  the  attack, 
it  is  as  yet  impossible  to  explain  with  certainty  the  nature  of  the  affection ; 
but  I  believe  that  the  above  solves  the  question  of  the  origin  of  the  char- 
acteristic mucus  formation,  and  that  the  other  symptoms  of  the  disease 
may  be  brought  into  relation  with  this  without  accepting  a  doubtful 
hypothesis. 

PROGNOSIS 

In  regard  to  life  the  prognosis  is  generally  favorable;  but  the  disease 
may  lead  to  a  lowered  state  of  nutrition  and  loss  of  strength,  and  thus 
result  in  chronic  invalidism.  As  a  rule,  however,  the  patient  attains  old 
age,  and  later  gradually  outgrows  the  affection.  The  disease  may  also 
be  cured  by  proper  treatment,  combined  with  good  nutrition  and  the 
regulation  of  the  mode  of  life;  usually,  however,  there  is  a  tendency  to 
relapses.  In  some  cases  the  disease  exhausts  itself  in  a  few  paroxysms, 
and,  in  the  first  attacks,  this  leads  us  to  hope  that  they  may  be  the  only 
ones;  decided  increase  in  weight,  improvement  of  the  general  condition, 
and  the  disappearance  of  other  nervous  disturbances  enhance  the  hope 
of  cure. 

DIAGNOSIS 

The  diagnosis  is  easy  when  we  find  in  the  dejecta  the  typical,  mem- 
branous, ribbon-shaped,  net-like  or  columnar  mucus  structures.  In  nerv- 
ous persons  who  now  and  then  suffer  from  severe  attacks  of  colic,  from 
tonesinus  and  constipation,  it  is  well  to  examine  the  feces,  and  to  ask 


TREATMENT  747 

the  patient,  or  those  about  him,  to  observe  whether  masses  of  this  kind 
are  discharged.  Cases  of  constipation  and  intestinal  catarrh  which  run 
their  course  with  colic  will  then  be  recognized  as  intestinal  colic  or  mem- 
branous catarrh.  It  is  true  we  must  guard  against  error  in  confounding 
these  masses  with  particles  of  connective  tissue  such  as  originate  from  meat 
and  other  constituents  of  the  food.  Frequently,  connective  tissue  masses 
containing  globules  of  fat  which,  by  the  effect  of  digestive  juices,  have 
become  saponified  and  have  therefore  a  whitish  color,  will  be  taken  for 
membranous  mucus  masses.  I  have  often  seen  them  after  the  eating  of 
raw  ham,  and  they  have  been  shown  me  by  anxious  patients  or  their 
physicians.  They  closely  resemble  the  mole-like  mass  which  Rosenheim 
depicts  in  his  text-book  in  the  chapter  devoted  to  enteritis.  By  their 
tenacity  when  we  attempt  to  separate  these  masses  and  entwine  them,  and 
the  microscopic  evidence  of  particles  of  transverse  muscle  between  the 
fibers,  and  the  clumps  of  whitish,  fatty  tissue,  we  may  easily  differentiate 
them;  moreover,  they  do  not  show  the  reaction  from  mucus  mentioned 
above,  nor  do  they  present  coarser  connective  tissue  fibrillaB  with  remains 
of  vessels,  elastic  fibers,  etc. 

Besides  tendons  and  fascia,  the  lumen  of  arteries  and  veins,  remains 
of  oranges,  milk  coagula,  masses  of  fungi  having  membranes,  such  as 
the  oidium,  may  be  confounded  with  mucus  dejecta,  but  the  chemical 
and  microscopical  investigation  of  these  objects  will  enlighten  us. 

The  typical  mucus  masses  are  disentangled  upon  shaking  in  water  and 
are  dissolved  into  countless  small  particles,  which,  upon  standing,  again 
separate  from  the  turbid  fluid  and  collect  upon  the  surface.  This  does  not 
happen  with  the  particles  of  food,  etc.,  referred  to  above. 

Admixture  of  blood  in  the  mucus  masses  favors  ulcerative  processes; 
therefore,  either  dysentery  or  tuberculous  disease  of  the  intestine,  deeply 
invading  follicular  ulceration  or  ameba  enteritis  may  be  simulated. 

TREATMENT 

The  treatment  must  be  designed  to  combat  the  various  factors  which 
have  been  operative  in  the  development  of  the  disease,  and  which  are  the 
individual  components  of  the  clinical  picture.  It  must  therefore  control 
the  irritation  of  the  intestinal  mucous  membrane,  the  motor  intestinal 
disturbance,  and,  particularly,  the  general  changes  in  the  nervous  system, 
the  hysterical,  neurasthenic  and  hypochondriacal  symptoms.  This  may  be 
attained  by  careful  regulation  of  the  diet,  for,  on  close  investigation,  we 
usually  find  here  much  at  fault!  Often  the  patients,  from  a  fear  that 
certain  food  will  disagree,  limit  their  diet  too  much.  Mechanical  and 
drug  treatment  of  constipation  must  also  be  instituted.  All  irritation  of 
the  intestine  should  be  avoided,  and  when  there  is  decided  evidence  of 
bacterial  decomposition  of  the  intestinal  contents,  the  administration  of  dis- 


748       MUCOUS  COLIC  AND  MEMBRANOUS   INTESTINAL  CATARRH 

infcctants  is  indicated.  All  means  to  regulate  and  strengthen  the  nerv- 
ous system  are,  in  general,  to  be  employed  to  the  fullest  extent. 

As  the  clinical  picture  varies  greatly  in  the  individual  patient,  at  one 
time  this,  at  another  time  that,  symptom  becoming  more  prominent,  special 
attention  must  be  given  to  the  intestinal  catarrh  and  the  accompanying 
constipation;  in  other  cases,  however,  in  which  the  catarrhal  symptoms 
are  less  marked,  and  a  more  or  less  purely  nervous  affection,  therefore 
Nothnagel's  mucous  colic,  appears  to  be  present,  the  main  stress  must  be 
laid  upon  the  regulation  of  the  mode  of  life  so  as  to  avoid  deleterious 
effects  which  might  react  upon  the  central  nervous  system, — the  psychical 
element.  All  means  must  be  employed  to  strengthen  the  tone  of  the 
nervous  system. 

If  examination  reveals  a  well-developed  catarrh  of  the  large  intestine, 
tliis  must  first  be  treated,  primarily  by  laxatives,  such  as  castor  oil,  rhu- 
liarli  and  the  like,  thoroughly  to  cleanse  the  intestine  of  long- retained, 
irritating  masses,  the  generators  of  fermentation  and  decomposition.  For 
the  latter  calomel,  a  single  dose  of  0.3-0.5  grams,  or,  upon  continuance 
of  the  bactericidal  action,  the  dose  repeated  for  several  days,  or  a  dose 
three  times  daily  of  0.05-0.2  grams  will  be  serviceable.  To  empty  the 
intestine  we  employ  purgatives,  and  we  assist  their  action  by  the  use  of 
injections  in  a  manner  to  be  later  described;  the  laxatives  render  the  in- 
testinal contents  fluid  and  propel  them,  but,  frequently,  in  the  lower  part 
of  the  intestine,  this  effect  is  lost,  and  the  fecal  masses  collect  here  and 
are  not  discharged.  The  prolonged  use  of  purgatives  and  also  mineral 
waters,  such  as  the  purgative  water  and  springs  containing  Glauber's  salt, 
is  not  advisable,  as  these  often  have  a  most  unfavorable  effect  upon  the 
motor  irritation  and,  in  general,  upon  the  nervous  condition.  Therefore, 
a  treatment  at  Carlsbad,  Marienbad,  etc.,  or  at  the  saline  springs,  such  as 
ITomburg  and  Kissingen,  is  generally  not  so  beneficial  as  in  a  simple 
chronic  catarrh  of  the  large  intestine. 

Sometimes  the  use  of  astringents,  bismuth  subnitrate  or  bismuth  sal- 
icylate, and  in  cases  of  decided  flatulence  magnesia,  is  also  of  value.  These 
remedies  may  be  combined,  or  an  extract  of  hyoscyamus  or  oil  of  pepper- 
mint and  the  like  may  be  included  to  allay  intestinal  irritation. 

In  the  removal  of  the  motor  disturbances  in  the  intestine,  careful  mas- 
sage will  be  found  serviceable  in  the  interval  between  the  attacks,  and  the 
application  of  the  faradic  or  galvanic  current,  cautious  gymnastic  exer- 
cises for  the  trunk  and  leg,  moderate  physical  exercise,  such  as  walking, 
liorseback  riding,  bicycling,  to  combat  the  frequently  coexisting  atony  of 
ilie  intestine.  In  such  instances  laxatives  should  be  avoided  as  much  as 
])nssil)le,  enemata  taking  their  place,  and  where  there  is  decided  irritability 
of  the  intestines,  warm  injections  of  Ems  water,  or  a  f  per  cent,  saline 
solution  in  quantities  up  to  one  liter.  Previous  to  this  olive  oil  may  be 
injected,  provided  the  intestine  is  but  slightly  sensitive.     Enemata  of  ^  a 


TREATMENT  749 

liter  of  oil,  according  to  the  methods  of  Kussmaul  and  Fleiner,  are  also 
valuable.  The  addition  of  irritating  astringents  or  disinfectants,  such  as 
silver  nitrate,  tannin,  corrosive  sublimate  and  the  like,  had  better  be 
avoided.  Drugs  which  have  an  anodyne  effect,  as  oil  of  peppermint,  starch, 
etc.,  may  be  added  to  the  injections  of  water,  or  the  injections  may  be  of 
chamomile  or  peppermint  tea.  These  intestinal  washings  act  especially 
well  during  the  attack;  they  assist  in  discharging  the  hard  scybala  and 
masses  of  mucus,  as  well  as  the  flatus  which  inconveniences  the  patient 
greatly,  and  thus  serve  to  quiet  the  intestine.  In  the  interval  between 
the  attacks,  preparations  of  strychnin  are  best  employed,  such  as  the  tinc- 
ture of  nux  vomica  with  tincture  of  rhubarb,  which  mildly  stimulate  the 
intestinal  movements;  during  the  attack  of  colic  the  belladonna  prepara- 
tions, such  as  extract  of  belladonna,  in  doses  of  0.02-0.04,  or  atropin  sul- 
phate, etc.,  afford  relief.  Even  where  the  spasmodic  contractions  of  the 
intestine  are  painless,  these  drugs  are  to  be  recommended.  Morphin  and 
opium  should  only  be  employed  in  cases  of  necessity.  To  allay  the  spas- 
modic pain,  heat  may  be  applied  in  the  form  of  cataplasms,  such  as  may 
be  combined  with  the  use  of  the  Quincke  heat  apparatus,  or  as  hot  woolen 
cloths,  thermophores,  etc. 

In  cases  of  a  more  catarrhal  character,  therefore,  in  enteritis  mem- 
branacea,  the  diet  should  be  non-irritating,  and  acids,  spices,  fats,  foods 
rich  in  cellulose,  and  those  which  ferment  readily,  should  be  avoided. 
But  this  restriction  in  diet  must  be  only  until  the  marked  catarrhal  symp- 
toms, such  as  periodically  appearing  diarrhea,  fermentation,  and  profuse 
gas  formation,  are  removed.  As  a  rule,  a  strengthening  and  nutritious 
mixed  diet  is  more  stimulating  and  serviceable  in  the  treatment.  A  con- 
tinuous filling  of  the  large  intestine  with  cellulose  and  other  remains  of 
food  decidedly  stimulates  peristalsis  without  leading  to  spasm,  which  read- 
ily occurs  in  an  empty  intestine  on  account  of  the  difficulty  of  propelling 
the  compact  mucus  masses.  For  this  reason  plentiful  amounts  of  bread 
are  usually  ordered,  not  fine  wheat  bread  but  the  coarser  varieties  which 
must  be  well  baked;  vegetables  rich  in  cellulose,  as  well  as  berries  and 
fruits;  meats  which  contain  fat,  also  bacon  and  butter.  Patients  are  usu- 
ally anxious  to  avoid  such  a  diet,  for  they  believe  their  intestines  to  be 
much  too  sensitive  to  retain  this  food,  and,  if  a  few  attacks  recur,  it  re- 
quires great  powers  of  persuasion  to  induce  them  to  resume  this  diet.  All 
strongly  spiced  food,  as  well  as  cabbage  and  other  vegetables  which  are 
apt  to  generate  quantities  of  gas,  must  be  excluded,  for  this  accumulation 
of  gas  in  the  intestine  causes  great  distress  to  the  patient,  and  readily 
induces  colic;  the  plentiful  ingestion  of  fat  and  carbohydrates  has  the 
further  advantage  of  increasing  the  accumulation  of  fat  in  the  body,  which 
should  be  particularly  borne  in  mind  in  the  case  of  nervous,  thin  individ- 
uals who  have  a  do\\Tiward  displacement  of  the  stomach,  intestine,  kidney, 
etc. ;  that  is,  when  enteroptosis  is  present.     The  fact  that  in  this  condi- 


750       MUCOUS  COLIC   AND  MEMBRANOUS   INTESTINAL  CATARRH 

tiou  the  organs  are  better  supported,  that  the  large  intestine  has  a  firmer 
hold  upon  the  mesentery  and  omentum  rich  in  fat,  that  torsion  of  the 
organs  and  their  nerves  is  lessened,  and  movements  of  the  colon  are 
increased  conduces  to  improvement.  In  cases  where  the  marked  effect  of 
lacing  exists,  proper  corsets  should  be  worn  and  the  dress  so  arranged  that 
the  weight  of  the  clothes  will  rest  upon  the  shoulders  rather  than  upon 
the  abdomen.  In  cases  of  pendulous  abdomen  with  marked  flaccidity  of  the 
abdominal  walls  after  pregnancy,  or  from  a  previous  abdominal  tumor, 
etc.,  the  wearing  of  an  elastic  abdominal  bandage  is  advisable,  prolonged 
standing  or  sitting  is  to  be  avoided,  and  there  should  be  frequent  rest  in 
tlie  recumbent  posture. 

In  controlling  the  nervous  symptoms,  general  rules  must  be  enforced 
which  cannot  hero  be  described  in  detail.  This  necessitates  careful  atten- 
tion to  the  complaints  of  the  patient,  an  accurate  study  of  his  mode  of 
life,  his  manner  of  thought,  and  the  possible  unfavorable  factors  in  his 
occupation,  his  family  relations,  etc.,  which  excite  and  disquiet  the  psy- 
chical sphere,  shock  the  nervous  system,  reduce  the  normal  resistance  to 
pain  and  unpleasant  sensations,  and  frequently  lead  to  nervous  tension. 
Sufficient  rest  at  night,  occasional  interruption  of  the  day's  activity  by 
intervals  of  rest,  and  especially  a  certain  freedom  in  diet  must  be  insisted 
upon.  Detailed  hygienic  instruction  by  the  physician  will  often  relieve 
these  conditions.  In  cases  of  necessity,  change  of  climate,  residence  in  a 
(juiet  place  in  the  mountains  or  at  the  seashore,  will  be  serviceable.  Ex- 
citing life  at  summer  resorts  or  at  the  seaside  is  to  be  avoided.  These 
measures  may  be  assisted  by  carefully  chosen  local  hydriatic  procedures, 
such  as  cold  rubbings,  baths,  or  douches,  general  massage  and  faradization, 
to  the  abdomen.  Finally,  as  previously  mentioned,  a  generous  diet  con- 
sisting of  fat  and  carbohydrates  will  be  useful  in  promoting  the  accumula- 
tion of  fat  in  the  body. 

In  general,  the  treatment  of  enteritis  membranacea  and  mucous  colic 
is  not  easy;  but  a  careful  study  of  the  intestinal  and  nervous  disturbances 
present  as  well  as  of  the  circumstances  of  the  patient,  and  the  investigation 
of  all  the  varying  symptoms,  may  enable  us  in  many  cases,  with  the  patient 
help  of  the  sufferer,  to  cure  the  affection,  or  at  least  to  alleviate  it,  so  that 
he  has  intervals  of  relief  from  the  affection,  and  it  does  not  so  decidedly 
interfere  with  his  occupation. 


INTESTINAL  CONSTRICTION   AND 
INTESTINAL  OCCLUSION 

By  H.  NOTHNAGEL,  Vienna 

I.  INTESTINAL  CONSTRICTION 

The  two  clinical  histories  which  we  shall  here  analyze  and  discuss 
belong  to  the  severest  forms  of  disease  with  which  the  physician  is  brought 
into  contact;  chronic  constriction  of  the  intestine  in  the  one  case,  and 
acute  occlusion  in  the  other.  I  shall  detail  the  pathology  of  these  two 
conditions  as  definitely  as  brevity  will  permit,  and  shall  first  describe 
stenosis,  then  intestinal  occlusion,  proceeding  from  the  simple  to  the 
more  complex. 

The  first  patient,  a  woman  aged  37,  states  that  she  has  had  five  normal 
labors,  and,  with  the  exception  of  an  acute  febrile  articular  rheumatism 
in  her  eighteenth  year  from  which  she  recovered,  has  always  been  well. 
Three  months  ago  she  began  to  suffer  from  constipation,  while  previously 
the  bowels  were  normal.  This  symptom  developed  quite  insidiously  with- 
out any  preceding  change  in  the  mode  of  life  of  the  patient.  She  was 
compelled  to  take  purgatives,  which  formerly  had  never  been  necessary. 
In  addition  there  was  pain  of  a  colicky  character,  which  occurred  daily, 
never  lasted  more  than  a  few  minutes,  and  frequently  subsided  with  the 
passage  of  flatus.  Moreover,  the  patient  had  observed  that,  for  about  five 
weeks,  during  the  attacks  of  pain,  the  intestines  and  different  parts  of 
the  abdomen  bulged  and  formed  prominences  (as  she  expressed  it).  In  the 
last  three  months  she  has  emaciated  appreciably. 

The  totality  and  grouping  of  these  symptoms  are  characteristic,  and 
must  at  once  arouse  a  suspicion  of  intestinal  narrowing.  Constipation 
developing  insidiously  without  recognizable  external  cause,  frequent  pain 
of  a  colicky  nature,  and,  above  all,  the  bulging  coils  of  intestines,  form 
the  characteristic  features.  The  sjnnptomatology  of  intestinal  constriction 
is  simple  and  comprehensive:  The  clinical  picture  is  dominated  by  the 
fact  that  the  propulsion  of  the  contents  of  the  intestine  meets  resistance 
at  a  certain  point  due  to  some  anatomical  obstruction. 

SYMPTOMATOLOGY 

Chief  among  the  symptoms  are  alterations  in  the  fecal  movements. 
Constipation  develops  slowly  and  gradually,  since  the  affection  which  causes 

751 

COLLIZGIS   01- 


752      INTESTINAL  CONSTRICTION   AND  INTESTINAL  OCCLUSION 

the  stenosis  also  almost  invariably  arises  insidiously.  This  kind  of  con- 
stipation is  important  in  diagnosis  for  the  reason  that  it  occurs  in  persons 
who  have  previously  had  regular  evacuations,  and  no  other  cause  can  be 
assigned  for  its  presence.  At  the  onset,  according  to  the  situation  of 
the  stenosis,  mild  therapeutic  measures  are  suflficient  for  its  amelioration — 
purgatives  by  the  mouth  or  irrigations  per  rectum;  gradually,  however, 
oilier  symptoms  appear  while  evacuation  of  the  intestines  becomes  more 
and  more  difficult. 

The  degree  of  intestinal  activity  is  pre-eminently  influenced  by  the 
seat  of  the  stenosis;  therefore,  while  the  contents  are  still  fluid  or  semi- 
solid in  the  jejunum  and  ileum  their  passage  is  not  greatly  interfered 
with,  or,  at  least,  only  late  in  the  course  of  the  affection;  on  the  other 
hand,  this  is  marked  in  the  lower  portions  of  the  large  intestine.  It 
ha})pens  occasionally  in  stenosis  of  the  colon,  even  in  advanced  stricture 
of  the  sigmoid  flexure,  that  the  daily  evacuations  continue  for  a  long 
time  to  be  regular. 

Occasionally,  constipation  is  interrupted  by  the  appearance  of  diarrheal 
discharges,  and  then  enormous  masses  may  be  passed.  This  diarrhea  is 
the  consequence  of  irritation  of  the  walls  of  the  intestine  above  the  stenosis 
by  the  retained  contents  and  may  persist  for  a  long  time.  Blood  and 
pus  are  sometimes  admixed  with  the  dejecta,  originating,  in  rare  instances, 
in  a  secondary  decubital  ulcerative  change  in  the  mucous  membrane  above 
the  stenosis,  more  frequently  due  to  definite  anatomic  forms  of  stenosis, 
particularly  carcinomatous  changes.  Special  importance  in  diagnosis  is 
often  attributed  to  changes  in  the  shape  of  the  fecal  masses  {feces  of 
stenosis)  :  small  balls  resembling  sheep  feces,  containing  one  or  two  grooves; 
or  thin,  lead-pencil-like,  or  flattened  ribbon-like,  columns  of  feces.  For- 
mations of  this  nature  are  not  often  observed,  but,  in  such  cases,  they 
cause  confusion  for  they  may  occur  without  any  anatomic  change  in 
nervous  spastic  constipation  or  in  cases  of  so-called  starvation  intestine. 

These  changes  in  the  feces,  considered  individually,  are  of  slight  diag- 
nostic value,  and  this  is  also  true  of  the  other  symptom  which  is  sooner 
or  later  added,  namely,  the  colicky  attacks  of  pain.  The  intensity  of  these 
pains  varies  greatly;  sometimes  they  are  extraordinarily  severe.  In  char- 
acter they  are  like  other  paroxysms  of  intestinal  colic.  Their  seat  is  gen- 
erally the  region  of  the  stenosis,  and  from  this  the  pain  radiates  to  other 
areas  of  the  abdomen ;  rarely  are  they  more  severe  anywhere  than  at  the 
point  of  their  origin.  Gurgling,  rumbling  sounds  are  often  noticed  during 
the  paroxysms.  Their  "^ physiologic  foundation  is  the  increased  resistance 
to  tlie  propulsion  of  the  intestinal  contents,  and  the  decided  intestinal 
conti-actions  thereby  produced. 

One  of  the  most  significant  symptoms,  often  decisive  in  diagnosis  and 
occasionally  pathognomonic,  is  the  plastic  prominence  of  the  tetanicalhj 
dilaffd,  tense  coils  of  intestines,  with  or  without  visibly  increased  peristal- 


INTESTINAL  CONSTRICTION  763 

sis.  This  tetanic,  visible,  and  palpable  phenomenon,  designated  by  me 
as  intestinal  stiffening,  finds  conditions  for  its  development  only  in  the 
presence  of  intestinal  stenosis,  with  accumulation  of  intestinal  contents  in 
a  gaseous  or  fluid  form,  with  energetic  contraction  of  the  intestine  as  a 
result  of  hypertrophy  of  its  walls,  and  resistance  to  the  propulsion  of  the 
intestinal  contents.  We  distinctly  see  and  feel  how  a  portion  of  the  intes- 
tine (perhaps  already  distended  with  gas  but  still  soft)  is  changed,  usually 
quite  suddenly,  into  a  ridge  standing  out  prominently  and  rigidly  above 
the  surrounding  area  and  actually  to  be  grasped  by  the  fingers,  which 
remains  in  this  condition  for  a  short  time,  and  then  returns  to  its  former 
elastic  state.  After  a  few  minutes  this  is  repeated.  The  patient  suffers 
severe  colicky  pain  which  is  produced  by  the  tetanic  condition  of  the  in- 
testines. For  the  diagnostic  employment  of  this  phenomenon,  it  must 
be  shown  that  tetany  does  not  occur  in  an  empty  coil,  or  one  that  can 
be  emptied,  but  in  a  dilated  coil,  one  filled  with  gas  and  intestinal  contents, 
which,  on  account  of  the  obstruction  (stenosis  or  pcclusion),  cannot  relieve 
itself. 

Besides  intestinal  stiffening,  increased  peristalsis  is  often  present,  and 
is  manifested  by  a  tortuous,  more  or  less  active  forward  motion,  visible 
over  limited  or  extensive  areas. 

The  symptom  just  mentioned  (with  changeable  conditions)  is  char- 
acteristic of  intestinal  constriction;  all  other  symptoms  occurring  in  a 
concrete  case  are  incidental  consequences,  or  due  to  the  nature  and  ana- 
tomical composition  of  the  stenosis.  The  external  condition  of  the  abdo- 
men varies  as  much  as  the  results  of  percussion;  both  are  determined  by 
the  fulness  of  the  intestines,  be  it  with  gaseous  or  compact  or  fluid 
contents,  which  vary  from  day  to  day  or  from  hour  to  hour.  General 
diagnostic  rules  cannot  be  formulated.  One  condition  must  be  briefly 
described;  occasionally  the  fluid  mass  which  has  accumulated  above  the 
stenosis  becomes  so  massive  that  the  greatly  dilated  coils  (on  account  of 
their  weight)  drop  from  their  horizontal  position  to  the  sides  of  the 
abdomen,  thereby  simulating  ascites,  especially  since,  with  this  change  in 
position,  the  full  coils  of  intestines  may  also  change  their  location.  I 
have  observed  in  stenoses  of  the  sigmoid  flexure  as  well  as  of  the  ileum 
that  coils  of  the  small  and  also  of  the  large  intestine  may  fall  into  the 
flanks.  A  very  simple  maneuver  will  decide  in  such  cases  whether  ascites 
or  the  fluid  contents  are  present  in  the  lumen  of  the  small  intestine.  If  a 
few  sharp  taps  are  made  longitudinally  upon  this  area,  dull  upon  percus- 
sion, and  a  splashing  sound  is  produced,  it  is  certain  that  fluid  is  inside 
the  lumen  of  the  intestine. 

In  the  case  whose  history  has  just  been  detailed  the  characteristic 
symptoms  were  present  and  the  diagnosis  of  enterostenosis  could  be  made 
with  absolute  certainty,  but  this  is  not  always  the  case.  The  diagnosis 
is  sometimes  simply  impossible,  if  no  obstruction  can  be  felt,  and  when 


754      IXTESTLNAL  CONSTRICTION  AND  INTESTINAL  OCCLUSION 

the  contents  of  the  intestines  are  still  expelled,  either  because  very  fluid, 
as  in  the  small  intestine,  or  because  the  obstruction  is  not  yet  suflBciently 
advanced.  Between  these  extremes  is  a  series  of  cases  which  seem  more 
or  less  probable,  but  which  necessitate  great  care  in  the  diagnosis.  A 
positive  decision  in  a  given  case  depends  upon  two  things :  either  we  must 
feel  the  stenosis  directly  in  the  rectum — ^that  is,  we  must  palpate  a  tumor, 
a  peritoneal  band — or,  upon  the  surface  of  the  intestines,  we  must  detect  a 
special  configuration,  the  tetanic  intestinal  rigidity  and  increased  peristalsis 
during  an  attack  of  colic. 

What  lends  to  the  rigid,  chronic  stiffening  of  dilated  coils  its  great 
diagnostic  value,  particularly  for  stenosis?  The  anatomical  change  above 
the  narrow  area  furnishes  the  explanation  of  this.  The  intestine  is  here 
dilated,  usually  only  to  a  limited  extent  and  moderate  degree,  but  some- 
times over  large  areas  until  an  extreme  degree  is  reached.  Macroscopically, 
the  distinctly  visible  muscularis  of  the  intestine  is  hypertrophic,  in  cases 
that  are  prolonged  often  decided,  increased  over  great  areas,  for  instance, 
in  stenosis  of  the  sigmoid  flexure,  up  to  the  ileo-cecal  valve.  This  thicken- 
ing of  the  intestinal  wall,  which  in  acute  stenosis  may  even  be  recognized 
upon  the  fourth  or  fifth  day,  is  the  product  of  a  true  hypertrophy  of 
individual  fibers  and  muscles  which  owe  their  origin  to  increased  muscular 
exertion  that  is  absolutely  necessary  to  propel  the  intestinal  contents 
through  the  narrowed  area.  And  as  such  a  marked  muscular  hyper- 
trophy, capable  of  developing  an  enormous  rigid  stiffening,  only  arises 
in  extreme  stenosis,  the  diagnostic  importance  of  intestinal  rigidity  is  clear. 


ETIOLOGY 

We  now  turn  to  the  question:  What  etiologic  factors  are  capable  of 
producing  such  a  change  in  the  intestinal  lumen  that  the  propulsion  of 
the  contents  becomes  difficult?  This  condition  we  designate  as  constric- 
tion of  the  intestines  (stenosis)  in  contrast  to  intestinal  obstruction  (oc- 
clusion) in  which  the  lumen  is  completely  closed,  and  any  propulsion  of 
the  contents  downward,  i.  e.,  in  a  physiologic  direction,  is  absolutely 
impossible. 

The  form  of,  and  the  causes  which  may  'produce,  narrowing  of  the 
lumen  of  the  intestine,  are  manifold. 

We  should  digress  far  beyond  the  limits  of  this  article  if  we  attempted 
minutely  to  investigate  these,  and  must  content  ourselves  with  their  simple 
enumeration,  giving  to  each  the  brief  consideration  necessary  for  our 
concrete  purpose. 

First,  it  must  be  stated  that  the  condition  designated  as  intestinal 
stenosis  is,  in  a  clinical  sense,  always  due  to  anatomical  changes  and  rela- 
tions. Certainly,  a  spastic  contraction  of  the  musculature  of  the  intestines 
will  cause  a  narrowing  of  its  lumen.     This,  however,  is  but  a  temporary 


INTESTINAL  CONSTRICTION  755 

condition,  and  does  not  produce  the  clinical  picture  characterized  by  the 
term  "  intestinal  stenosis/'  The  fecal  masses  which  accumulate  in  the 
intestine,  especially  in  habitual  constipation,  also  narrow  the  intestinal 
passage;  but  in  this  condition  the  picture  of  intestinal  stenosis  with  mus- 
cular hypertrophy  and  tetanic  stiffening  does  not  develop;  should  any 
serious  local  consequences  arise,  the  symptom-complex  of  complete  intes- 
tinal occlusion  results. 

Chief  among  the  causes  of  stenosis  of  the  intestine  are  the  following: 

1.  Carcinomata  of  the  intestine.  These  are  almost  always  primary; 
only  very  exceptionally  does  a  carcinoma  develop  in  the  intestines  by  way 
of  metastases,  through  the  blood,  or  through  the  lymph-vessels.  Naturally 
we  must  consider  very  differently  those  not  infrequent  cases  in  which  the 
neoplasm  proliferates  from  a  neighboring  organ  (the  stomach,  the  uterus, 
the  gall-bladder)  to  the  intestines. 

Universal  experience  teaches  us  that  carcinoma  in  the  small  intestine  is 
very  rare,  is  frequent  in  the  colon,  and  most  frequent  in  the  rectum.  To 
illustrate,  we  will  mention  only  those  figures  which  are  taken  from  the 
autopsy  reports  of  the  Pathological  Institute  of  the  Vienna  General  Hos- 
pital. In  twenty-four  years,  among  41,838  autopsies  there  were  343  intes- 
tinal cancers.  Of  these  7  were  in  the  duodenum,  10  in  the  ileum  (none 
in  the  jejunum),  164  in  the  colon,  and  163  in  the  rectum.  Accordingly — 
and  other  autopsy  statistics  agree  in  this — the  number  of  colon  and  rectal 
carcinomata  is  almost  equal.  In  contrast  to  this,  the  statistics  in  the 
living  show  the  very  extraordinary  preponderance  of  rectal  cancers,  80 
per  cent,  of  all  intestinal  cancers  being  here  included.  The  discrepancy 
in  these  statistics  may  probably  be  largely  explained  by  the  fact  that  cancer 
of  the  rectum  is  much  more  susceptible  to  diagnosis  and  more  readily 
operable,  so  that  many  carcinomata  of  the  rectum  are  operated  upon,  and 
do  not  come  to  autopsy  in  the  Hospital. 

Clinically,  the  fact  is  noteworthy  that  cancer  of  the  intestine  occurs 
with  relative  frequency  in  the  first  half  of  life,  usually  developing  before 
the  fortieth  year.  The'  anatomical  peculiarity  of  intestinal  cancer,  that  it 
often  distributes  itself  in  a  markedly  annular  form,  occasionally  encircling 
the  intestinal  lumen  like  a  cicatricial  ring,  makes  it  possible  for  the 
neoplasm  to  produce  decided  narrowing  which  may  be  so  extreme  that 
only  a  thin  pencil  or  a  sound  can  be  introduced.  The  same  stenotic 
effect,  however,  may  occasionally  be  produced  by  all  other  forms  of  the 
neoplasm. 

2.  Sarcomata  may  also  narrow  the  lumen,  but  this  effect  is  only  rarely 
observed.  On  the  contrary,  in  this  form  of  tumor,  the  intestinal  passage 
is  but  little  influenced;  on  account  of  the  peculiar  distribution  of  the 
neoplasm  mass  into  the  musculature,  the  intestinal  wall  rather  becomes 
paretic. 

3.  I  include  here  tuberculomata  of  the  intestinal  walls,  which,  like  car- 


756      INTESTINAL  CONSTRICTION  AND  INTESTINAL  OCCLUSION 

cinomata,  and  in  identically  the  same  manner,  may  bring  about  stenosis. 
I  have  observed  several  cases  of  this  form  of  tumor  and  the  literature  of 
the  past  year  also  furnishes  examples. 

4.  Benign  intestinal  tumors  (myomata,  lipomata,  angiomata,  fibromata, 
adenomata)  only  exceptionally  form  the  cause  of  stenosis;  their  entire 
composition  and  anatomical  formation  is  but  little  conducive  to  this  and 
their  occurrence  is  quite  rare.  At  the  most  they  indirectly  cause  a  limita- 
tion in  the  passage  by  becoming  the  starting  point  of  an  invagination  as 
pediculated  polypi.  The  majority  of  benign  tumors  which,  by  direct 
limitation  of  space,  cause  stenosis  are  situated  in  the  rectum  and  usually 
occur  in  children. 

5.  Internal  cicatricial  strictures  are  produced  from  connective  tissue, 
from  cicatrices  of  ulcers.  Of  the  many  varying  etiologic  forms  of  ulcer 
in  the  intestine,  few  terminate  in  a  cicatrix  which  causes  a  stricture. 
The  most  frequent  are  the  tuberculous  and  stercoraceous  ulcerations,  more 
rarely  the  round  ulcer  of  the  duodenum,  the  dysenteric  and  catarrhal 
follicular  ulcerations,  the  syphilitic  forms  of  disease,  finally,  traumatic 
lesions  and  enteric  fever  ulcerations.  This  scale  of  frequency  is  dif- 
ferent from  that  commonly  given,  in  which  the  dysenteric  cicatricial 
ulcers  occupy  the  first  place,  and  the  tuberculous  and  typhoid  ulcers  the 
last.  According  to  the  comprehensive  statistics  compiled  by  Woodward, 
we  can  hardly  doubt  the  rarity  of  dysenteric  strictures.  On  the  other  hand, 
Konig  has  called  attention  to  the  fact,  opposed  to  former  views,  that 
tuberculous  cicatricial  strictures  have  been  frequently  observed,  and  this 
coincides  with  my  own  personal  experience. 

Tuberculous  cicatricial  strictures  occur  mostly  in  the  small  intestine, 
particularly  in  the  ileum,  as  do  also  the  very  rare  typhoid  strictures; 
those  due  to  ulcer  of  the  duddenum  are  naturally  found  in  its  region; 
dysenteric  and  stercoraceous  (decubital),  in  the  colon  and  rectum.  The 
cicatricial  stenoses  after  catarrhal  follicular  ulcers,  which  are  also  exceed- 
ingly uncommon,  are  met  with  in  the  small  as  well  as  in  the  large  intes- 
tine; those  due  to  syphilis  preponderate  in  the  large  intestine,  moje  accu- 
rately, in  the  rectum.  This  latter  region,  more  often  than  any  other  part 
of  the  intestine,  may  become  stenosed  by  cicatrices  which  originate  from 
trauma, — operations  for  prolapse  of  the  rectum,  destruction  of  hemor- 
rhoidal nodules,  injury  from  syringes  or  introduced  foreign  bodies,  and 
to  these  perforating  periproctitic  abscesses  are  superadded.  Cases  of  ste- 
nosis of  the  intestine  are  rarely  observed,  and  up  to  this  time  have  been 
exclusively  in  the  small  intestine,  after  severe  trauma  of  the  abdomen 
which  has  produced  a  lesion  in  the  wall  of  the  intestine.  These  anoma- 
lies liavo  a  purely  clinical  interest  from  the  fact  that  when  a  portion 
of  the  intestine  is  implicated  in  a  strangulation,  or  after  the  desquama- 
tion of  an  intussuscepted  portion  of  the  intestine  in  invagination,  a  stric- 
ture may  subsequently  develop. 


INTESTINAL  CONSTRICTION  757 

6.  External  constriction  of  the  intestine  hy  peritoneal  processes,  the 
anatomical  appearancer  of  which  has  been  portrayed  by  Treves.  It  is  im- 
possible for  us  here  to  give  a  detailed  description;  only  the  most  important 
general  features  will  be  emphasized.  In  this  etiologic  group  we  invariably 
deal  with  chronic  peritoneal  adhesions,  indurations  or  bands,  which  have 
made  a  portion  of  the  intestine  adherent  either  to  another  part  of  the 
intestine,  to  any  area  of  the  abdominal  walls,  or  to  another  organ,  and, 
in  the  latter  case,  to  one  normally  in  the  neighborhood  of  the  intestine 
or  abnormally  situated  there. 

In  very  different  ways  the  lumen  of  the  intestine  may  be  occluded  by 
the  action  of  chronic  peritonitis.  Peritoneal  indurations  which  are  isolated 
and  circumscribed  usually  encircle  the  intestine  in  a  ring-shape,  or,  at  a 
circumscribed  point  on  the  lateral  surface,  the  adherent  intestine  becomes 
more  or  less  decidedly  twisted,  when  we  have  a  volvulus  of  the  intestine. 
Or,  a  general  peritonitis  leads  to  concretions,  partly  of  the  intestinal  coils 
among  each  other,  and  partly  of  the  parietal  serosa  with  the  solid  abdom- 
inal organs.  Occasionally,  constriction  occurs  as  the  result  of  peculiar 
extension  of  the  intestinal  wall  by  traction  of  a  diverticulum. 

I  must  refrain  from  the  enumeration  of  the  various  anatomical  causes 
and  the  etiologic  modes  of  development  of  this  chronic  adhesive  peritonitis, 
and  shall  only  state  that  this  etiologic  form  of  stenosis  may  affect  the 
different  portions  of  the  intestine  quite  irregularly. 

7.  The  intestine  may  he  constricted  hy  a  tumor  or  hy  any  other  mass 
acting  similarly  hy  pressure  (gravid  uterus,  dislocated  organs,  inflamma- 
tory abscesses).  In  this  group  those  portions  of  the  intestine  are  most 
frequently  occluded  which,  on  account  of  their  anatomical  position,  and 
their  tense,  mesenteric  fixation,  are  least  able  to  elude  pressure;  first,  the 
rectum,  then  the  descending  colon  and  the  sigmoid  flexure,  the  duodenum, 
the  ileum  infimum,  the  upper  portions  of  the  ileum  very  slightly,  the  jejunum 
and  the  transverse  colon. 

Besides  the  factors  which  have  been  mentioned,  in  very  rare  cases 
other  conditions  may  bring  about  a  constriction  of  the  lumen  of  the  intes- 
tine, such  as  a  chronic  invagination,  or  even  sometimes  an  obstruction 
from  hard  fecal  masses,  gall-stones,  or  a  foreign  body.  But  this  is  excep- 
tional ;  for  the  most  part  the  conditions  enumerated  are  the  causative  ones. 

We  now  return  to  our  special  case  with  the  question:  What  causes  the 
stenosis  in  this  patient?  In  which  portion  of  the  intestine  is  it  situated? 
I  will  recapitulate  briefly  the  important  results  of  our  investigation:  The 
patient  is  afebrile;  moderately  emaciated;  there  is  pallor  of  the  face; 
the  radial  pulse  is  normal;  there  is  constipation  and  the  previously  men- 
tioned abdominal  pain.  Upon  inspection  the  upper  portion  of  the  abdo- 
men shows  nothing  abnormal.  It  is  situated  below  the  level  of  the  thorax ; 
the  lower  half,  from  the  navel  downwards,  is  somewhat  inflated;  there  is 
no  meteoric  bulging  of  the  flanks.  In  the  lower  half  of  the  abdomen, 
49 


758      INTESTINAL  CONSTRICTION   AND  INTESTINAL  OCCLUSION 

occasional  tetanic  intestinal  rigidity  and  progressively  energetic  peristalsis 
are  noted.  Most  decided  bulging,  in  extent  that  of  a  dinner-plate,  is 
periodically  observed  in  the  ileo-cecal  region.  This  area  is  also  the  seal 
of  the  severest  pain.  These  phenomena  appear  spontaneously,  causing  pain 
which  ceases  after  a  few  seconds,  at  most  after  a  few  minutes.  Occasion- 
ally loud  gurgling  and  rumbling  are  heard.  Stress  must  be  laid  upon  the 
following:  If  the  abdominal  surface  is  perfectly  quiet,  it  is  sometimes 
possible  to  produce  peristalsis  and  intestinal  tetany  by  gentle  palpation, 
but,  more  certainly,  by  short,  energetic  taps  which  invade  deeply  or  by 
flagellations  with  a  cold,  damp  towel. 

The  seat  and  the  relief-like  arrangement  of  these  characteristic  signs 
must  be  accurately  studied;  as  their  presence  permits  the  diagnosis  of 
intestinal  stenosis,  their  seat  and  arrangement  furnish  valuable  and,  as  a 
rule,  the  most  important  aid  in  answering  the  question  in  which  part 
of  tlie  intestine  the  stenosis  is  situated.  I  go  still  further  since,  upon 
the  average,  the  determination  of  the  seat  in  chronic  stenosis  of  the  intes- 
tine is  easier  than  giving  an  opinion  in  regard  to  its  anatomical  nature; 
as  is  shown  by  the  above  compilation  of  the  anatomico-etiological  condi- 
tions, certain  processes  which  cause  stenosis  occur  very  frequently  in  indi- 
vidual portions  of  the  intestine,  in  others  very  rarely  or  not  at  all,  and 
by  determining  the  seat  we  indirectly  gain,  at  the  same  time,  certain 
points  of  support  for  the  recognition  of  the  anatomical  process.  For  this 
reason,  I  generally  advise  that  we  first,  if  possible,  determine  the  seat  of 
the  obstruction,  and  then  its  nature. 

Descriptions  of  the  various  forms  of  intestinal  stiffening  and  peristalsis 
wliich  occur  in  individual  cases  are  hardly  possible;  illustrations  convey 
a  much  clearer  idea  of  the  condition.  I  shall,  therefore,  limit  myself  to 
tlie  enunciation  of  a  few  general  principles. 

As  a  rule,  the  arrangement  and  position  of  the  intestinal  areas  correspond 
with  the  normal. 

Distention  of  the  flanks  and  of  the  upper  abdominal  regions  primarily 
points  to  the  colon.  If  the  flanks  are  not  at  all  distended,  if  they  follow 
a  horizontal  line,  or  are  even  concave,  stenosis  of  the  colon  may,  with 
great  probability,  be  excluded;  but  the  possibility  of  congenital  or  acquired 
anomaly  of  position  must  always  be  considered.  The  inverse,  however,  is 
not  true ;  i.  e.,  that  extension  of  the  flanks  may  be  caused  by  tensely  filled 
and  prolapsing  coils  of  the  small  intestine.  The  diagnostic  importance  of 
extension  of  the  flanks  is  especially  convincing  when  the  obstruction  is 
situated  in  that  portion  of  the  colon  from  the  hepatic  flexure  to  the  splenic 
flexure;  here  the  right  flank  alone  is  distended.  In  the  majority  of  cases 
of  chronic  stenosis,  the  dilated,  stiffened  or  extremely  peristaltic  large 
intestine  is  in  its  normal  situation  (while  the  enormous  degree  of  infla- 
tion in  acute  obstruction,  especially  in  sigmoid  volvulus,  creates  the  most 
ieiiiarkal)le  topographical  positions). 


INTESTINAL  CONSTRICTION  759 

Abnormally  situated  intestinal  coils,  with  alternating  and  disappearing 
peristalsis  or  stiffening,  indicate  the  small  intestine.  The  same  is  true 
of  several  (2,  3  or  more)  adjacent,  oblique  or  vertical  (organ-like)  coils 
upon  the  longitudinal  axis  of  the  body. 

The  most  extreme  thickening,  as  a  rule,  must  be  referred  to  the  intes- 
tinal portion  situated  nearest  the  obstruction,  which  is  accompanied  by 
marked  muscular  hypertrophy.  An  exception  to  this  occurs  only  when 
the  intestine  has  become  paretic  by  long-continued  over-distention. 

The  fact  is  noteworthy  that  movements  in  the  colon  are  usually  slow, 
in  the  small  intestine  they  are  more  rapid  and  irregular.  It  is  often  noted 
that  they  cease  in  a  definite  locality,  with  absolute  regularity,  for  example, 
in  the  ileo-cecal  region,  and  if  there  is  irregular  peristalsis  of  the  small 
intestine,  if  the  lateral  walls  invariably  remain  quiet,  we  conclude  that 
the  obstruction  is  in  the  region  of  the  cecum. 

These  relief-like  circumscribed  inflations  and  changes  in  the  shape  of 
the  abdominal  surface  may,  however,  be  entirely  absent.  The  seat  of  the 
stenosis  is  then  much  more  difficult  to  decide,  but  it  may  occasionally 
be  made  with  certainty,  provided  physical  examination  reveals  such  rela- 
tions as  are  calculated  to  influence  directly  or  indirectly  the  permeability 
of  the  intestine.  To  this  category  belong  the  proof  of  tumors  of  a  neo- 
plasmatic  or  inflammatory  nature,  changes  in  position  of  the  solid  abdom- 
inal organs,  tumors  from  invagination,  chronic  peritoneal  bands,  and  old 
external  hernias. 

The  results  of  percussion  and  auscultation  are  less  valuable  in  deciding 
upon  the  seat,  are  only  to  be  utilized  most  cautiously,  and  then  rather 
in  cases  of  occlusion;  in  stenosis  little  or  no  value  can  be  attached  to  this 
method  of  examination. 

Vaginal  exploration  is  an  important  aid,  and  even  of  greater  signifi- 
cance is  digital  rectal  examination,  by  which  we  may  directly  demonstrate 
the  obstruction  which  produces  the  stenosis.  These  examinations  should 
never,  under  any  circumstances,  be  neglected,  for  with  the  regular  exam- 
ination of  the  hernial  rings  they  become  a  duty  upon  which  too  great 
stress  cannot  be  laid. 

Pain  is  a  very  unreliable  symptom.  Only  when  it  is  closely  circum- 
scribed, accurately  located,  of  uniform  degree,  and  permanent,  can  we  trace 
its  seat  to  a  definite  locality,  and  not  always  then. 

The  stenoses  of  the  duodenum  and  the  rectum  call  for  special  dis- 
cussion. 

Chronic  stenosis  of  the  duodenum  gives  rise  to  varying  symptoms, 
according  to  whether  the  narrowed  area  is  situated  above  or  below  the 
common  gall-duct  and  the  pancreatic  duct.  The  clinical  picture  in  the 
former  case  so  closely  resembles  that  of  stenosis  of  the  pylorus  that  a 
differential  diagnosis  is  impossible.  Where  the  constriction  is  deeply  situ- 
ated there  is  also  gastric  dilatation ;  in  this  case,  however,  there  are  charac- 


760      INTESTINAL  C0;NSTRICTI0N   AND  INTESTINAL  OCCLUSION 

teristic  symptoms  in  addition.  Bile  flows  profusely  and  continuously  into 
the  stomach  so  that  massive  bilious  vomiting  occurs;  or,  after  gastric 
lavage,  large  quantities  of  pure  bile  may  flow  from  the  tube.  Pan- 
creatic juice  may  also  be  present  in  the  stomach,  so  that  in  this  organ 
duodenal  digestion  with  distinct  splitting  of  fat  may  take  place. 

Stenosis  of  the  rectum  is  easily  and  most  positively  diagnosticated,  as, 
in  the  majority  of  cases,  it  may  be  reached  by  the  palpating  finger.  Some- 
times suspicion  is  awakened  by  the  apparently  causeless  development  of 
hemorrhoids  and  hemorrhages;  also  by  tenesmus.  In  the  main,  general 
diagnostic  laws  are  here  applicable. 

The  employment  in  our  special  case  of  the  rules  which  have  been 
briefly  sketched  forces  us  to  the  view  that  the  seat  of  the  stenosis  is  in 
tlie  lowest  part  of  the  ileum,  in  the  neighborhood  of  the  ileo-cecal  valve 
(tlie  details  of  proof  may  be  omitted,  and  we  may  assume  the  diagnosis 
to  be  correct  since  later,  when  laparotomy  was  performed,  this  view  was 
confirmed). 

Another  question  arises:  What  is  the  nature,  what  the  anatomical 
composition,  of  the  obstruction  which  causes  this  stenosis?  The  deter- 
mination of  the  anatomical  nature  of  the  intestinal  obstruction  is  hedged 
in  by  enormous  difficulty,  and,  in  our  opinion,  forms  one  of  the  most 
perplexing  points  in  diagnosis.  Only  the  most  careful  consideration  of 
each  individual  symptom  enables  us  to  proceed,  and  we  should  never 
forget  that  each  concrete  case  may  deviate  from  the  symptomatologic  type. 

The  general  rules  must  be  first  mentioned. 

Primarily,  the  hernial  rings  should  be  examined.  Hernias  are  not 
only  of  great  importance  in  acute  intestinal  occlusion,  but  old  hernias 
may  also  form  a  focus  for  chronic  constriction  by  means  of  peritoneal 
adhesions  wliieh  lead  to  constriction  and  volvulus  of  the  intestine. 

Exact  digital  investigation  of  the  rectum  and  vagina  must  be  made; 
tliis  occasionally  furnishes  the  direct  clue  to  the  diagnosis,  or  points  the 
way  to  it. 

If  examination  of  the  hernial  rings,  of  the  rectum  and  vagina,  is  nega- 
tive, the  abdomen  must  be  carefully  palpated.  In  a  certain  number  of 
cases  a  tumor  will  be  found,  and  we  must  decide  whether  it  be  a  malignant 
growth  or  chronic  invagination,  a  fecal  mass  or  an  inflammatory  infiltra- 
tion. The  points  of  support  operative  here  cannot  be  described.  Natu- 
rally tumors,  particularly  those  not  circumscribed,  may  be  present  and 
escape  detection,  either  because  they  are  too  small  (which  is  particularly 
the  case  in  carcinoma),  or  because  they  are  concealed  by  inflated  coils  of 
intestine,  or  for  other  accidental  reason. 

Occasionally  we  succeed  in  palpating  isolated,  thicker,  peritoneal  bands. 
of  irregular  contour.  If  we  are  dealing  with  tough,  massive,  distributed 
and  chronic,  inflammatory  adhesions,  such,  for  example,  as  are  produced 
Itv  tubercular  peritonitis,  the  anatomical  situation  clears  at  once. 


INTESTINAL  CONSTRICTION  761 

If,  however,  no  clue  is  found  which  may  directly  lead  to  the  recogni- 
tion of  the  anatomical  nature  of  the  obstruction,  then  an  explanation  must 
be  sought  in  the  history,  in  the  course  of  development,  and  from  other 
circumstances.  Chronic  inflammatory  processes  in  the  pelvis,  a  preceding 
perityphlitis,  and  similar  anamnestic  data  indicate  peritoneal  fixation,  dys- 
enteric and  other  ulcerative  intestinal  processes  point  to  cicatricial  stric- 
tures, very  insidious  development  of  the  symptoms  of  stenosis  without  pre- 
ceding disease  indicates  carcinoma.  Under  these  circumstances,  it  is  of 
special  importance  in  the  diagnosis  to  determine  in  which  portion  of  the 
intestine  is  the  narrowed  area. 

Let  us  apply  this  mode  of  investigation  to  our  special  case. 

The  hernial  rings  are  free.  Palpation  of  the  abdomen  reveals  the  in- 
testinal rigidity  and  increased  peristalsis  which  have  been  described,  which 
justify  the  conclusion  that  the  seat  of  the  obstruction  is  the  lowest  por- 
tion of  the  ileum — but,  beyond  this,  absolutely  nothing  to  assist  in  ex- 
plaining the  nature  of  the  obstruction,  no  palpable  tumor  or  i)eritone-I 
band,  not  even  an  area  painful  upon  pressure.  On  the  other  hand,  vaginal 
and  rectal  examinations  yield  positive  findings:  In  the  left  vaginal  vault, 
a  prominent  crescentic  cicatrix,  on  the  right  side  a  narrow  cicatricial  band 
extending  to  the  posterior  wall  of  the  vagina.  These  cicatricial  adhe- 
sions render  a  positive  palpation  of  the  adnexa  difficult.  Palpation  by 
rectum  shows  the  pelvis  to  be  filled  with  markedly  inflated  intestinal  coils, 
and,  besides,  particularly  upon  the  right  posterior  surface  of  the  uterus, 
posteriorly  toward  the  ligamentum  latum,  thin,  tendinous,  coarse  bands  of 
adhesions  may  be  distinctly  felt.  A  preceding  pelvic  peritonitis  must, 
therefore,  be  diagnosticated. 

On  account  of  these  conditions,  the  opinion  naturally  forces  itself  upon 
us  that  these  chronic  peritoneal  processes  arising  from  the  internal  genitalia 
are  connected  with  intestinal  stenosis,  the  latter  being  due  to  constriction  or 
volvulus.  In  connection  with  the  otherwise  entirely  negative  findings,  this 
conclusion  must  be  recognized  as  logical,  and  no  direct,  forcible  objection 
to  it  can  be  raised. 

Nevertheless,  we  must  be  careful  not  to  assume  without  more  ado  that 
this  conclusion  is  correct.  This  caution  is  not  based  upon  forcible  reasons 
in  the  particular  case,  but,  on  the  contrary,  upon  general  experience  gained 
by  much  observation  at  the  bedside,  which  may  be  expressed  by  saying 
that  we  cannot  he  too  cautious  with  these  diagnoses.  Any  one  who  ba-; 
observed  many  of  these  cases  knows  how  often  and  how  readily  mistakes 
and  diagnostic  errors  arise,  even  when  everything  has  been  carefully  inves- 
tigated in  logical  sequence.  My  method  of  reasoning  in  such  a  case  is  the 
following : 

The  diagnosis  obtained  by  direct  analysis,  it  is  true,  primarily  and 
immediately  leads  to  the  presumption,  just  expressed,  of  an  intestinal  con- 
striction or  volvulus  which  is  the  result  of  peritoneal  adhesions  arising  from 


762      INTESTLNAL  CONSTRICTION  AND  INTESTINAL  OCCLUSION 

the  genitalia.  But — as  has  been  taught  us  by  quite  analogous  cases — 
something  else  might  be  present,  and  it  is  advisable  to  keep  these  other 
possibilities  always  in  mind.  What  conditions  must  be  considered  here? 
Basis  of  support  is  given  by  two  factors :  The  very  insidious  onset,  and  the 
seat  of  the  stenosis  in  the  lower  portion  of  the  small  intestine.*  Both  these 
facts  coincide  with  the  assumption  of  cicatricial  stricture  or  neoplasm.  In 
fact  long  experience  has  taught  me  to  formulate  the  following  law :  When 
there  is  an  unquestioned  stenosis  of  the  ileum,  and  absolutely  no  point  by 
which  we  may  recognize  its  anatomical  nature,  we  should  primarily  con- 
sider cicatricial  stricture  following  tuberculous  ulcers  of  the  ileum,  even 
although  no  other  evidence  of  tuberculosis  can  be  determined.  I  have  seen 
conditions  exactly  as  in  this  case ;  i.  e.,  stenosis  of  the  small  intestine  in 
women  in  whom  peritoneal  bands  originating  from  the  genitalia  were 
palpable,  yet  nevertheless,  at  the  operation  or  autopsy,  not  these  but  cica- 
tricial strictures  after  healed  tuberculous  ulcers  of  the  ileum  were  shown  to 
be  the  cause  of  the  stenosis;  or,  a  small  neoplasm,  either  carcinomatous  or 
tuberculous,  not  palpable,  situated  in  the  lowest  portion  of  the  ileum  or  at 
the  ileo-cecal  valve,  might  also  be  considered. 

From  this  framework  the  diagnosis  must  be  evolved;  we  cannot  express 
ourselves  more  definitely  or  more  carefully.  Our  diagnosis^  therefore,  in 
this  case  is  as  follows:  Peritoneal  constriction  or  volvulus,  or  a  tuberculous 
cicatricial  stricture  or  neoplasm  {carcinoma,  tuberculoma),^ 

PROGNOSIS 

The  prognosis  of  constriction  of  the  intestine  is  always  serious  although 
not  always  equally  so.  The  gravity  is  determined  less  by  the  spat  than  by 
the  nature  of  the  obstruction.  In  some  forms,  although  naturally  very 
rarely,  spontaneous  recovery  may  result;  a  benign  polypoid  neoplasm,  even 
an  invaginated  portion  of  the  intestine,  may  be  thrown  off,  an  exudate 
which  causes  pressure  may  be  resolved,  a  uterus  in  abnormal  position  may 
be  replaced,  and  thus  the  cause  of  the  stenosis  is  removed.  But  these  are 
all  exceptions. 

Without  treatment  stenosis  almost  always  causes  serious  consequences. 
If  no  complications  occur,  the  course  of  a  benign  stenosis  is  as  follows: 

1  I  here  include  the  following : 

Laparotomy  revealed  the  existence  of  pelvic  peritoneal  bands;  but  these  were 
diiefly  found  in  the  large  intestine,  and  there  was  no  causal  connection  with  the 
stenosis  of  the  ileum.  In  the  ileum  not  one  but  two  stenoses  were  found,  removed 
about  6  era.  from  each  other.  A  portion  of  the  intestine  about  13  cm.  in  length  was 
excised;  examination  revealed  two  ring-shaped,  coarse,  fibrinous,  cicatricial  stric- 
tures. The  mesentery  belonging  to  this  coil  of  ileum  contained  glands  which  were 
hard  and  the  size  of  a  hazelnut;  microscopic  examination  revealed  tubercular  disease. 
Accordingly  the  intestinal  strictures,  also,  must  be  looked  upon  as  originating  from 
tuberculous  ulcers. 


INTESTINAL  CONSTRICTION  763 

For  a  long  time  the  compensatory  hypertrophy  of  the  musculature  over- 
comes resistance,  making  the  propulsion  of  the  intestinal  contents  possible. 
Gradually,  however,  insufficiency  of  the  musculature  appears;  it  becomes 
paretic;  fecal  stasis  follows,  and  finally,  all  the  consequences  which  char- 
acterize intestinal  occlusion — operation  or  death.  In  other  cases  the  changes 
in  the  mucous  membrane  above  the  stenosis  determine  the  further  course. 
Diffuse  peritonitis  or  sacculated  fecal  abscesses  may  result  from  decubital 
ulcers,  also  severe  septic  conditions,  or  perforation  with  its  fatal  issue. 
In  carcinomatous  stricture  the  process  is  hastened  by  the  malignant  nature 
of  the  growth. 

Here  and  there  intermediate  conditions  may  add  to  the  constriction 
and  lead  to  sudden  and  complete  occlusion.  Thus,  solid  foreign  bodies 
(fruit-stones,  asparagus)  or  even  a  coarse  particle  of  feges  may  com- 
pletely occlude  the  narrow  opening  of  the  intestinal  lumen.  Or  the  heavy 
intestinal  coil  above  the  stenosis  which  is  filled  with  feces  may  descend, 
causing  torsion  of  the  axis  and  volvulus.  If  the  antecedents  are  unknown, 
or  have  been  disregarded,  cases  of  this  kind  may  occasionally  simulate  acute 
intestinal  occlusion.  Sometimes  the  true  condition  may  be  suspected  if 
active  peristalsis  and  rigid  stiffening  arise,  for  these  permit  the  conclu- 
sion of  hypertrophy  of  the  intestinal  musculature ;  therefore,  of  an  obstruc- 
tion which  has  existed  for  a  long  time. 


TREATMENT 

In  conclusion  we  must  discuss  the  treatment. 

This  may  be  instituted  with  two  objects:  To  limit  the  disease  to  a 
symptomatic  course,  or  to  attempt  the  radical  removal  of  the  obstruction. 
We  shall  begin  with  the  latter. 

Except  in  very  isolated  cases  the  removal  of  the  stenotic  obstruction 
is  possible  only  by  surgical  measures.  Fecal  masses  in  the  interior  of  the 
intestine  narrow  it  but  do  not  cause  total  occlusion;  an  inflammatory  exu- 
date capable  of  resorption  gives  rise  to  external  pressure;  these  belong  to 
the  greatest  rarities.  In  such  instances  treatment  must  be  instituted  in 
accordance  with  the  well-known  laws  which  apply  in  the  concrete  case. 
In  others  only  the  knife  can  aid  us;  it  is  superfluous  to  explain  this  in 
detail,  for  a  glance  at  the  previously  described  anatomical  causes  of  con- 
striction proves  this  convincingly.  The  question  is  only  this:  When  shall 
we  operate  ?  The  answer  to  this  must  be :  As  soon  as  the  diagnosis  of  con- 
striction has  been  made  with  certainty.  For,  if  left  to  itself,  the  condition 
can  never  ameliorate  but  steadily  becomes  more  serious.  In  the  case  of 
carcinoma,  operative  interference  as  early  as  possible  is,  in  fact,  our  duty, 
for,  apart  from  the  consequences  due  to  the  stenosis,  the  danger  of  metas- 
tasis from  the  prolonged  existence  of  the  neoplasm  constantly  increases, 
and  the  chances  of  a  successful  operation  constantly  decrease.     In  cica- 


764      INTESTINAL  CONSTRICTION  AND  INTESTINAL  OCCLUSION 

tricial  strictures  and  in  constricting  indurations  we  are  not  influenced  by 
this  latter  consideration,  but  even  a  speedy  operation  is  indicated,  as  a 
spontaneous  recovery  is  not  to  be  expected  under  any  circumstances.  Nev- 
ertheless, here  we  may  more  reasonably  temporize  a  little,  and  only  insist 
upon  the  operation  when  the  clinical  conditions  of  the  pathologic  picture 
(unbearable  pain,  transitory  intestinal  occlusion)  make  it  necessary. 

Symptomatic  treatment  must  be  based  upon  three  different  points  of 
view:  The  period  of  time  between  the  individual  attacks  of  colic,  the  par- 
oxysms themselves,  and  the  appearance  of  complete  intestinal  occlusion. 

The  first  object  is  attained  by  regulating  the  diet  and  evacuating  the 
bowels.  Large  quantities  of  food  should  never  be  taken  at  one  time.  Its 
quantity  must  be  definitely  arranged ;  everything  is  to  be  absolutely  avoided 
that  is  unsuitable  in  volume  to  the  digestive  powers,  or  which  might  even 
itself  produce  an  obstruction,  such  as  rye-bread,  slices  of  potato,  fibrous 
and  tendinous  meat,  above  all,  most  vegetables  and  fruit  with  their  skins 
and  seeds.  It  is  best  only  to  give  pappy,  finely  divided,  or  finely  chopped 
food;  in  the  more  marked  grades  of  stenosis  only  fluid  or  semi-solid  food. 

It  is  clear  that  a  regular  daily  evacuation  of  the  bowels  must  be  care- 
fully brought  about.  According  to  the  seat  of  the  stenosis  serviceable 
remedies  are  irrigations  (of  water,  oil,  or  soap  and  water)  or  purgatives 
administered  internally,  among  which  the  neutral  salts  and  purgative 
waters,  preparations  of  senna  or  rhamnus  and  colocynth  are  preferable. 

The  attacks  of  colic  necessitate  the  complete  withdrawal  of  food  and 
the  employment  of  purgatives;  if  active  peristaltic  movements  and  intes- 
tinal stiffening  which  show  activity  above  the  stenosis  are  present,  irriga- 
tions but  no  eccoprotica  by  the  mouth  are  indicated.  Where  the  pain  is 
unbearable,  warm  compresses  to  the  abdomen,  and  occasionally  even  an 
opiate  must  be  resorted  to. 

A  further  indication  may  be  the  appearance  of  complete  occlusion.  It 
is  of  the  greatest  importance  that  we  understand  clearly  in  the  individual 
case  how  this  serious  result  has  arisen,  as  very  different  measures  may  be 
necessary  in  the  relief  of  this  condition. 

If  the  stenosed  area  is  still  permeable,  and  only  accidentally  occluded 
by  compact  intestinal  contents,  irrigations  and  salines  which  reduce  the 
intestinal  contents  to  a  fluid  may  relieve  this  condition. 

If  paresis  of  the  musculature  above  the  constriction  is  the  cause  of  the 
so-called  symptoms  of  ileus,  to  these  evacuants  we  add  the  employment  of 
electricity  and  massage,  also  gastric  lavage,  and  a  trial  of  the  atropin  treat- 
ment which  will  be  described  more  in  detail  in  the  article  upon  complete 
intestinal  occlusion.  These  non-surgical  measures  must  be  carried  out 
with  a  clear  conception  of  the  anatomical  conditions  and  functional  dis- 
turbances. Their  employment  is  limited  to  a  very  brief  period.  As  soon  as 
stasis  of  the  intestinal  contents  assumes  a  threatening  aspect,  particularly 
as  soon  as  the  cardiac  action  begins  to  weaken,  operative  interference  affords 


INTESTINAL  OCCLUSION  765 

the  only  hope  of  saving  life.  This  should  never  be  long  postponed,  even 
although  strangulation  of  the  intestine  have  not  supervened,  which,  in  acute 
occlusion,  causes  very  fulminant  symptoms;  a  possible  cardiac  insufficiency 
should  always  be  taken  into  consideration.  What  the  operative  process 
would  be  in  a  concrete  case  cannot  be  here  described. 


II.  INTESTINAL   OCCLUSION 

The  second  history  which  I  shall  relate  refers  to  an  acute  invagination 
of  a  portion  of  the  intestine  into  an  adjacent  part.  This  process  led  to 
the  complete  closure  of  the  intestinal  lumen,  and  produced  a  symptom- 
complex  which  is  usually  grouped  under  the  designation  "  ileus."  As  this 
symptom-complex  depends  not  only  upon  mechanical  closure  of  the  intes- 
tine but  also,  in  spite  of  complete  permeability,  upon  paralysis  of  the 
musculature  of  the  intestine,  in  the  former  case  we  speak  of  "  mechan- 
ical," in  the  latter  of  "  paralytic "  or  "  dynamic "  ileus.  The  clinico- 
symptpmatologic  limits  of  this  term  are  by  no  means  exact  or  sharply 
defined.  It  appears  to  me  that  occasionally  there  is  danger  in  the  use  of 
this  elastic  term,  inasmuch  as  by  its  use  in  a  concrete  case  the  impression 
may  be  given  that  the  diagnosis  has  been  clearly  established.  For  this 
reason,  I  think  it  wise  to  reject  the  term  ileus,  although  it  is  undoubtedly 
useful  on  account  of  its  brevity.  In  its  place,  however,  in  every  case  where 
possible,  not  only  a  functional  but  an  anatomical  diagnosis  should  be  made. 

PATHOLOGY 

The  pathology  of  intestinal  occlusion  is  much  more  complicated  than 
that  of  intestinal  stenosis.  In  a  single  concrete  case  it  is  impossible  to 
analyze  all  of  its  features;  therefore,  in  describing  this  condition  I  shall 
pursue  a  method  different  from  that  used  in  presenting  stenosis. 

Let  us  then  begin  upon  the  firm  foundation  of  the  anatomical  changes. 

In  occlusion  the  permeability  of  the  intestine  is  completely  arrested. 
Neither  compact,  nor  fluid,  nor  gaseous  contents  pass  downward.  As  in 
stenosis  a  marked  contrast  exists  between  the  intestinal  coils  situated  above 
and  those  below  the  occlusion;  the  picture,  however,  is  not  uniform,  but 
varies  according  to  the  causal  relations  of  the  process. 

In  those  cases  in  which  a  slowly  progressive  stenosis  gradually  leads 
to  complete  occlusion,  the  same  anatomical  condition  is  found  which  I 
sketched  in  describing  stenosis;  often  there  is  decided  thickening  of  the 
intestinal  wall,  with  catarrhal  and  ulcerative  implication  of  the  mucous 
membrane  above  the  area  of  occlusion. 

On  the  other  hand,  in  acute  occlusion  which  occurs  suddenly  in  an  in- 
testine previously  healthy,  the  distention  of  the  upper  intestinal  coils  is 
occasionally  enormous,  but  the  wall  is  not  thickened  by  muscular  hyper- 
trophy; on  the  contrary,  according  to  the  nature  of  the  anatomical  process 


766      INTESTINAL  CONSTRICTION   AND   INTESTINAL   OCCLUSION" 

causing  the  condition,  it  is  sometimes  thin  and  pale,  at  other  times  dark 
blood-red  and  succulently  thick.  The  distention  is  usually  caused  by  a 
so-called  stasis  meteorism,  i.  e.,  by  stasis  of  the  intestinal  contents  and  gas 
above  the  occluded  area.  The  intensity  and  distribution  of  the  same 
toward  the  stomach  varies  in  individual  cases;  if  the  seat  of  the  occlu- 
sion be  in  the  colon,  the  resistance  of  the  ileo-cecal  valve  is  overcome  with- 
out difficulty. 

Wahl  and  Zoege  v.  Manteuffel  have  recognized,  in  contrast  to  the  usual 
form,  another  variety,  the  so-called  local  meteorism.  This  appears  when, 
besides  the  narrowing  of  the  intestinal  lumen,  severe  circulatory  disturb- 
ance in  the  sense  of  a  venous  stasis  simultaneously  occurs  in  the  intestinal 
wall  and  in  the  mesentery;  this  is  most  frequently  observed  in  torsion  and 
kinking,  occasionally  also  in  internal  forms  of  incarceration  resembling 
hernia.  Stasis  meteorism  may  happen  in  these  forms,  but  may  also  be 
absent.  In  the  latter  case,  the  intestines  above  and  below  the  area  of 
occlusion  are  absolutely  empty;  on  the  other  hand,  the  coils  between  the 
points  of  occlusion  are  dilated  (particularly  in  volvulus  and  in  kinking), 
they  are  dark  blood-red,  their  walls  are  thickened  by  an  accumulation  of 
fluid ;  gas,  blood  and  fluid  fill  the  interior — and  this  condition  in  particular 
is  designated  as  local  meteorism.  In  complicated  noose  formation  empty 
and  local  meteoric  coils  may  vary,  and  present  anomalous  pictures.  The 
development  of  gas  is  due  to  the  strangulation,  i,  e.,  to  the  venous  circu- 
latory disturbance  which,  in  the  previously  mentioned  varieties  of  occlu- 
sion, is  found  in  the  intestinal  wall  and  in  the  mesentery  (an  implication 
of  the  mesenteric  nerves  in  the  strangulation  may  also  be  possible).  In 
spite  of  the  fact  that  some  authors  still  raise  objections  to  the  assump- 
tion of  a  local  meteorism,  it  nevertheless  appears  to  me  that  this  certainly 
occurs  if  the  conditions  necessary  for  its  development  are  present;  and  its 
exceptional  absence  in  spite  of  the  latter  may  be  explained  by  special  cir- 
cumstances in  the  individual  case. 

Other  anatomical  changes,  in  so  far  as  they  present  themselves  in  the 
various  forms  of  peritonitis,  will  be  considered  under  the  description  of  the 
clinical  picture. 

To  ol)tain  a  clear  conception  of  the  clinical  picture  of  complete  intes- 
tinal occlusion,  a  few  fundamental  laws  must  be  first  laid  down. 

While  stenosis  always  comes  on  slowly  (with  the  single  exception  of 
an  acutely  arising  invagination  which  merely  causes  stenosis  of  the  lumen 
I)ut  not  entire  occlusion)  and  insidiously,  occlusion  in  quite  a  number  of 
cases  appears  suddenly  in  the  midst  of  perfect  health,  and  only  in  those 
cases  in  which  it  is  due  to  stenosis  do  the  symptoms  gradually  appear. 

Even  more  significant  is  the  following  law: 

In  some  cases  the  symptoms  are  the  result  of  phenomena  produced  by 
the  entire  cessation  of  the  passage  of  feces  (symptoms  purely  of  occlu- 
sion).    This  usually  occurs  when  the  occlusion  develops  from  stenosis. 


INTESTINAL  OCCLUSION  767 

In  other  cases  symptoms  appear  which  are  to  he  attributed  to  strangu- 
lation, and  these  consist  of  disturbances  of  the  circulation  in  the  intestinal 
wall  and  in  the  mesentery  combined  with  toxic  symptoms  and  those  de- 
pendent upon  derangement  of  the  nervous  system.  The  clear  recognition 
of  this  condition  is  not  only  necessary  for  the  understanding  of  the  patho- 
logical process,  but  in  a  high  degree  will  also  decide  the  therapeutic  indica- 
tions and  methods. 

I  shall  first  describe  the  symptom-complex  of  pure  occlusion,  i.  e.,  the 
symptoms  which  characterize  simple  occlusion;  this,  as  a  rule,  comes  on 
slowly  and  gradually  and  is  caused  by  a  cicatricial  or  carcinomatous  stric- 
ture, or,  more  rarely,  appears  acutely,  in  consequence  of  the  impaction  of 
foreign  bodies  or  gall-stones. 

SYMPTOMS 

The  passage  of  retained  gas  as  well  as  of  compact  and  fluid  masses 
ceases  entirely.  Absolute  constipation  follows  and  the*  complete  cessation 
of  flatus  per  anum.  Particles  of  feces  which  may  perhaps  be  expelled  by 
irrigation  proceed  from  that  part  of  the  intestine  below  the  occlusion  and 
have  been  retained  in  parts  of  the  colon. 

The  patient  is  attacked  by  severe  pain.  This  presents  itself  as  a  pain- 
ful attack  of  colic  such  as  I  have  described  in  the  article  upon  stenosis 
(which  see),  and  in  which  energetic  peristalsis  and,  occasionally,  extreme 
intestinal  rigidity  become  visible  and  palpable.  In  the  acute  cases  of 
intestinal  occlusion — and  this  is  a  valuable  diagnostic  point — these  con- 
spicuous symptoms  are  absent,  and  the  conditions  for  their  development, 
particularly  decided  muscular  hypertrophy,  do  npt  exist.  Therefore,  in 
most  of  the  cases  in  which  the  intestine  shows  excessive  and  marked  mus- 
cular hypertrophy  with  symptoms  of  occlusion,  we  may  suspect  an  ana- 
tomical process  that  has  gradually  produced  occlusion  from  stenosis. 

Step  by  step,  deflcient  appetite,  nausea,  eructation  and  vomiting  appear. 
Usually  the  gastric  contents  are  evacuated,  and  then  bile.  The  vomited 
matter  soon  reveals  a  feculent  odor,  and  finally  the  dreaded  fecal  vomiting 
takes  place. 

Fecal  vomiting — it  may  be  remarked  in  passing  that  some  authors 
employ  the  term  "  ileus  "  only  when  this  symptom  appears — on  account  of 
its  offensiveness  has  been  duly  studied  from  the  earliest  times.  The  fecu- 
lent character  of  the  vomited  material  is  readily  diagnosticated  by  the 
sense  of  smell.  The  color  is  usually  a  dirty  yellow,  or  it  may  be  greenish 
or  brownish.  Almost  invariably  it  is  fluid,  and  resembles  watery  diarrheic 
discharges.  That  more  compactly  formed  feces  have  been  discharged  by 
the  mouth,  as  has  been  positively  reported  by  some  observers,  cannot  be 
denied,  but  such  cases  certainly  belong  to  the  greatest  rarities,  and  then 
should  be  analyzed  individually,  as  these  disagreeable  symptoms  may  be 
simulated  by  malingerers  and  hysterical  individuals.     Sausage-like  masses 


768      LNTESTLNAL  CONSTRICTION   AND   INTESTINAL  OCCLUSION 

resembling  formed  feces  may  be  discharged  from  the  mouth,  but  more 
minute  investigation  reveals  that  they  are  composed  of  coagulated  milk  the 
surface  of  which  has  been  stained  yellow  by  bile.  True,  formed  feces  may 
be  vomited  in  consequence  of  the  rare  occurrence  of  a  communication  be- 
tween the  stomach  and  the  colon;  but  this  phenomenon  cannot  be  consid- 
ered as  a  parallel  with  fecal  vomiting  in  intestinal  occlusion. 

The  opinion  previously  maintained  that  fecal  vomiting  denotes  posi- 
tively that  the  seat  of  the  occlusion  is  in  the  colon,  or,  at  least,  in  the 
lower  portion  of  the  ileum,  has  for  some  time  been  recognized  as  erroneous. 
We  now  know  that  this  symptom  may  arise  even  in  occlusion  of  the  upper 
part  of  the  jejunum.  The  explanation  is  simple.  The  disagreeable  odor 
caused  by  the  decomposition  of  albumin  bodies,  and  which  lends  to  the 
intestinal  contents  their  feculent  character,  occurs  also  under  the  influ- 
ence of  definite  varieties  of  bacteria.  A  prolonged  action  is  necessary  for 
this,  such  as  occurs  normally  in  the  large  intestine,  but  not,  however,  in 
the  contents  which 'rapidly  pass  through  the  small  intestine.  If,  on  ac- 
count of  occlusion,  the  contents  are  retained  for  a  long  time  in  the  small 
intestine,  here  also  they  may  denote  a  feculent  composition.  Vice  versa, 
this  explains  how  fecal  vomiting  may  be  absent  even  with  absolute  occlu- 
sion of  the  intestinal  passage:  namely,  when  death  occurs  very  early,  or 
when  severe  vomiting  does  not  permit  prolonged  stagnation. 

As  to  the  manner  in  which  fecal  vomiting  occurs,  there  is  unanimity 
of  opinion.  In  the  first  place,  it  is  not  caused  by  a  motus  antiperistalticus. 
It  is  true  there  is  actual  antiperistalsis,  but  the  requirements  for  its  de- 
velopment under  the  conditions  here  operative  are  not  present.  A  detailed 
exposition  of  this  interesting  question  is  at  this  point  impossible.  Usu- 
ally the  explanation  given  by  Haguenot-van  Swieten  is  accepted.  If  the 
intestine  is  occluded,  more  or  less  rapidly  the  portion  above  the  occluded 
area  is  filled  with  gas  and  fluids  furnished  by  the  gastric  contents  and  the 
secretions  which  enter  the  intestine  and  attempt  to  pass  onward.  When 
the  stasis  reaches  a  point  immediately  above  the  obstruction,  formed  by  the 
distended  intestinal  wall,  the  retained  mass  is  gradually  forced  upward 
in  the  direction  of  the  stomach.  Vomiting  now  occurs  which  may  be  due 
to  any  cause.  During  this  act  the  diaphragm  and  abdominal  muscles  con- 
tract, the  area  of  the  abdominal  cavity  diminishes,  and  pressure  is  exerted 
upon  the  intestine  and  its  contents.  The  volume  of  the  fluid  contents 
cannot  be  propelled  downward  toward  the  anus  on  account  of  the  insur- 
uiouiitahle  obstruction,  nor  can  it  be  pressed  upward,  and  thus,  in  a  retro- 
gressive manner,  it  is  forced  toward  the  stomach,  and  fecal  vomiting  re- 
sults. It  is  readily  perceived  that,  analogous  to  the  act  of  vomiting,  the 
contractions  of  the  intestine,  moving  in  a  normal  direction,  must  mechan- 
ically affect  the  contents  in  its  lumen,  thus  causing  a  regurgitation  of  the 
contents.  That  the  act  of  vomiting  as  such,  and  not  antiperistalsis,  is  the 
cause  of  the  expulsion  of  th^  intestinal  contents  is  borne  out  by  an  expe- 


INTESTINAL  OCCLUSION  769 

rience  of  my  own  that  in  an  enterostenosis  of  the  sigmoid  flexure  the  entire 
colon  and  the  small  intestine  up  to  the  jejunum  were  filled  with  thin  feculent 
contents,  yet  fecal  vomiting  did  not  occur.  The  patient  did  not  vomit  during 
the  entire  course  of  the  disease  and  retching  even  was  not  present. 

Meteorism  occurs,  but  by  no  means  in  the  same  form  and  to  the  same 
extent  in  all  cases.  This  depends  upon  the  etiologico-anatomical  form  of 
the  intestinal  occlusion.  It  is  true  that  the' passage  of  flatus  ceases  entirely, 
but  the  more  important  resorption  of  gas  from  the  intestine  into  the  blood 
may  continue  as  long  as  a  simple  stenosis  of  its  lumen  without  an  altera- 
tion of  its  wall  exists,  and  in  case  the  formation  of  gas  due  to  the  acci- 
dental presence  of  abnormal  quantities  of  fermentative  material  does  not 
preponderate  over  the  absorption  of  gas.  Under  these  circumstances  me- 
teorism will  be  but  moderate.  This  is  more  frequently  observed  in  occlu- 
sion which  develops  from  stenosis  of  the  intestine;  quite  as  frequently  also 
in  the  case  of  internal  occlusion  of  the  intestine  (ohturatio  intestinalis) 
by  foreign  bodies,  gall-stones,  intestinal  stones  and  fecal  masses ;  and  also 
in  cases  of  external  compression.  On  the  other  hand,  in  the  forms  of  acute 
occlusion  which  run  their  course  with  strangulation  of  the  intestinal  wall 
and  of  the  mesentery,  marked  degrees  of  meteorism  may  be  observed.  Here 
the  areas  nearest  the  occlusion  show  the  greatest  distention,  and  from  the 
peculiar  formation  and  situation  of  the  inflated  coils  important  data  not 
only  for  the  localization  of  the  seat  of  the  obstruction  but  occasionally 
even  indicative  of  its  anatomical  nature  may  be  obtained. 

Finally,  as  a  direct  symptom  of  occlusion,  the  increased  excretion  in  the 
nrine  of  indican  and  other  combined  ethereal  sulphates  must  be  mentioned, 
of  which  indicanuria  is  the  most  important  in  practice  because  of  the 
readiness  with  which  it  may  be  chemically  determined.  In  occlusion  of 
the  small  intestine  there  is  a  large,  and  occasionally  enormous,  increase 
of  indican  in  the  urine;  in  occlusion  of  the  colon  only  when  this  lasts  a 
long  time,  and  when  there  is  stagnation  of  its  contents  above  the  ileo-cecal 
valve.  In  the  use  of  this  symptom  embarrassment  has  arisen  from  the  fact 
that  under  some  conditions  which  must  be  here  considered,  very  frequently, 
in  addition  to  the  occlusion  and  also  as  produced  by  it,  a  diffuse  peritonitis 
which  runs  its  course  with  decided  indicanuria  is  superadded. 

All  of  the  symptoms  which  have  as  yet  been  described  are  the  direct  or 
indirect  consequence  of  the  arrested  impermeability  of  the  intestinal  lumen, 
and  they  appear  when  the  cause  of  the  impermeability  in  its  nature  has  this 
effect  only,  and  does  not,  at  the  same  time,  cause  strangulation.  Only  in 
isolated  cases,  especially  in  acute  obstruction  by  large  gall-stones,  do  other 
symptoms  appear  which  resemble  the  severe  clinical  picture  of  strangu- 
lation. 

We  shall  now  turn  to  these. 

It  must  first  be  remarked  that  the  clinical  picture  in  which  symptoms 
of  occlusion  and  strangulation  appear  simultaneously  is,  without  excep- 


770     Ix\TESTINAL  CONSTRICTION  AND  INTESTINAL  OCCLUSION 

tion,  produced  by  acute  processes.  These  are  acute  strangulation,  volvulus, 
noose  formation,  and  particularly  also  invagination.  Each  of  these  forms 
presents  typical  peculiarities  which  are  not  characteristic  in  every  concrete 
case.  But  the  main  features  of  the  clinical  picture  are  common  to  all,  and 
these  I  shall  now  enumerate. 

Suddenly,  sometimes  in  the  midst  of  perfect  health,  and,  in  any  event, 
without  preceding  abdominal  disturbance  or  external  cause,  occasionally 
after  a  prior  mild  or  indistinct  intestinal  disturbance  and  pain,  or  follow- 
ing jumping,  a  fall,  or  a  blow,  the  patient  is  seized  with  severe  pain  in  the 
abdomen.  This  is  sometimes  localized,  at  other  times  diffuse;  occasion- 
ally persistent,  at  other  times  remittent  and  colicky.  To  this  is  added 
nausea,  vomiting,  singultus.  The  vomiting  may  then  sooner  or  later 
assume  a  feculent  character.  Sometimes  (in  invagination,  in  volvulus) 
tenesmus  appears.  If,  after  the  pains  set  in,  a  movement  of  the  bowels 
occurs,  the  passage  of  feces  and  gases  subsequently  ceases  entirely.  Me- 
teorism  appears,  sometimes  moderate,  at  other  times  intense,  according  to 
the  nature  and  the  seat  of  the  occlusion;  there  may  be  extreme  distention 
of  definite  configuration. 

The  symptoms  of  strangulation  are  added  to  these  symptoms  of  occlu- 
sion which,  except  for  their  usually  rapid  development,  externally  resem- 
ble those  before  described,  although  pathogenetically  they  differ  some- 
what. 

A  serious  condition  now  sets  in,  which  profoundly  implicates  the  whole 
constitution.  The  expression  of  the  face  denotes  anxiety  and  pain;  the 
nose,  the  ears  and  extremities  are  cool  and  livid;  the  pulse  is  frequent, 
small,  and  easily  compressible;  the  respiration  is  often  rapid  and  super- 
ficial. There  is  a  feeling  of  oppression;  the  secretion  of  urine  ceases.  Yet 
the  mind  retains  its  clearness.  Unless  nature  or  art  comes  to  our  aid  the 
disease  progresses  to  its  highest  degree,  the  skin  becomes  withered  and 
flaccid,  is  cool  and  livid  and  often  covered  with  cold  sweat.  The  features 
are  sunken,  the  pulse  thready  and  extreme  prostration  is  the  prelude  to 
death. 

This  is  an  outline  of  the  clinical  picture  of  acute  strangulation,  but  the 
individual  symptoms  must  be  briefly  analyzed. 

A  merely  superficial  glance  permits  the  recognition  of  two  groups  of 
symptoms:  On  the  one  hand  the  gastrointestinal,  and,  on  the  other  hand, 
phenomena  dependent  upon  the  nervous  system  and  upon  the  circulation. 

Of  the  former  group  of  symptoms,  the  majority  are  unquestionably  the 
direct  and  mechanical  consequences  of  occlusion;  namely,  the  absolute 
stoppage  of  the  bowels,  the  passage  of  flatus,  and  the  occurrence  of  fecal 
vomiting.  On  the  other  hand,  the  initial  simple  vomiting,  the  pain,  and 
the  meteorism  may  have  an  indirect  cause,  and  not  be  exclusively  and 
immediately  the  consequences  of  occlusion  of  the  intestinal  lumen. 

The  initial  pain  is  one  of  the  most  invariable  and  conspicuous  symp- 


INTESTINAL  OCCLUSION  771 

toms  of  acute  occlusion,  and  is  rarely  absent  in  incarceration,  in  volvulus, 
and  in  invagination.  If  localized  and  fixed,  it  owes  its  origin  to  a  sudden, 
local  irritation  of  the  nerves  of  the  intestinal  wall;  this  is  also  true  of 
the  colicky  pain  which  occurs  in  paroxysms,  of  the  energetic  peristalsis 
which  increases  and  decreases,  and  of  the  tetanic  intestinal  stiffening.  Be- 
sides the  pain  which  is  localized,  there  may  be  more  diffuse  pain  which 
is  also  initial,  which  is  not  increased  by  external  pressure,  and  which  is 
not  as  yet  the  consequence  of  peritonitis.  This  is  caused  by  the  irradiating 
stimulation  of  the  large  ganglion  plexuses  and,  according  to  my  experience, 
is  more  severe  in  occlusion  of  the  small  intestine  than  in  that  of  the  large 
intestine,  more  severe  in  incarceration,  which  usually  attacks  the  ileum, 
than  in  volvulus  which  is  most  common  in  the  sigmoid  flexure.  In  com- 
plete acute  intestinal  occlusion  even  without  peritonitis,  the  pain  is  almost 
always  constant,  although  there  are  remissions  and  exacerbations;  as  the 
lethal  termination  approaches,  it  sometimes  ceases  in  consequence  of  intes- 
tinal paralysis. 

In  the  onward  course  of  the  disease,  vomiting,  although  not  yet  fecu- 
lent, must  be  considered  so  pathogenetically.  The  initial  vomiting  which 
occurs  at  the  onset  of  acute  occlusion,  and  the  hiccough  which  appears 
simultaneously,  are  unquestionably  of  reflex  origin,  and  due  to  the  sudden, 
severe  irritation  of  the  nerves  of  the  peritoneum  and  of  the  intestine.  This 
process  of  development  explains  the  constancy  of  vomiting  in  acute  occlu- 
sion of  the  small  intestine  which  is  richly  supplied  with  nerves,  and  in  this 
form  of  the  disease  it  is  rarely  absent. 

I  have  previously  mentioned  that  in  the  development  of  meteorism 
in  occlusion  combined  with  strangulation,  not  only  in  stenosis  of  the  intes- 
tine a  cause  but  also  the  cessation  of  gas  resorption  from  the  lumen  of  the 
intestine  in  consequence  of  alteration  in  its  walls.  This  alteration  in  the 
intestinal  wall  occurs  in  the  area  of  the  strangulation,  and  accounts  for 
the  fact  that  in  this  form  of  occlusion  a  peculiar  configuration  is  occasion- 
ally met  with  which  has  been  designated  above  as  "  local "  meteorism. 

This  is  most  characteristic  in  acute  volvulus,  which  occurs  with  great- 
est frequency  in  the  sigmoid  flexure,  and  to  such  an  extent  that  volvulus, 
either  in  its  own  longitudinal  axis  or  in  the  axis  of  the  mesentery,  is  greater 
than  in  any  other  portion  of  the  intestine.  In  volvulus  of  the  sigmoid 
flexure,  as  a  rule,  local  meteoric  distention  in  the  sigmoid  flexure  sets  in 
very  rapidly,  and  after  forty-eight  to  seventy-two  hours  it  may  attain  such 
enormous  dimensions  that  the  entire  abdomen  appears  inflated  like  a  bal- 
loon. This  inflation  begins  in  the  first  hours  of  the  disease  in  the  left 
lower  abdominal  region;  the  inflated  coil  then  extends  toward  the  right 
and  upper  abdominal  areas,  and  finally  distends  the  entire  abdomen  to  a 
globular  form.  Xowhere  is  peristalsis  observed;  the  percussion  note  over 
the  distended  region  is  tympanitic,  exceptionally  dull,  the  latter  condition 
being  explained  by  the  circumstance  that  the  walls  of  the  intestine  are 


772      INTESTINAL  CONSTRICTION   AND  INTESTINAL  OCCLUSION 

markedly  edematous  and  thickened,  and  the  contents  of  the  sigmoid  flex- 
ure consist  "of  blood  and  feces.  In  the  other  forms  of  acute  occlusion  which 
accompan}'  strangulation,  namely,  internal  incarceration  and  invagination, 
local  meteorism  either  does  not  occur  at  all  or  scarcely  develops  to  such 
an  extent  as  to  be  of  clinico-diagnostic  importance. 

Although  it  has  been  already  mentioned,  the  importance  of  the  subject 
leads  me  to  reiterate  that  in  acute  occlusion,  if  this  attack  an  intestine 
previously  permeable,  peristalsis  that  is  distinctly  visible  and  tetanic  in- 
testinal stiffening  only  occur  exceptionally,  and  never  to  the  extent  seen 
in  occlusion  which  follows  a  slowly  growing  stenosis.  The  reasons  for  this 
are  obvious:  In  the  first  place,  there  is  no  muscular  hypertrophy  of  the 
intestinal  wall  in  acute  occlusion,  and  the  paralysis  of  the  musculature 
Avhich  occurs  develops  with  particular  rapidity  in  the  doubly  occluded  and 
strangulated  intestinal  areas  in  which  local  meteorism  has  developed;  para- 
lyzed muscles,  of  course,  do  not  contract. 

The  extremely  rare  occurrence  of  diarrhea  in  acute  occlusion  (in  in- 
vagination, incarceration),  is  deserving  of  brief  mention,  since,  at  first, 
it  may  lead  to  gross  errors  in  diagnosis.  This  is  explained  by  the  hypo- 
tlietic  assumption  of  a  hypersecretion  of  fluid  from  the  intestinal  wall  in 
consequence  of  paralysis  of  the  mesenteric  nerves. 

Besides  this  group  of  symptoms,  other  symptoms  on  the  part  of  the 
circulatory  apparatus  are  noted;  these  dominate  the  situation,  and  impress 
their  stamp  upon  the  affection,  the  clinical  condition  closely  resembling 
"  collapse  "  from  other  causes.  The  extent  of  these  phenomena  may  vary 
in  individual  cases;  as  a  rule,  however,  they  are  decidedly  marked. 

In  regard  to  their  occurrence  two  views  are  maintained  at  the  present 
time:  A  nervous  reflex  theory,  and  an  intoxication  theory.  In  my  opinion 
the  latter  is  operative  only  for  certain  rare  symptoms  and  cases.  On  the 
other  hand,  the  nervous  reflex  theory  readily  explains  the  majority  of 
symptoms  which  are  clinically  common  and  important,  and  which  usually 
ap])ear  at  the  onset  of  the  affection. 

I  cannot  here  analyze  the  reflex  theory  in  detail,  but  will  only  remark 
that  in  accoi-dance  with  well-known  physiological  facts  the  severe  clinical 
picture  is  caused  by  decided  irritation  of  the  sensory  nerves  of  the  intes- 
tine and  of  the  peritoneum;  that  is,  of  the  mesentery,  which  results  with 
tlie  acute  onset  of  volvulus,  incarceration,  invagination,  obstruction  from 
gall-stones,  etc.  Occlusion  thereby  leads  to  an  alteration  of  cardiac  activity 
and  of  the  entire  distribution  of  the  blood,  this  being  brought  about  by 
tlie  reflex  influence  of  the  cardiac  vagus  and  of  the  splanchnic  nerve.  In 
fact,  the  majority  of  the  symptoms  may  be  thus  explained,  particularly 
those  nl)ove  described  and  also  some  rare  ones;  as,  for  example,  the  albu- 
niiniiria  and  cylindruria  which  are  occasionally  obsierved  in  'mcarcerated 
lu'(  nia. 

The  idea  of  the  "intoxication  theory"  is  this,  that  in  the  closed' in- 


INTESTINAL  OCCLUSION  773 

testinal  passage  the  arrested  products  of  bacterial  proteid  decomposition 
which  had  formed  in  large  amounts  (phenol,  indol,  skatol,  the  aromatic 
ox3^acids)  are  absorbed  by  the  blood,  and  thus  exert  their  toxic  action. 
A  modification  of  the  intoxication  theory,  designated  as  "  septic  collapse," 
assumes  that  the  intestinal  microbes  reach  the  peritoneum  through  the 
intestinal  wall,  which  is  damaged  by  the  strangulation,  and  thence,  even 
without  causing  peritonitis,  infect  the  entire  organism.  The  following 
may  be  stated  in  criticism  of  these  views:  It  is  possible  that  a  few  very 
rare  symptoms  of  strangulation  shock  may  be  referred  to  intoxication  of 
this  kind,  and  among  these  delirium  or  coma,  rise  of  temperature  without 
peritonitis,  and  the  so-called  "  incarceration  typhoid.''  But  the  facts  have 
by  no  means  been  determined  with  certainty,  and  against  its  general 
acceptance  very  important  clinical  objections  may  be  raised;  for  instance, 
that  the  severest  picture,  the  most  profound  collapse,  may  develop  in  from 
six  to  twenty-four  hours  after  the  occlusion;  that,  as  a  rule,  the  intoxica- 
tion is  in  proportion  to  the  suddenness  of  the  incarceration  and  the  severity 
of  the  initial  pain;  that  in  occlusion  which  develops  gradually  it  may  be 
entirely  absent. 

The  course  of  the  disease  is  not  always  the  same;  it  varies  according 
to  the  anatomical  foundation,  the  cause  of  the  occlusion,  and  particularly 
according  to  whether  simple  occlusion  or  accompanying  strangulation 
exists. 

In  occlusion  with  strangulation  occurring  suddenly,  death  may  follow 
in  a  few  hours  (eight)  with  all  the  symptoms  of  collapse.  At  other  times 
peritonitis  is  added  and  brings  about  the  lethal  termination.  Its  devel- 
opment in  these  forms  is  favored  by  the  fact  that  in  the  area  of  the  stran- 
gulated region  there  is  a  histological  alteration  in  the  intestinal  wall  which 
makes  it  possible  for  microbes  to  penetrate  into  the  peritoneal  cavity.  To 
this  already  alarming  picture  more  circumscribed  or  distributed  sponta- 
neous painfulness  upon  pressure  is  added,  according  to  the  distribution  of 
the  peritonitis.  This  peritonitis  may,  although  rarely,  develop  in  pure 
occlusion.  On  the  other  hand,  if  no  relief  is  brought  about,  death  usually 
occurs  by  gradual  exhaustion  in  consequence  of  the  absence  of  nourish- 
ment and  of  continuous  vomiting. 

What  are  the  conditions  which  lead  to  complete  intestinal  occlusion? 

I  have  already  mentioned  quite  a  number  of  the  causes  under  intestinal 
stenosis  (which  see).  All,  or  nearly  all,  of  the  processes  there  enumerated 
are  capable,  either  directly  or  indirectly,  of  causing  complete  occlusion 
of  the  intestinal  lumen.  They  furnish  the  cases  in  which  occlusion  forms, 
as  a  rule,  by  gradual  stages  from  the  constantly  advancing  stenosis,  and 
in  which  the  clinical  picture  is  composed  of  the  symptoms  of  pure  occlu- 
sion. Exceptionally,  and  under  special  circumstances,  the  stenosis  sud- 
denly and  rapidly  increases  to  entire  impermeability;  as  when  a  coarse  for- 
50 


774      INTESTINAL  CONSTRICTION   AND   INTESTINAL  OCCLUSION 

eign  body  entirely  occludes  the  narrow  passage,  or  the  dilated  portion  of 
the  intestine  above  the  stenosis,  which  is  filled  with  contents,  descends  and 
leads  to  volvulus  and  the  like. 

A  second  series  of  cases  is  furnished  by  complete  occlusion  of  the  intes- 
tinal lumen  by  any  large  impacted  masses  there  present  (obstruction  of 
the  intestine).     Of  this  variety  are: 

(a)  Enormous  fecal  masses  which,  in  addition  to  their  direct  consti- 
pating effect,  produce  a  paralytic  weakness  of  the  musculature  of  the 
intestine ; 

(b)  Intestinal  calculi; 

(c)  Gall-stones; 

(d)  Foreign  bodies. 

In  this  series  of  cases  the  clinical  picture  exhibits  exclusively  the  83Tnp- 
toms  of  occlusion.  Only  in  obstruction  due  to  gall-stones  are  symptoms  of 
collapse  occasionally  observed  which,  as  stated  previously,  are  produced  by 
the  severe  sensory  irritation  of  the  stone  upon  the  intestinal  wall. 

A  third  series  of  cases  is  formed  by  processes  which  not  only  cause  oc- 
clusion but,  at  the  same  time,  produce  strangulation  of  the  intestine,  that 
is,  of  the  mesentery: 

1.  Volvulus; 

2.  Noose  formation — which,  at  this  time,  is  usually  included  under  the 
designation  volvulus ; 

3.  Hernia,  internal  incarceration; 

4.  Invagination,  intussusception. 

These  conditions  almost  invariably  occur  acutely,  and  are  accompanied 
by  the  distressing  symptoms  of  the  clinical  picture  last  mentioned. 

In  conclusion,  an  affection  must  be  mentioned  which  mechanically  has 
not  the  remotest  connection  with  occlusion  of  the  intestinal  lumen,  but 
whose  physiologic  termination  is  nevertheless  the  same. 

This  is  paralysis  of  the  intestine.  Here,  the  lumen  is  wide  open,  the 
passage  mechanically  unhindered;  nevertheless,  its  function  has  ceased 
because  motor  paralysis  in  a  large  or  small  portion  of  the  intestine  makes 
tlie  propulsion  of  the  contents  through  this  area  impossible. 

We  require  no  explicit  description  to  make  it  clear  that,  besides  these 
conditions  which  in  combination  form  the  clinical  picture  of  occlusion, 
or  of  occlusion  with  strangulation  added,  each  individual  one  may  pro- 
duce in  the  clinical  picture  its  own  distinctive  symptoms.  In  this  article, 
which  is  merely  a  comprehensive  review  of  intestinal  occlusion,  it  is  impos- 
si])le  to  enter  more  minutely  into  the  subject.  Each  of  the  various  condi- 
tions would  require  special  description. 


INTESTINAL  CXXLUSION  775 


DIAGNOSIS 

Although  the  analysis  of  the  symptoms  which  make  up  the  clinical  pic- 
ture of  occlusion  is  simple,  in  reality  it  may  be  extraordinarily  difficult  to 
make  the  diagnosis  at  the  bedside.  In  fact,  when  the  individual  points 
are  considered,  and  occasionally  even  in  deciding  the  fundamental  ques- 
tion, this  proves  a  most  difficult  task  for  the  physician.  The  most  expe- 
rienced and  the  most  careful  investigator  is  liable  to  err,  and  yet,  in  this 
grave  affection,  not  only  is  certainty  but,  especially,  rapidity  of  diagnosis 
of  the  utmost  importance  in  the  treatment. 

In  each  individual  case  the  diagnosis  must  be  based  upon  the  answers 
to  three  distinct  questions: 

1.  Is  intestinal  occlusion  present? 

2.  In  what  portion  of  the  intestine  does  it  exist  ? 

3    What  is  the  anatomical  foundation  of  the  condition  ? 

In  regard  to  the  first  question :  Is  intestinal  occlitsion  present  ?  Errors 
in  diagnosis  may  be  made  in  two  ways.  Intestinal  occlusion  is  assumed 
because  the  symptom-complex  is  more  or  less  completely  developed ;  yet, 
notwithstanding,  this  condition  is  not  present,  but  the  symptoms  are  due 
to  another  affection.  Or  the  symptoms,  which  but  partially  indicate  the 
condition,  divert  the  attention  of  the  physician  into  another  channel,  and 
the  actually  existing  occlusion  is  overlooked. 

The  diagnosis  is  based  mainly  upon  the  local  intestinal  symptoms :  Ab- 
solute impermeability  for  gas  as  well  as  feces,  meteorism,  vomiting,  fecal 
vomiting.  ' 

That  the  first  three  symptoms,  taken  individually,  furnish  but  limited 
proof  need  not  be  dwelt  upon.  Even  fecal  vomiting  is  of  no  pathogno- 
monic diagnostic  value.  Apart  from  its  possible  appearance  in  hysteria, 
and  from  its  actual  but  very  rare  occurrence  in  fistulas  between  the  colon 
and  stomach,  it  may  also  appear — as  well  as  absolute  constipation,  meteor- 
ism, and  vomiting — in  intestinal  occlusion  from  paralysis  of  the  intestine 
and  from  peritonitis  (in  the  latter  instance  also  it  is  pathogenetically  due 
to  intestinal  paralysis).  Under  the  following  circumstances,  the  physician 
must  consider  the  possibility  of  pure  intestinal  paralysis  without  mechan- 
ical occlusion:  When  fecal  vomiting  appears  after  some  dull  trauma  has 
affected  the  abdomen;  when  it  persists  in  incarcerated  hernia  after  the 
mechanical  obstruction  has  been  removed  by  the  knife  or  other  means;  in 
general,  when  it  appears  after  surgical  operation  upon  the  intestine  itself 
or  in  its  immediate  vicinity;  or  when  it  has  developed  in  disease  of  the 
testicles^  in  the  inguinal  region,  in  the  inflammation  of  hemorrhoids,  in 
renal  colic,  in  gall-stone  colic,  in  recent  acute  appendicitis  and  perityph- 
litis. To  this  must  be  added  the  possibility  of  the  appearance  of  intes- 
tinal paralysis  in  embolism  of  the  mesenteric  artery,  in  habitual  constipa- 
tion, in  over-distention  from   excessive  meteorism  and,  perhaps,  also  in 


776      INTESTINAL  CONSTRICTION   AND   INTESTINAL  OCCLUSION 

consequence  of 'bacterial  peritoneal  infection  without  peritonitis.  Under 
all  these  circumstances  fecal  vomiting  and  the  entire  symptom-complex 
may  be  caused  by  pure  intestinal  paralysis,  and  the  physician  must  always 
bear  this  possibility  in  mind,  and  should  never  forget  that  in  the  concrete 
case  actual  mechanical  occlusion  may  also  be  present. 

The  most  frequent  and  the  greatest  perplexity  is  caused  by  the  question : 
Occlusion  or  peritonitis,  or  their  combination?  Its  vital  importance  con- 
strains me  to  dwell  somewhat  more  explicitly  upon  the  individual  points 
which  may  aid  us  in  the  differential  diagnosis. 

The  pain  is  of  great  significance.  Severe  pain  occurs  spontaneously  in 
acute  peritonitis  as  well  as  in  acute  occlusion.  If  to  this,  however,  diffused, 
well-developed  tenderness  of  the  entire  abdomen  upon  palpation  is  soon 
added,  if  the  patient  lies  very  quiet  and  carefully  avoids  voluntary  move- 
ment, this  is  more  in  favor  of  peritonitis.  Naturally,  the  latter  condition 
may  very  rapidly  develop  in  occlusion,  but  scarcely  sooner  than  after 
forty-eight,  or,  at  the  earliest,  twenty-four  hours.  The  possibility  of 
examination  within  the  first  or  the  second  day  may,  therefore,  give  us 
important  data  to  clear  the  diagnosis.  Of  course  absence  of  pain  upon 
pressure  is  by  no  means  absolute  proof  of  occlusion  and  disproof  of  peri- 
tonitis, for,  on  the  one  hand,  even  in  acute  and  purulent  peritonitis  spon-* 
taneous  pain  as  well  as  pain  upon  pressure  may  be  only  of  minimal  degree, 
and,  on  the  other  hand,  the  rapidly  developing  meteorism  in  volvulus  and 
in  internal  incarceration  may  occasionally  run  its  course  with  quite  marked 
sensitiveness  to  pressure;  nevertheless,  decided  painfulness  upon  pressure 
more  strongly  indicates  peritonitis. 

Sometimes  in  acute  cases  the  degree  of  meteorism  will  establish  the 
diagnosis.  If,  at  the  onset,  it  develops  decidedly  as  local  meteorism,  if 
it  is  possible  to  detect  circumscribed,  inflated,  extremely  tense  portions 
of  the  intestine  by  simultaneous  percussion  and  auscultation,  we  may  as- 
sume volvulus  or  an  internal  incarceration.  Diffuse  meteorism,  on  the  con- 
trary, may  be  observed  in  occlusion  as  well  as  in  peritonitis,  and  for  this 
reason  cannot  be  utilized  in  a  differentio-diagnostic  respect;  the  enormous 
balloon-like  inflation  makes  a»  accurate  examination  impossible. 

The  significance  of  the  intestinal  movements  in  such  conditions  has 
been  several  times  described,  I  believe  it  to  be  certain  that  positive,  decided 
peristalsis  and,  particularly,  paroxysmal  intestinal  stiffening  always  shows 
an  obstruction  in  the  passage.  Inversely,  if  it  has  been  determined  after 
careful  examination  by  means  of  inspection,  palpation,  and  auscultation 
that  there  is  absolutely  no  sign  of  intestinal  movement,  this  points  with 
great  likelihood  to  peritonitis  with  intestinal  paralysis.  But  the  occur- 
rence of  intestinal  movement  is,  unfortunately,  not  absolute  and  positive 
proof.  For  complete  stoppage  may  also  occur  without  peritonitis  in  conse- 
quence of  enormous  over-distention,  and,  inversely,  it  may  continue  even 
after  the  development  of  peritonitis. 


INTESTINAL  OCCLUSION  777 

The  presence  of  a  fluid  exudate  is  in  favor  of  peritonitis,  but  here  it  is 
necessary  for  us  to  be  cautious;  since,  on  the  one  hand,  in  internal  incar- 
ceration, particularly  in  volvulus  in  consequence  of  mesenteric  venous 
stasis,  such  a  profuse  hemorrhagic  transudation  may  occur  in  the  perito- 
neal cavity  that  a  peritoneal  effusion  is  simulated;  on  the  other  hand,  the 
latter  may  be  actually  present,  but,  because  masked  by  peculiar  physical 
conditions,  may  not  be  recognized. 

Fever  points  to  peritonitis;  but  the  absence  of  the  same  does  not  ex- 
clude peritonitis,  as  any  form  of  this  affection  may  sometimes  run  its 
course  without  fever  and  even  with  subnormal  temperatures. 

Occasionally  the  presence  of  indicanuria  may  be  of  diagnostic  impor- 
tance, naturally  only  under  very  definite  conditions.  The  positive  proof  of 
increased  indicanuria  coincides  with  the  existence  of  a  diffused  peritonitis 
as  well  as  an  occlusion  of  the  small  intestine.  However,  its  absence  is 
against  the  presence  of  either  of  these  processes,  and  the  same  is  true  of 
an  occlusion  of  the  large  intestine,  for  example,  volvulus  of  the  sigmoid 
flexure. 

Naturally  other  factors  may  be  utilized  in  the  diagnostic  consideration 
of  the  concrete  case.  For  example,  the  presence  of  florid  ulcerative  pro- 
cesses in  the  stomach  or  intestine  is  an  indication  of  peritonitis.  Care- 
ful analysis  will  very  frequently  reveal  the  true  situation,  but  there  are 
cases  in  which  the  diagnosis,  either  of  peritonitis  or  intestinal  occlusion, 
may  be  impossible. 

If  the  presence  of  intestinal  occlusion  has  been  determined  the  question 
next  arises :  In  what  portion  of  the  intestine  does  it  exist  ?  To  answer  this 
is  extremely  difficult.  As  a  positive  aid  it  is  well  first  to  determine  clearly 
whether  the  occlusion  has  developed  from  stenosis  or  whether  its  onset  was 
acute,  that  is,  simultaneously  with  symptoms  of  strangulation.  In  the 
former  case  its  localization  is  readily  decided,  and  as  guides,  the  factors 
which  I  have  mentioned  in  the  article  upon  intestinal  stenosis,  to  which 
I  here  refer,  may  be  utilized. 

If  we  are  dealing  with  acute  occlusion,  that  is,  with  strangulation,  the 
most  minute  manual  exploration  of  the  hernial  rings,  as  well  as  of  the  rec- 
tum and  vagina,  is  necessary.  Occasionally,  by  this  means,  important  data 
are  revealed,  particularly  in  incarcerated  external  hernias. 

Irrigation  of  the  rectum,  which  is  much  practised  in  order  to  determine 
the  seat  of  the  occlusion  from  the  amount  of  fluid  which  may  be  injected, 
is  sometimes  impracticable  on  account  of  the  condition  of  the  patient,  and 
even  when  possible  the  result  is  frequently  unreliable.  A  deep-seated  ob- 
struction may  be  determined  only  when,  after  repeated  irrigations,  but 
little  fluid  can  be  forced  into  the  intestine,  and  this  invariably  returns 
rapidly.  But  we  must  not  forget  that  the  rectum  with  its  ampulla  may 
take  up  from  one  to  one  and  a  half  liters  of  fluid.  Sounding  of  the  rectum 
is  also  unreliable. 


778      INTESTINAL  CONSTRICTION   AND   INTESTINAL   OCCLUSION 

In  acute  strangulated  occlusions,  local  meteorism  in  the  individual 
case  may  occasionally  enable  us  to  come  to  a  decision  in  regard  to  the  seat 
of  the  occlusion,  particularly  if  volvulus  of  the  sigmoid  flexure  is  present 
and  the  development  of  meteorism  is  observed  by  the  phys'ician  himself, 
who  can  refer  it  to  the  coils  of  the  sigmoid  flexure.  The  points  of  support 
which  we  assume  from  the  functional  symptoms  on  the  part  of  the  intes- 
tine are,  as  a  rule,  susceptible  of  various  explanations  and  untrust- 
worthy. 

In  insidious  occlusion  there  is  sometimes  entire  absence  of  pain.  In 
the  acute  forms,  naturally,  it  is  usually  present,  but  only  when  it  is  nar- 
rowly circumscribed,  definitely  fixed,  persistent,  uniform,  and  localized, 
should  pain  be  utilized  as  a  guide,  and  even  then  cautiously;  and  I  regard 
its  importance  in  localization  as  of  greater  significance  when  it  is  not  only 
spontaneously  present  but  may  also  be  developed  in  the  same  area  upon 
pressure.  The  law  that  in  acute  occlusion  of  the  small  intestine  the  pain 
sets  in  earlier,  more  severely,  and  is  more  continuous  than  in  that  of  the 
large  intestine,  is  in  itself  subject  to  many  exceptions,  and  to  this  may  be 
added  that  in  volvulus  of  the  sigmoid  flexure  also  the  pain  may  be  exceed- 
ingly severe. 

Vomiting  may  be  of  importance  in  the  diagnosis  in  so  far  that  gener- 
ally— concrete  exceptions  may  occur  in  either  direction — in  acute  occlu- 
sions of  the  small  intestine  it  is  more  regular,  more  continuous  and  severe 
than  in  those  of  the  large  intestine.  Fecal  vomiting,  as  I  have  previously 
remarked,  may  occur  in  any  localization,  even  in  high-seated  jejunal  occlu- 
sion. 

Very  little,  but  occasionally  something,  may  be  learned  from  the  state 
of  the  feces.  Marked  tenesmus  may  occur  when  the  seat  of  an  acute  occlu- 
sion is  in  the  lower  colon.  An  admixture  of  blood  is  more  apt  to  be  ob- 
served in  this  condition  when  the  occlusion  extends  from  the  cecum  far 
downwards. 

The  value  of  indicanuria  as  pointing  to  the  seat  of  the  affection  may 
be  formulated  in  the  following  manner :  If,  in  a  previously  healthy  person, 
the  symptoms  of  acute  occlusion  (but  without  symptoms  of  peritonitis) 
appear,  and  if  upon  the  second  or  third  day  marked  indicanuria  is  pres- 
ent, this  points  to  the  small  intestine  and  is  against  the  large  intes- 
tine. With  a  prolonged  duration  of  the  occlusion,  its  absence  also 
favors  the  large  intestine,  its  presence,  however,  no  longer  furnishes 
any  clue. 

Some  general  view-points  have  been  made  use  of  in  deciding  upon  the 
seat  of  the  occlusion.  It  was  formerly  believed  that  with  a  very  rapid 
course  and  markedly  developed  s3nnptoms  of  occlusion  the  seat  might  be 
referred  to  the  small  intestine.  This  is,  however,  absolutely  incorrect,  for, 
if  tlie  seat  be  in  the  small  intestine,  the  symptoms  at  the  onset  need  not 
necessarily  be  very  severe,  and  vice  versa.    In  volvulus  of  the  sigmoid  flex- 


INTESTINAL  OCCLUSION  779 

ure  the  symptoms  may  rapidly  appear  and  be  exceedingly  severe.  If,  in 
the  concrete  case,  the  anatomical  nature  of  the  occlusion  is  readily  per- 
ceived, this  may  sometimes  also  facilitate  the  recognition  of  its  seat. 

The  third  part  of  the  diagnosis,  namely,  the  determination  of  the  ana- 
tomical nature  of  the  pathological  process,  is  sometimes  easy,  usually  diffi- 
cult, and,  in  a  few  instances,  impossible.  Nevertheless,  we  should  always 
attempt  to  decide  it,  and  for  this  purpose  the  following  method  has  been 
found  useful: 

The  hernial  rings,  which  should  be  first  examined,  and  the  rectum 
sometimes  directly  furnish  the  anatomical  diagnosis  (hernia,  intestinal 
invagination). 

If  an  old  hernia  exist,  even  although  it  be  not  directly  (incarceration, 
inflammation)  and  solely  the  cause  of  the  symptoms,  nevertheless  its  util- 
ization must  be  held  in  reserve  until  investigation  discloses  another  un- 
doubted cause  (volvulus  or  internal  incarceration  from  peritoneal  adhe- 
sions originating  in  the  hernia). 

If  hernia  or  an  obstruction  in  the  rectum  be  excluded,  the  history 
must  be  accurately  reviewed.  If  this  denotes  chronic  stenosis  from  which 
complete  occlusion  has  finally  developed,  the  same  examination  and  con- 
siderations must  be  pursued  as  in  the  diagnosis  of  that  form  of  the 
disease  which  I  have  already  described  in  stenosis  of  the  intestine. 

If  we  are,  however,  dealing  with  acute  occlusion  in  an  individual 
previously  healthy — acute  peritonitis,  naturally,  does  not  here  come  into 
question — the  following  anatomical  conditions  are  possible:  Obstruction  by 
foreign  bodies  or  from  gall-stones,  volvulus,  internal  incarceration,  invagi- 
nation, intestinal  paralysis. 

The  view  of  obstruction  from  foreign  bodies  must  be  at  once  rejected 
or  maintained  according  to  the  history  (except  in  insane  patients).  In 
obstruction  due  to  gall-stone,  the  history  almost  invariably  furnishes  data 
which  point  to  gall-stone  disease;  moreover,  we  have  usually  the  picture 
of  occlusion  and  not  of  strangulation.  If,  as  often  occurs,  the  history 
furnishes  no  points,  and  if,  besides,  the  symptoms  of  collapse  be  added  to 
those  of  occlusion,  for  instance,  such  as  are  produced  by  the  sensory 
irritation  of  the  stone  upon  the  nerves  of  the  intestine,  a  diagnosis  becomes 
impossible. 

VohTilus,  internal  incarceration,  invagination,  all,  as  a  rule,  set  in 
with,  severe  pain  and  vomiting.  The  same  is  true  of  acute  peritonitis. 
The  perplexity,  which  sometimes  cannot  be  overcome,  in  differentiating 
from  acute  peritonitis,  which  begins  in  the  same  manner,  I  have  already 
emphasized  and  have  indicated  the  steps  toward  a  possible  solution.  The 
factors  which  may  lead  to  the  assumption  of  intestinal  paralysis — under 
the  picture  of  occlusion — have  also  been  previously  mentioned.  These  two 
possibilities,  acute  peritonitis  and  intestinal  paralysis,  must  always  be 
minutely  considered.     If  there  is  no  foundation  for  their  diagnosis,  if  the 


780      INTESTINAL  CONSTRICTION   AND  INTESTINAL  OCCLUSION 

conditions  incline  us  to  the  assumption  of  volvulus,  of  incarceration,  or 
of  invagination,  other  points  of  support  must  be  present  to  make  possible 
the  differentiation  of  these  processes. 

Pain  is  here  of  the  less  importance,  because  it  is  common,  almost 
invariable,  and  usually  the  initial  symptom  in  these  conditions.  Perhaps 
its  primary  seat  may  indicate  the  anatomical  diagnosis :  If  extending  from 
the  left  hypogastrium  to  the  sigmoid  flexure,  volvulus;  if  in  the  right 
hypogastrium,  to  an  invagination  of  the  ileum  and  cecum ;  if  in  the  middle 
and  upper  abdominal  region,-  to  an  internal  incarceration  or  volvulus  of 
the  small  intestine. 

Even  less  significant  is  vomiting. 

Absolute  constipation  is  the  rule  in  internal  incarceration,  in  volvulus, 
and  in  obstruction  from  gall-stones,  sometimes  too  in  invagination,  but 
here  diarrhea  occasionally  alternates  with  constipation.  Hemorrhagic  dis- 
charges are  most  frequently  observed  in  invagination,  rarely  in  volvulus 
of  the  sigmoid  flexure,  very  exceptionally  in  internal  incarceration,  and 
not  at  all  in  obstruction  due  to  gall-stones.  The  same  laws  exist  for 
tenesmus  as  in  regard  to  hemorrhagic  discharges. 

Collapse  suddenly  appearing  may  occur  in  all  forms  of  occlusion,  most 
markedly  in  internal  incarceration,  next  in  volvulus,  and  to  a  less  degree 
(oven  entirely  absent)  in  invagination  and  obstruction. 

Better  grounds  for  the  diagnosis  may  be  furnished  by  the  local  findings 
in  the  abdomen,  if  it  be  possible  to  obtain  these.  Above  all,  acute  local 
mcteorism  may  lead  to  definite  conclusions.  If  we  can  be  sure  that  the 
tensely  inflated,  elastic,  motionless,  intestinal  coil  rises  from  the  left  lower 
side  of  the  abdomen,  this  is  in  favor  of  volvulus  of  the  sigmoid  flexure. 
Invagination  may  be  determined  with  certainty  if  a  tumor  is  present 
which  possesses  the  characteristic  properties  of  an  invagination  tumor; 
namely,  that  it  is  usually  soft  but  periodically  becomes  hardened  by  rigid 
contractions  of  the  wall. 

TREATMENT 

Among  the  most  difficult  and  responsible  duties  of  the  physician  is 
the  treatment  of  intestinal  occlusion.  Upon  his  decided  opinion,  based 
directly  upon  his  definite  conclusions,  naturally,  the  life  of  the  patient 
often  depends.  While  this  opinion  in  the  case  of  occlusion  developing 
from  chronic  stenosis  occasions  no  immediate  anxiety,  the  situation  in 
acute  occlusion  often  necessitates  most  urgent  measures;  within  a  few 
hours  the  most  far-reaching  decisions  must  sometimes  be  made,  and  this 
oftentimes  when  we  only  indistinctly  recognize  the  seat  and  the  nature 
of  the  occlusion,  and  occasionally  are  even  in  doubt  as  to  whether  an 
occlusion  or,  on  the  contrary,  a  paralysis  of  the  intestine  is  present.  Con- 
sider the  distressing  picture  with  its  characteristic  features — features 
mostly  uniform  and  which  repeat  themselves — when  the  patient,  collapsed 


INTESTINAL  OCCLUSION  781 

and  vomiting,  is  found  .to  have  complete  intestinal  obstruction,  his  abdo- 
men distended  like  a  drum,  and  all  diagnostic  points  which  aid  in  the 
determination  of  the  nature  of  the  affection  are  absent!  Nevertheless, 
the  physician  must  act.  The  patient,  unless  already  in  the  terminal 
agony,  must  not  be  left  to  his  fate.     What  is  to  be  done? 

Some  authors  absolutely  deny  the  occurrence  of  a  spontaneous  cure, 
that  is,  without  surgical  interference,  in  an  internal  incarceration,  a 
volvulus,  or  kinking.  Others,  upon  a  basis  of  actual  experience,  believe 
this  to  be  possible  in  favorable  anatomical  conditions  and  in  the  earlier 
periods  of  the  affection,  although  exceedingly  rare.  The  first  contingency, 
however,  absolutely  requires  operative  interference;  the  latter  permits, 
within  definite  limits  and  even  here  in  a  certain  period  of  time,  non- 
surgical treatment.  Naturally,  the  latter  does  not  and  cannot  decide  the 
treatment,  and  this  statement  is  only  made  to  show  how  a  very  surprising 
course  may  be  occasionally  explained. 

In  regard  to  treatment,  we  must  differentiate  between  simple  occlusion 
and  occlusion  with  strangulation. 

In  occlusion  with  strangulation  it  is  the  rule  to  operate  as  soon  as 
the  symptoms  of  the  latter  become  at  all  marked.  If  the  diagnosis  of  the 
seat  and  the  nature  of  the  disease  can  be  made,  exploratory  laparotomy 
and  removal  of  the  obstruction  is  in  place.  The  chances  of  operation  are 
best  if  it  be  done  within  the  first  forty-eight  hours  after  the  appearance 
of  the  symptoms  of  occlusion:  75  per  cent,  recover;  after  the  third  day, 
the  percentage  of  recoveries  falls  rapidly  to  35  to  45  per  cent.  It  remains 
on  this  plane  even  when  the  operation  is  done  only  in  the  course  of  the 
second  week. 

If  the  physician  recognizes  that  the  intestinal  occlusion  is  either  in- 
ternal incarceration  or  volvulus,  no  time  is  to  be  lost  by  attempting  any 
other  method  of  treatment.  For  the  psychical  effect  upon  very  anxious 
patients  and  to  relieve  the  minds  of  friends  and  relatives  during  the  time 
when  preparations  for  the  operation  are  being  made,  at  most  only  a  brief 
trial  of  non-surgical  measures  is  allowable. 

It  appears  that  twists,  if  not  of  marked  extent,  may  occasionally  re- 
cover under  non-surgical  treatment.  This  may  also  be  resorted  to  in 
invagination,  but  in  these  two  conditions  operation  should  be  attempted 
early,  provided  non-surgical  measures  do  not  rapidly  bring  relief. 

If  gall-stones  cause  intestinal  occlusion,  experience  has  shown  that  the 
outlook  for  a  spontaneous  recovery  or  by  internal  remedies  is  not  unfavor- 
able. In  this  case,  we  should  decide  upon  laparotomy  only  when  the 
symptoms  indicate  direct  danger  to  life.  The  gauge  for  this  is  furnished 
by  the  cardiac  activity;  we  shall  revert  to  this  later. 

What  has  been  said  of  gall-stones  is  also  true  of  large  and  round  foreign 
bodies.  When  sharp  or  angular  substances  cause  obstruction  purgatives 
must  be  avoided,  and  in  their  place  soft  food  should  be  taken  and  potatoes. 


782      INTESTINAL  CONSTRICTION   AND  INTESTINAL  OCX^LUSION 

rice,  oatmeal  grits,  which  form  a  mass  safely  enclosing  the  foreign 
bodies. 

I  shall  now  return  to  the  question  of  operation. 

Experience  teaches  that  the  chances  of  operation  not  only  depend  upon 
its  early  performance,  but  also  increase  with  the  recognition  of  the  nature 
and  location  of  the  obstruction,  as  this  makes  possible  a  direct  attack  at 
its  seat.  If,  however,  the  diagnosis  is  obscure,  and  only  peritonitis  and 
intestinal  paralysis  are  excluded,  what  is  to  be  done?  The  answer  must 
certainly  be:  Operate  at  once,  provided  the  operation  in  itself  would  be 
a  harmless  affair.  This  is,  however,  not  the  case  if  sjnnptoms  of  strangu- 
lation are  at  all  marked.  Although  the  modem  surgeon  may,  with  some 
degree  of  certainty,  exclude  septic  infection  in  peritonitis,  other  dangers 
threaten,  particularly  in  these  laparotomies,  and  especially  if  the  seat  of 
the  disease  must  first  be  searched  for  (intestinal  paralysis,  reflex  influences 
upon  the  nervous  system  and  upon  the  circulatory  apparatus).  Here,  that 
is,  with  an  uncertain  diagnosis,  two  kinds  of  cases  must  be  differentiated. 
If  the  course  is  very  acute,  if  there  are  severe  symptoms  of  shock,  probably 
only  the  operation  can  save  life.  Without  this  almost  all  patients  perish, 
and  one  saved  by  this  means  may  be  looked  upon  as  pure  gain.  If,  how- 
ever, the  course  is  more  moderate,  the  entire  picture  not  too  severe, 
so-called  internal  treatment  may  be  resorted  to  with  a  definite  view  and 
purpose  which  shall  be  later  explained. 

In  attempting  this  therapy,  the  physician  must  carefully  observe  the 
cardiac  activity,  as  shown  by  the  quality  of  the  pulse.  In  these  cases 
the  condition  of  the  pulse  will  correctly  indicate  the  best  time  in  which 
to  perform  the  operation.  If  the  pulse  begins  to  increase  in  frequency,  the 
tension  to  sink  but  a  little,  it  is  time  to  operate,  for  somewhat  later  this 
may  become  impossible.  The  weakened  cardiac  activity  is  no  longer  suf- 
ficient to  meet  the  requirements  of  an  operation.  In  such  cases  it  is  much 
better  to  operate  several  days  before  this  critical  cardiac  change  than  to 
wait  but  a  few  hours  after  it  has  taken  place. 

If  the  symptoms  of  occlusion  exclusively  appear  in  the  clinical  picture, 
while  those  of  strangulation  are  absent,  often  an  operation  alone  can  save 
the  life,  but  in  the  less  fulminant  course  of  the  affection  there  is  time  to 
try  non-surgical  measures.  In  quite  a  number  of  cases  these  may  entirely 
relieve  the  threatening  situation. 

There  has  been  much  discussion  of  late  as  to  the  cases  of  intestinal 
occlusion  in  which  a  resort  to  non-operative  treatment  is  at  all  permissible, 
under  what  circumstances,  and  as  to  the  factors  upon  which  the  decision 
depends. 

Primarily,  a  point  of  support,  as  I  have  already  mentioned,  is  the  gen- 
eral condition  as  expressed  in  the  cardiac  activity  and  in  the  condition 
of  the  pulse,  while  the  local  symptoms  of  occlusion  (meteorism,  vomiting) 
are  of  less  import.     But,  I  repeat,  if  the  diagnosis  at  the  onset  is  un- 


INTESTINAL  OCCLUSION  783 

certain,  and  if  the  cardiac  condition  is  good,  relief  by  non-surgical  measures 
may  be  attempted,  for,  during  this  time,  by  rapid  decision,  we  may  obtain 
more  data  in  support  of  the  local  and  collective  diagnosis  to  improve  the 
chances  of  operation.  If  by  the  application  of  these  principles  the  possi- 
bility and  justification  of  a  brief  delay  is  gained,  the  question  then  arises 
which  non-surgical  measures  are  most  likely  to  be  successful. 

First,  a  method  which  is  not  to  be  resorted  to  must  be  pointed  out. 
In  all  forms  of  acute,  subacute,  chronic,  and  complete  intestinal  occlusion 
purgatives  are  decidedly  dangerous,  and  for  this  reason  must  be  absolutely 
avoided — with  the  single  exception,  in  case  the  obstruction  is  due  to  fecal 
masses.  With  a  positive  or  lightly  acute  occlusion  by  incarceration,  tor- 
sion, kinking,  or  obstruction  by  gall-stones  and  foreign  bodies,  as  well  as 
whenever  the  diagnosis  is  questionable,  purgatives  should  never  be  em- 
ployed !  Only  when  in  a  concrete  case  obstruction  due  to  feces  is  almost 
certain  may  purgatives  be  administered  by  the  mouth.  Mercury,  formerly 
so  much  used,  may  be  entirely  dispensed  with,  for  it  is  occasionally  directly 
harmful  and  still  more  so  indirectly,  as  valuable  time  is  lost  in  its  em- 
ployment. 

Enemata  and  rectal  irrigations  are  often  advised,  but  very  little  more 
may  be  expected  from  them  than  from  purgatives  by  the  mouth.  If  they 
do  not  flow  off  again  they  also  have  a  harmful  effect,  since  by  their  massive- 
ness  they  raise  the  already  increased  intra-abdominal  pressure.  These  facts 
must  always  be  taken  into  consideration.  A  priori,  and  according  to 
experience,  enemata  and  large  injections  are  useless  in  nearly  all  forms 
of  acute  occlusion;  the  only  exception  to  this  is  formed  by  acute  invagina- 
tion which,  if  it  have  occurred  in  the  large  intestine,  may,  in  fact,  be  caused 
to  disappear  by  forced  massive  enemata  or  by  the  introduction  of  air. 
In  one  form  of  chronic  occlusion  these  are  almost  indispensable,  and  com- 
bined with  internal  purgatives  they  form  a  most  valuable  therapeutic  agent, 
namely,  in  obstruction  from  feces,  immaterial  whether  this  takes  place 
in  a  free  atonic  intestine  or  above  the  point  of  stenosis.  But  we  must 
be  very  careful  in  their  use  if  there  is  a  well-founded  suspicion  of  ulcerative 
processes  or  fissures  in  the  intestine. 

For  irrigation,  water  (1-5  liters)  or  oil  (^1  liter)  is  employed.  The 
temperature  of  the  water  should  be  that  of  the  air;  ice-water  injections 
are  no  more  beneficial,  and  are  contraindicated  in  all  debilitated  patients. 
Highly  irritating  additions,  particularly  of  table  salt  (5  to  8  per  cent.), 
are  perhaps  only  of  use  in  acute  invagination.  The  value  of  the  irriga- 
tion depends,  in  the  main,  upon  its  softening  property,  and  for  this 
purpose  pure  water,  or  soapy  water,  or  oil  is  sufficient.  The  fluid  must 
always  be  introduced  with  only  slight  force  and  very  slowly,  from  one-half 
to  one  hour  being  required. 

Lately  carbonic  acid  enemata  have  been  employed,  of  which  about  the 


784      INTESTINAL  CONSTRICTION   AND  INTESTINAL  OCCLUSION 

same  is  to  be  said  as  of  injections  of  water.  The  inflation  of  gas  into 
the  rectum,  as  occasionally  practised,  is  naturally  useless  in  obstruction 
due  to  feces;  in  the  acute  forms  of  occlusion  the  same  is  true  as  of  the 
irrigations  with  water,  i.  e.,  an  effect  is  only  occasionally  to  be  expected 
in  acute  invagination. 

Massage  of  the  abdomen,  as  well  as  the  application  of  the  faradic 
current  in  the  milder  degrees  of  the  affection,  may  prove  useful  in  a 
single  form,  namely,  that  of  obstruction  due  to  feces.  On  the  contrary, 
massage  as  well  as  faradism  is  to  be  absolutely  rejected  in  all  forms  of 
acute  occlusion  with  strangulation,  and  also  when  the  possibility  of  peri- 
tonitis or  hernia  may  be  assumed,  which,  in  the  case  of  strangulation, 
often  begins  very  early.  In  invaginations  of  very  recent  origin,  massage 
(with  simultaneous  narcosis)  is  said  to  be  occasionally  useful;  but  even 
here  the  greatest  caution  is  necessary  and,  in  my  opinion,  rectal  injections 
and  inflations  are  generally  more  successful  and  considerably  less  dangerous. 

An  important  enrichment  of  our  therapy  in  acute  intestinal  occlusion, 
gastric  lavage,  has  been  introduced  by  Kussmaul.  Its  value  consists  in 
this,  that  the  evacuation  of  the  gastric  contents  facilitates  the  regurgita- 
tion of  the  intestinal  contents  into  the  stomach.  This  causes  the  cessation 
of  retching  and  fecal  vomiting  and  a  subjective  feeling  of  amelioration  is 
produced.  Experience  shows,  however,  that  the  employment  of  gastric 
lavage  occasionally  does  even  more  than  this;  an  absolute  cure  of  the 
severest  forms  of  complete  intestinal  occlusion  in  cases  lasting  from  eight 
to  nine  days  has  been  brought  about  by  its  use.  This  treatment  should 
not  be  deferred  until  too  late,  and  we  should  never  rest  content  with  a 
single  lavage,  but  the  method  must  be  employed  frequently,  often  being 
repeated  every  two  or  three  hours,  since  the  regurgitation  of  the  contents 
of  the  small  intestine  into  the  stomach  may  take  place  with  extraordinary 
rapidity.  The  same  objection  has  been  made  to  gastric  lavage  as  to  opium 
treatment,  that  it  brings  about  a  deceptive  euphoria  while  the  local  process 
remains  unchanged  or  advances.  As  stated,  these  agents  occasionally  have 
a  curative  effect,  and,  apart  from  this  fact,  the  patient  who  suffers  severely 
must  not  have  such  a  beneficial  remedy  withdrawn  from  him  even  although 
it  have  but  a  symptomatic  effect.  Far  it  is  the  duty  of  the  intelligent 
and  conscientious  physician  constantly  to  keep  in  mind  the  question  of  an 
operation,  and,  in  spite  of  apparent  subjective  improvement,  closely  to 
observe  the  most  decisive  local  symptoms  (passage  of  feces  and  flatus) 
as  well  as  to  watch  over  the  cardiac  activity. 

I  must  still  refer  to  two  drugs  used  internally.  One  of  these  is  opium 
and  its  preparations,  which  may  be  administered  either  by  the  mouth  or 
by  subcutaneous  injection  in  the  form  of  morphin.  There  is  great  differ- 
ence of  opinion  as  to  their  use.  That  they  may  be  given,  or  must  be 
frivon.  to  tide  the  suffering  patient  over  a  few  hours  of  misery  when  the 
situation  is  hopeless  and  operative  interference  is  no  longer  possible,  is 


INTESTINAL  OCCLUSION  785 

generally  recognized.  In  some  cases  its  eniplo3anent  is  permitted  by  even 
its  most  bitter  opponents ;  for  instance,  if  in  high-graded  stenosis,  enormous 
peristalsis  and  intestinal  stiffening  make  us  fear  early  paralysis  of  the 
musculature  of  the  intestine,  and  if,  during  this  time,  attempts  have  been 
made  to  overcome  the  obstruction  by  rectal  irrigation  and  other  measures. 
The  dispute,  on  the  contrary,  is  concerning  the  question  whether  or  not 
opium  may  be  given,  that  is,  must  be  given  at  the  beginning  of  acute 
occlusion.  Some  surgeons  are  decidedly  opposed  to  its  use  for  the  follow- 
ing reasons:  Because  the  treatment  by  opium  brings  about  only  an  appar- 
ent improvement,  and  by  masking  important  symptoms  renders  the  diag- 
nosis diflficult,  increases  the  danger  of  collapse,  and  facilitates  the  onset 
of  intestinal  paralysis;  also  because  the  patient,  on  account  of  apparent 
improvement,  rejects  an  operation.  In  opposition  to  this  the  following 
may  be  said :  The  feeling  of  intense  anxiety,  the  nausea  and  vomiting, 
the  severe  pains,  frequently  cease.  If  given  at  the  right  time,  i.  e.,  imme- 
diately at  the  onset,  opium  occasionally  has  a  surprising  effect  upon  the 
symptoms  of  initial  reflex  collapse.  And  even  if  this  were  its  only  effect — 
which  is  not  the  case,  as  it  occasionally  influences  peristalsis,  even,  per- 
haps, makes  possible  the  spontaneous  improvement  of  the  anatomical  dis- 
turbance— treatment  by  opium  should  not  be  rejected  for  it  brings  great 
relief  to  the  suffering  patient.  The  dreaded  deleterious  effects  may  be 
obviated  if,  as  I  have  just  remarked  concerning  gastric  lavage,  the  physi- 
cian does  not  permit  himself  to  be  deceived,  and  continually  keeps  in 
mind  the  local  intestinal  symptoms  and  the  cardiac  condition;  if,  more- 
over, the  employment  of  opium  is  instituted  only  upon  the  first  or  second 
day  of  the  disease,  and,  notwithstanding  its  apparently  good  effect,  the 
question  of  operation  is  decided  according  to  the  principles  which  I  have 
indicated. 

The  other  remedy,  quite  recently  introduced  into  the  treatment  of 
"  ileus,"  is  atropin  given  subcutaneously  in  decided  doses,  0.001  to  0.005 
at  a  dose,  and  repeated  if  necessary.  In  the  last  few  years  a  series  of  cases 
has  been  reported  in  which  atropin  was  used  under  most  desperate  circum- 
stances when  for  many  reasons  an  operation  was  out  of  the  question;  it 
freed  the  intestinal  tract,  and  recovery  followed.  It  is  impossible  to  base  an 
opinion  upon  the  statistics  at  hand.  In  the  cases  in  which  atropin  was  inef- 
fectual, an  anatomical  intestinal  occlusion  was  shown.  In  the  single  case  in 
which  I  have  had  opportunity  to  observe  its  favorable  effect,  the  symp- 
toms were  those  of  severe  intestinal  occlusion  in  consequence  of  obstruc- 
tion due  to  gall-stone.  I  presume  that  the  effect  of  atropin  in  intestinal 
occlusion  may  best  be  observed  when  the  underlying  condition  is  that  of  a 
spastic  or  paralytic  obstruction. 

In  acute  occlusion  the  ingestion  of  food  must  be  absolutely  suspended 
from  the  first  day.  When  the  thirst  is  tormenting  small  pellets  of  ice 
may  be  given  by  the  mouth  or  minimal  amounts  of  ice  water  may  be  swal- 


786      INTESTINAL  CONSTRICTION  AND  INTESTINAL  OCCLUSION 

lowed.  In  case  of  profuse  loss  of  fluid  by  vomiting,  fluid  may  be  injected 
into  the  rectum  or  subcutaneous  infusions  of  normal  salt  solution  may  be 
employed.  Where  the  course  of  the  disease  is  prolonged,  nutritive  enemata 
are  to  be  advised. 

For  severe  cases  of  well-developed  intestinal  paralysis  the  measures 
previously  described  (massage,  electricity)  have  proven  ineffectual.  Fur- 
ther experience  will  show  whether  physostigmin  (physostigmin  salicylate, 
0.0005  per  dose),  recently  introduced  by  v.  Noorden,  will  furnish  any  bet- 
ter results. 


INDEX  OF  AUTHORS 


As6e,  300. 
Abelmann,  311,  314. 
Abramow,  334. 
ACHARD,  411. 
V.   ACKEREN,  315. 

AcKERMANN,  361,  362,  385,  386,  393. 

Aezel,  398. 

Apfanassiew,  330,  370. 

Ag6ron,  207,  216. 

Albers,  397,  419. 

Alberti,  195,  216. 

Albrecht,  126,  127,  145. 

Albu,  152,  597. 

V.  Aldor,  98,  109. 

Alison,  369. 

Andral,  187,  407. 

Anschutz,  313,  318. 

Apolant,  40. 

Arcelet,  417. 

AscHOFP,  575, 

Ashe,  O.,  216. 

AuERBACH,  40,  316,  317. 

AuFRECHT,  197,  332,  371,  385. 

Backman,  109,  152,  163,  216. 

Bagot,  440. 

Baillie,  397,  398. 

Bakman,  93. 

Baldi,  311. 

Balzer,  166,  220. 

Bamberger,  368,  444,  477,  479,  484. 

Banti,  331. 

Bar-Bacci,  166. 

Bard,  430,  434. 

Bardenheuer,  277,  404,  408. 

Baumler.  127. 

Bayer,  440. 

Bayle  443. 

Beard,  79. 

Beaumetz,  370,  383. 

Becher,  282,  283,  287. 

V.  Beck,  B.,  546. 

Behm,  104,  107. 

V.  Behring,  637,  688,  698. 


Belin,  441. 

Benedictxjs,  Alexander,  419. 

Benzon,  282. 

Berg,  440. 

V.  Bergmann,  443. 

Bernard,  Claude,  311. 

Bettmann,  349. 

BiACH,  398. 

Bial,  277. 

BiCKEL,  342. 

Bidder,  327. 

BiEDERT,  Th.,  41,  166,  640,  641. 

BlENSTOCK,  640. 

Bier,  281,  294. 

BlERMER,  41,  447. 
BlERNACKI,  327. 

Billroth,  45,  221,  236,  637,  638. 

BiNz,  407. 

Bleichroder,  220. 

Blocher,  294. 

Block,  441. 

Blocq,  370. 

Blumenfeld,  700. 

Bltjmensath,  F.,  216. 

Blumenthal,  F.,  252. 

Boas,  J.,  66,  83,  97,  104,  116,  121,  122, 
169,  174,  175,  205,  216,  221,  225,  232, 
259,  280,  573,  574,  588,  590,  599,  632, 
652,  704,  724. 

Bochdalek,  446. 

boeniger,  93. 

Bogdan,  449. 

BoHM,  327. 

Bohnstedt,  424,  432. 

Boix,  370. 

BoKAi,  636,  643,  654. 

BoLDS,  417. 

Bollinger,  269. 

BORRMANN,  167,  216. 

BoTKiN,  337,  363. 

Bouchard,  345,  377,  383,  644,  711. 

BoUCEtARDAT,  306. 
BOUILLAUD,  184. 

BouissoN,  419. 

787 


788 


INDEX  OF  AUTHORS 


BOURCERET,  429. 

BouRGET,  L.,  201,  216. 

bouveret,  107. 

bowditch,  37. 

Bradbury,  429. 

Bramwell,  177,  216. 

Brandenburg,  140. 

Bkasch,  215. 

Brauer,  348,  355,  369,  372. 

Bbaun,  L.,  296,  298. 

Braun,  W.,  414. 

Braunstein,  340. 

Bret,  160. 

l^RiEGER,  L.,  327,  362,  376,  393,  455,  643, 

644. 
Bright,  306. 

Brinton,  164,  170,  176,  211,  216,  222. 
Brodowski,  398. 
Brosch,  339. 
Browicz,  331,  333,  468. 
Brunner,  Fr.,  184,  214,  216. 
Bruns,  463. 
Budd,  166,  183,  199. 
Bum,  a.,  267. 
BuNGE,  639. 
Bi trker,  330. 
burkhart,  80. 
Buxbaum,  280. 
VAN  der  Bye,  419. 

Cabot,  216. 
Cahn,  43,  91. 
Calabrese,  378. 
Calzavara, 419. 
Canstatt,  263. 
Cantani,  291,  372. 
Carlau,  358. 
Carle,  213,  216,  258. 
Carpentier,  347. 
Cavazzani,  308,  311,  315. 
Cayol,  443. 
Chadbourne,  233. 
CiiARroT,  .385,  386,  502. 
C'harrin,  337. 
Chauffard,  331,  337,  365. 
("hauveau   308. 
(^HERCHEWSKI,  296,  298. 
Chervinsky,  439. 
Chiari,  397,  438. 
Chlumky,  258. 
Chopart,  306. 

ClIVOSTEK,   187. 

Cipriani,  316. 


Clark,  A.,  679. 

Classen,  417. 

Clemm,  109,  110. 

Cloetta,  108. 

CoHN,  A.,  178. 

CoHN,  Martin,  100. 

cohnheim,  o.,  644. 

Cohnheim,  p.,  90,  106,  154,  165  176  186^ 

187,  207,  208,  216,  606. 
Columbus,  Realdus,  485. 

COPEMAN,  414. 

Cornil,  187,  397. 

Cotton  Holland,  41. 

coupland,  429. 

Courtaqe,  672. 

CouRVOisiER,  397,  399,  400,  401    405, 

408,  413,  414,  419,  421,  424,  425,  427, 

429,  431,  432,  488. 
Cowley,  306. 
Cramer,  H.,  339,  631. 
Croner,  232. 

Cruveilhier,  159,  165,  203,  225,  428,  677. 
CSERY,  273. 
Cuilleret,  263. 
cullevrier,  167. 
curschmann,  24,  298. 
Cyr,  408. 
V.  CzERNY,  258,  260,  261  397,  404,  603. 

Damaschino,  416. 

Debove,  411. 

Dejerine,  408. 

Delitzin,  283. 

Delius.  H.,  729. 

Demel,  Cesaris,  167,  216. 

Dennig,  142,  264,  265,  266,  267. 

Destree,  397. 

Determann,  295,  296,  298. 

Deucher,  314. 

Diamare,  308. 

Dieckmann,  420. 

Dietrich,  198. 

DiEULAFOY,  161,  181,  579. 

Dinkler,  75. 

DiTTL,  286. 

Dittrich,  237. 

Dolmatow,  181,  216,  233. 

DoNATUs,  Marcellus,  419. 

DoNOP,  407. 

DoYON,  497. 

Dronke,  204. 

Drozda,  187. 

Drummond,  376,  384. 


INDEX  OF   AUTHORS 


789 


DUFRESNE,  491. 

DujARDiN,  370,  383. 
DuNiN,  213. 
DuPLAix,  363. 
DuRAND,  397,  419. 

DURET,   281. 

Eberle,  639. 

Ebstein,  29,  42,  73,  388,  711. 

Edebohls,  591. 

Edel,  111. 

Ehret,  381. 

Ehrlich,  504,  743. 

Ehrmann,  91. 

ElCHHORST,  201,  501. 

Eiger,  327. 

EiNHORN,  M.,  43,  90,  97,  107,  186,  216, 

228,  273,  726. 
V.  EisELSBERG,  180,  407,  439. 
EisELT,  442. 

ElSENHARDT,  166. 
ElSENLOHR,  674. 

Ekehorn,  232. 

Elsner,  H.,  186,  196,  216. 

Ely,  422. 

EMidH,  640. 

Emminghaus,  42. 

Encklin,  432. 

Engel,  167,  187. 

Eppinger,  Hans,  166,  216,  333,  334,  444. 

Escherich,  655. 

Esmarch,  708,  734. 

EsQuiROL,  263. 

EwALD,  C.  A.,  41,  66,  80,  97,  113,  119,  120, 
121,  159,  173,  181,  186,  201,  204,  216, 
223,  228,  232,  237,  263,  275,  282,  393, 
585,  588,  590  593,  677,  713,  715. 

Eysenhardt,  217. 

Faber,  Knud,  184,  711. 
Fagge,  Hilton  414. 
Fallopius,  465. 
Fantino,  213,  216. 
Fardel,  397,  419. 
Fauconneau,  491. 
Fauvel,  187. 
Fawitzky,  378. 
Federmann,  577. 
Felsenthal,  443. 
Feltz,  411. 
Fenwick,  210,  217. 
Fereol,  263. 
Fetzer,  444. 
51 


Fiedler,  339,  414. 

Field,  672. 

Fipield,  398. 

Fink,  Frz.,  192,  217. 

Finkelstein,  576. 

FiNsoN,  416. 

Fischer,  282. 

FiscHL,  Leop.,  208,  217,  603. 

Fleiner,  W.,  32,  78,  119,  121,  193,  205, 

217,  228,  273,  490,  504,  635   648,  709, 

727,  749. 
Fleischl,  431. 
Fles,  312,  315. 
Fleury,  439. 
Foote,  214. 
FoREL,  729. 
FoRSTER,  Balthazar,  201. 

FOURNIER,  487. 

Fox,  Wilson,  201. 

Frankel,  298,  339,  352. 

Eraser,  333. 

Frerichs,   187,  306,  341,  351,  400,  401, 

417,  470,  493. 
Freudweiler  238,  239. 
Friedenthal,  217. 
Friedmann,  384. 
Friedreich,  306. 
Fries,  177. 
Frison,  408. 
FucHs,  Th.,  473. 
Ftjtterer,  217. 

Gaertneb,  110. 

Gaillard,  167,  187,  217. 

Gairdner,  407. 

Galvagni,  367. 

Gartig,  252. 

Gebele,  224. 

Geis,  p.,  287. 

Gerber,  93. 

Gerhardi,  321. 

Gerhardt,  C.,  341,  356,  357,  603,  620. 

Gephardt,  D.,  161,  176,  193,  194,  217, 

296,  333,  469,  487. 
Gerlach,  670. 
Gersuny  482. 
van  Gieson,  422. 
Gilbert  337,  348,  349,  364,  439,  442,  444 

445,  447,  448. 
GiNTL,  113,  116. 
GiRODE,  331,  337. 
Giudiceandrea,  316. 
Glaessner,  95,  121. 


790 


•INDEX  OF  AUTHORS 


Glaister,  407. 

Glenard,  263,  264,  265,  275,  292. 

Glover,  414. 

Gluczinsky,  164,  173,  191,  217. 

goldbach,  584. 

goldschmidt,  140. 

Goldstein,  187. 

GOMBAULT,  386,  412. 

Gram,  498,  499. 

Grawitz,  331,  372,  406,  530,  631. 

Greenough,  185,  217. 

Griesinger,  263. 

Griffini,  161. 

Grote,  102. 

Grube,  443. 

Grundzach,  130. 

Gubler,  410,  539. 

GuMLicH,  378. 

gusenthal,  492. 

Gxtssenbauer,  260,  304. 

GUTTMANN,  P.,  282,  677. 

Guyon,  181. 

Haal,  349. 

Haarmann,  428. 

Haberer,  603. 

Habershow,  677. 

V.  Hacker,  29. 

HagedoRn,  439. 

Haguenot,  van  Swieten,  768. 

Hahn,  E.,  282,  290,  377,  579. 

Hall,  397. 

Hallervorden,  378. 

Hammerschlag,  92,  95,  98,  232   495. 

Hampeln,  179,  217,  238. 

Hanot,  364,  365,  367,  386,  410,  411,  412, 

439,  442,  444,  447,  448,  450. 
V.  Hansemann,  307,  309,  444,  577,  689. 
Hari    186. 
Harland,  184. 
Harley,  315,  402. 
Hartmann,  258. 
Hartung,  217,  362,  393. 
Hassmann,  233. 
Hauser,  G.,  167,  237,  400. 
Hayem,  167,  228,  331,  349,  386. 
Hecker,  166,  218. 
Heddaeus,  a.,  397,  405. 
Hkdon,  .307,  311. 
Heger,  377. 
Heidenhain,  330,  404. 
Heim,  .384. 
Heimann,  G.,  251. 


Heinecke,  195. 

Heitler,  337. 

Heller,  689, 

Helly,  304. 

Hemmeter,  78,  108,  186,  217,  228. 

Henke,  295. 

Henoch,  446. 

Henschen,  186. 

Hermann,  468. 

Hermes    O.,  575. 

Herz,  H.,  583. 

Herzen,  95,  102,  103. 

Heschl,  398. 

Hesse,  122,  476. 

Heubner,  670. 

VAN  Heukelom,  Siegenbeck,  442. 

Heyfelder,  397 

Heymanns,  370. 

HiLLER,  187,  729. 

Hippel,  419. 

HiRSCH,  A.,  102,  213,  217. 

Hirschfeld,  F.,  263,  279,  316. 

HiRSCHFELD,  P.,  167,  179,  217. 

Hochenegg,  404,  453. 

HODGEN,  40. 

Hoffmann,  A.,  233,  295  296,  298  718. 

Hofmeier,  331. 

Holzmann,  319. 

honigmann,  91. 

Hood,  W.  Charles,  176,  217. 

Hoppe-Seyler,  G.,    331,    421,   432,    434, 

460,  663,  678,  735. 
Howald,  M.,  420. 
Huber,  201. 

HXJETER,  440. 

HuTiNEL,  367,  450. 


Ignatowski,  351. 
Illoway,  105. 
lOANNOVICS,  330. 

Israel,  J.,  282,  284,  289,  290,  442. 
Italia,  Edoardo,  317. 

Jacob,  408, 

Jageh,  339, 

V.  Jaksch,  121,  239,  378. 

Janeway,  398. 

Janowski,  388,  389. 
'  Jaworski,  106,  107,  110,  131,  208. 
'  Jeanne,  576. 

Jeanselme,  318. 

JoEST,  637. 

Johnson,  104,  107. 


« 


INDEX  OF  AUTHORS 


791 


JosLiN,  168,  176,  185,  213,  217. 
JULIEN,  187. 

JiJHGENSEN,  39,  40,  41,  78,  142. 
JiJRSS,  358. 

V.  Kablden,  370,  441,  444. 

Kaltenbach,  440, 

ka.rlinsky,  339. 

Kast,  639. 

Katz,  307,  313,  321. 

Kaufmann,  231,  232,  308. 

Kaupe,  212. 

Kausch,  213,  217,  257,  258. 

Keen,  443. 

Kehr,  290,  404,  425,  427,  430,  432,  433, 

434,  435,  470,  475,  476,  499,  509. 
Keith,  581. 

Kelling,  G.,  213,  217,  235,  474. 
Kelsch.  337,  365,  444. 
Kermauner,  618. 
Kiener,  365,  444. 
KiMURA,  Tokuye,  336,  340. 
Kirch,  210. 

KiRCHHOFF,  294. 
KiTACfAWA,  741. 

Klebs,  187,  348,  400. 

Klein,  A.,  639. 

Klemperer,  G.,  140,  239,  252,  280,  382. 

Klingemann,  369 

Klob,  398,  400,  442. 

Klopp,  440. 

KoBERT,  358,  742. 

KOBLER,  711. 

Koch,  Robert,  687,  699,  700. 
KocHER,  217,  258. 
Kochmann,  230,  244. 
KoHLER,  G.,  172,  217. 

KOHLSTOCK,  729. 
KONITZKY,  407. 
KORANYI,  273. 

KoRTE,  217,  245,  260,  493,  580,  587,  591, 

596. 
KossEL,  639. 
KOSSOBXJDSKJ,  732. 

KovEsi,  107. 
v.  koziczkowzki,  93. 
Krafft,  161,  217. 
V.  Krannhals,  349. 
Kraske,  249,  261. 
Kraus,  Fedor,  252,  258. 
Kraus,  Fr.,  396,  470. 
Krauss,  J.,  397,  400. 
Kretz,  498. 


Krieger,  417. 
Kronig,  370,  609. 
Kronlein,  217,  258. 
Kruger,  90. 
Kkull,  357. 
Kuchenmeister,  454. 
KtJHNE,  653. 
KiJMMEL,  397,  408. 

KUNDRAT,  167. 
KUNZMANN,  312. 

KusNEZOW,  452. 

KussMAUL,  32,  33,  34,  35,  36,  37,  38,  41, 

43, 44,  45,  46,  53,  119,  126,  142,  170,  201, 

205,  225,  243,  648,  670,  676,  682,  749, 

784. 
KiJSTER,  287,  316. 
KuTTNER,  L.,  96,  179,  217,  232,  235,  263, 

275,  282,  285,  287. 

Laache,  181. 

Laboulais,  173. 

Lachmann,  417. 

Laennec,  367,  368,  371,  373. 

Laguesse,  308. 

Lambotte,  180. 

Lanceraux,  309,  397. 

Lancereaux,  187,  438. 

Landau,  L.,  263,  264,  271,  277,  282  286, 

291,  292. 
Landau,  Th.,  575,  576,  589. 
Landsberger,  379. 
Lang,  93,  167,  187,  352. 
Lange,  164,  217. 
Langenbuch,  404,  432,  452. 
Langerhans,  161,  218,  308,  309. 
Langowoi,  370. 
Lanz,  541. 
Lautenbach,  377. 
Lebert,  237,  239,  407. 
Ledden-Hulsebosch,  618. 
Legendre,  417. 
Leichtenstern,  75,  181,  381,  417,  421, 

422,  424,  425,  426,  430,  432,  434,  435, 

436,  468,  475,  497. 
Lenhartz,  121,  203,  204. 
Lennander,  581. 
Lennhof,  282,  283,  287. 
Lenzmann,  384. 

Leo,  H.,  63,  90,  91,  95,  120,  268. 
Lepage,  305. 
Lepine,  160,  307,  379. 
Lerebouillet,  348,  349. 
Leroboulet,  504. 


792 


INDEX   OF  AUTHORS 


Leser,  224. 

Letulle,  161,  178,  218. 

V.  Leube,  41,  42,  44,  65,  66,  67,  79,  83, 
119,  140,  176,  191,  194,  200,  201,  202, 
211,  218,  228,  254,  263,  319,  354,  359, 
413,  437,  450,  561,  631,  677. 

Leuckart,  454. 

Leudet.  167,  187. 

Leuk,  186,  218. 

Leusser,  296,  298. 

Levy,  349. 

V.  Leyden,  24  74,  80,  220,  253  411,  677. 

LiCHTHEIM,    116,  316. 
LlEBERMEISTER,  332,  347,  381. 
LlEBREICH,  204. 

Lindner,  232,  258,  286. 

LiNOSSIER,  90. 

Lion,  228. 

LiTTEN,  166,  218,  263,  282,  293,  388,  452, 

459,  677,  739. 
LoBKER,  400,  404,  406. 
Longuet,  228. 
LOUSTE,  210. 

Lovell-Keays,  L.,  185,  218. 
lowenthal,  43. 
Lubarsch,  186,  689. 
LiJCKE,  453. 
lijrmann,  338. 
Luschka,  51. 
LiJTJE  734. 

LiiTTKE,  121. 

Luxenburg,  167,  218. 

Macfadyen,  638. 

Machol,  212,  219. 

Madelung,  453. 

Maier,  439,  670. 

Malbranc,  43. 

Maly,  640. 

Mamlock,  210. 

Mangelsdorp,  368,  388. 

V.  Manteuffel,  Zoege,  766. 

Maragliano,  698. 

Marchand,  367,  745. 

Marchetti,  233. 

Marechal,  326.  , 

Marfan,  166,  218. 

Markel,  a.,  177.  ■ 

Marshall,  J.  N.,  218.  ■ 

Martini,  260. 

Martius,  76,  113   116,  121. 

Mathieu,    a.,    106,    107,    140,    173,   218, 


Matthes,  201,  205,  280. 

May,  223. 

V.  Maydl,  257. 

Meinert,  263,  264,  265,  266,  267,  274. 

Meister,  452. 

Meltzing,  273. 

V.  Merino,  36,  151,  201,  203,  213,  218, 

278,  303,  306,  311. 
Merkel,  H.,  218,  494. 
Mermann,  397. 
Mertens,  H.,  370. 
Metschnikoff,  640. 
Mett,  92,  95,  120. 
Mettenheimer,  449. 
Metzger,  103. 
Mey,  E.,  180,  218. 
Meyer,  Paul,  102. 
Michaelis,  W.,  147,  268. 

MiCHAILOW,  218. 

MicHAux,  414. 

V.    Mikulicz,    195,   200,  211,  218,    235. 

257,  258,  259,  404,  520,  522,  524,  525, 

533. 
Mills,  210. 
Minkowski,  O.,  131,  177,  179,  218,  227, 

303,  306,  307,  308,  310,  311,  325,  329, 

330,  331,  348,  352,  468. 
Mintz,  S.,  218. 
Mitchell,  Weir,  279. 

MOELLER,  700. 

Mohamed,  442. 

Moncorg6,  434. 

monneret,  439,  443. 

Morgagni,  443,  465,  495. 

MoRisoN,  384. 

MORITZ,  151. 

MoRNER,  90,  378. 

MoROUX,  364. 

MOSER,  180. 

MouRSON,  455. 

MoxoN,  398. 

MuLAT,  398. 

MtJLLER,  Fr.,  150,  170,  183,  252,  312,  313, 

314,  340,  359. 
MiJLLER,  Johannes,  107. 
MuLLER,  O.   166,  218. 

MULLERHEIM,    R.,  288. 
MUNNICH,  319. 

MuNZER,  339,  352,  378. 

MuRCHisoN,  167,  185,  187,  348,  414,  4l7. 

MURRELL,  Wm.,  168,  218. 

MussER,  J.  H.,  166.  185,  218,  397,  407. 

Myeh,  117. 


INDEX  OF  AUTHORS 


793 


Nauheim,  300, 

Naunyn,  177,  196,  329,  330,  331,  381, 
400,  402,  421,  424,  427,  429,  430,  432, 

434,  444,  499,  502,  507,  508,  509,  539. 
Nauwerck,  161,  218,  333,  339. 
Neisser,  416. 

Nencki,  377,  638. 

Neumann,  215,  339,  384. 

Neumeister,  644. 

Neusser,  E.,  409,  413,  426,  427,  429,  432, 

435,  436,  437,  464. 

NiCXJLADONI,  419. 
NiEWERTH,  407. 

Nikola YSEN, 213. 
NiKousKi,  690,  691. 

NiRENSTEIN,  121. 
NiSSEN,  211. 
NOLTE,  164. 

V.  NooRDEN,  91,  252,  313,  327,  378,  786. 

North,  440. 

NoTHNAGEL,  H.,  41,  225,  242,  243,  313, 
343,  422,  435,  524,  541,  571,  593,  594, 
605,  618,  622,  627,  631,  658,  670,  671, 
677,  ,679,  708,  715,  735,  740,  741,  742, 
744,  745,  748,  751. 

Obolensky,  371. 
Obrastzow,  248,  264,  590. 
Oderfeld,  213. 
Oeder,  731,  734. 
V.  Oefele,  652. 
Oertel,  278. 
Oestreich,  180. 
Ohloff,  397,  400. 
Ollivier,  386,  417. 
V.  Openchowski,  160,  218. 
Opie,  308,  318. 
Oppler,  97,  231. 
Oppolzer,  446. 
Ord,  W.,  207,  218. 
Orth,  362,  444,  689. 
Ortner,  426,  427,  429,  432. 
OsER,  41,  435. 
OSLER,  183. 
OSTERSPEY,   181,  218. 

Ostertag,  277. 

Pariser,  170,  186,  205,  207,  214,  218. 

Parish  97. 

Paulicki,  167,  219. 

Pawlow,  87,  95,  100,  102,  109,  117,  128, 

129,  304,  305,  377,  635. 
Pean,  221. 


Peiper,  E.,  454. 

Penski.  452. 

Penzoldt,  44,  289. 

Perez,  Akimow,  109. 

Perls,  443,  444. 

Peter,  485. 

Petersen,  212,  213,  219. 

Petit,  408. 

Petruschky,  193,  219. 

Pfaundler,  131. 

Pfluger,  311. 

Pfuhl,  339. 

Pfungen,  102. 

Phillips,  Rees,  281. 

Pic,  409,  430,  434. 

Pick,  A.,  296,  348,  468. 

Pick,  Fr.,  364,  380,  502,  503. 

PiLLIET,  439. 

Pisenti,  321. 
Plantenga,  201. 
Platter,  N.   186,  219. 
Ploss,  40. 
Podrou2ek,  441. 
Ponfick,  452. 
PORGES,  500. 
POSNER,  287. 

Posselt,  460. 
Pott,  327. 
Powell,  177. 
PftESCH,  B.,  289. 
Pribram,  312. 
Price,  368. 
Pringle,  414. 

PUPIER,  370. 
QUEIROLO    138. 

QuENU,  228,  432. 

Quincke,  73,  341,  366,  367,  375,  393,  394 
411,413,438. 

Ramskill,  408. 

Ranvier,  397. 

Raudnitz,  606. 

Reclus,  438. 

Regnard,  502. 

Regnier,  438. 

Reich,  43. 

Reichard,  179,  219. 

Reichmann,  118. 

Reinert,  181. 

Reinhard,  R.  219. 

R6MOND,  106,  107,  140. 

Rencki,  R.,  181,  213,  219,  233. 


794 


INDEX  OF  AUTHORS 


Renon,  210. 
Renvers,  24,  576. 
Renzi,  315. 
Rewidzoff  235. 
Rheinstein,  402. 
Rheinwald,  168,  172,  219. 

RiBBERT,  400. 

Richard,  407. 

RiEDEL,  397,  400,  404,  414,  465,  466,  471, 

472,  488,  500,  501,  505,  542,  543,  547, 

550,  553,  555,  570. 
RiEGEL,  F.,  64,  65,  73,  89,  90,  100,  104, 

111,  113,  114,  116,  118,  121,  122,  173, 

219,  228. 
RiEss,  239,  352,  420. 

RiNDFLEISCH    444. 
RiTTEH,  411. 

RizET,  338. 

Roberts,  398. 

Robin,  232. 

RoBsoN,  Mayo,  214,  219,  414. 

Rockwell,  79. 

Rodman,  177. 

Roger,  337,  377,  383. 

Rogner,  492. 

ROHMANN,  327. 

Rohmer,  384. 

RoKiTANSKY,  160,  237,  442,  500,  509. 

ROLLET,  446. 

Romberg,  298. 

Rose,  289. 

Rosenbach,  O.,  87. 

Rosenberg,   Siegfried,   311,   314,   315, 

316,  317. 
Rosenheim,  Th.,  1,  43,  83,  104,  118,  121, 

213,  219,  228,  232,  235,  237,  267,  268, 

313,  581,  747. 
Rosenstein,  331,  344,  368,  381,  386,  387, 

395. 
Rosenthal,  40,  439,  561. 
Rosin,  113,  326. 
RossEL,  174,  210. 
RossoNi,  211. 
RosT,  118,  201. 
Rotch,  417. 
Roth,  93,  500. 
Rothmann,  O.,  738. 
Rotter,  548. 
Roux,  218. 
RowsiNG,  281. 
Rxibner,  719. 
RuMPFF,  H.,  296,  298,  364. 

RUTIMEYER,  232. 


RuYSCH,  443. 
Rydygier,  221,  293. 

Sabourin,  367,  444,  450. 

Saburin,  Giles,  166. 

Saccharjin,  382,  387. 

Sachs,  177,  178. 

Sahli,  93,  215,  316,  317,  542,  544,  551, 
554,  595. 

Saint-Vel,  347. 

Samoilowicz,  334. 

Sandmeyer,  307,  311,  315. 

Sanger,  440. 

Saylor,  233. 

schachmann,  367,  386. 

Schiff,  95,  121,  232,  311,  377. 

schiffer,  40. 

Schittenhelm,  378. 

Schlagdenhauffen, 455. 

Schlange,  538. 

Schlatter,  257. 

Schlesinger,  231,  232. 

Schliep,  43. 

Schloffer,  194,  195,  219,  260. 

Schloth,  414. 

Schmauss,  174. 

Schmidt,  A.,  67,  100,  101,  110,  161,  219, 
296,  327,  487,  605,  606,  616,  617,  618, 
619,  621,  623,  625,  626,  627,  628,  630, 
638,  639,  653,  676,  741,  742,  743. 

Schmidt,  F.,  443. 

Schneider,  104,  172. 

Schneyer,  233. 

schnirer,  267. 

SCHORER,  39. 

Schorlemmer,  120,  618. 

Schott,  292. 

Schreiber,  24,  28,  30,  113,  715. 

Schreuer,  100. 

Schroder,  400,  700. 

V.  Schrotter,  713. 

V.  Schrotter,  Sr.,  180. 

Schuh,  439. 

ScHtJLE,  100,  102,  104,  105. 

SCHULTZE,  352. 

ScHULZ,  J.,  200,  219. 

ScHULZE,  Walter,  308,  309. 

ScHiJpPEL,  397,  400,  407,  408,  415    419 

427,  444. 
Schutz,  194,  219,  640,  665. 

SCHWARZ,  219. 

Schweninger,  278. 
Schwimmer,  167. 


INDEX  OF  AUTHORS 


795 


See,  G.,  207. 

Seegen,  306. 

Semmola,  381. 

Senator,  24,  29,  239,  282,  349,  352. 

Serejukow,  144. 

Sieber,  638. 

SlEBOLD,  454. 

Siegert,  400. 
SiGEL,  J.     191,  219. 
SiLBERMANN,  331. 
SiLBERMARK,    M.,  219. 
SiLBERSCHMIDT,  530,  531. 

SiMMONDS,  166,  219,  444. 
Simon,  111,  626. 
Singer,  G.,  593. 
SiPPY,  B.  W.,  24. 
Sjoquist,  378. 
Sklifosowski,  438. 
Smolenski,  407. 
SociN,  29,  404,  408,  438. 

SOETBEER,  352. 
SOHLERN,  163,  219. 
SOLOWIEFf,  363. 

SoNNENBURG,  525,  526,  544,  590. 

SORENSEN,    140. 

SouPAULT,  173,  339. 

Spicker,  184,  219. 

Spirack,  137. 

Stadelmann,  E.,  330,  331,  355,  361,  386, 

394,  395,  454. 
Stahl,  Georg  Ernst,  713. 
Stargard,  112. 
Steffen,  439. 
Steinhaus,  379. 
Stepp,  219. 
Stern,  162,  219,  329. 
Stiller,  264,  275. 
Stirl,  339. 

Stokes,  W.,  161,  407,  419. 
Stoll,  397,  443. 

Strasburger,  J.,  605,  606,  621,  639,  665. 
Strassmann,  370. 
Strauss,  87,  139,  140,  152,  203,  220,  232, 

355,  370,  379. 
Struppler,  167,  220, 
Stumm,  443. 
SURRE,  373. 
van  Swieten,  443. 
Szubinski,  333. 

Tait,  404. 

Takayasu,  319. 

Talamon,  166,  220,  574,  577,  584. 


Talma,  S.,  162,  220,  384. 
Tarchetti,  198,  228. 
Tavel,  541. 
Taylor,  233,  403. 
Teichmann,  633. 
Terillon,  440. 
Terrier,  258,  432. 
Thornton,  414. 
Tiegel,  M.,  220. 
TiLLMANN,  384. 

Todd,  410. 

TOELG,  409. 

Toldt,  C,  295. 

Traube,  170. 

Treves,  244,  585,  587,  588,  602*  757. 

Tricomi,  443. 

Trier,  199. 

Troller,  100. 

Trousseau,  470,  677. 

TUFFIER,  576. 

Tyson,  398. 

Uffelmann,  119. 
Ughetti,  365,  367. 
Ury,  626. 

Vassale,  161. 

Vater,  465. 

Vedova,  Dalla,  162,  220. 

Veit,  348. 

van  den  Velden,  231. 

Vierordt,  O.,  460,  513,  528,  534. 

ViLLARD,  397,  398. 

ViLLE,  311. 

ViRCHOw,   187,  240,  263,  282,  294,  439, 

444,  454,  615. 
VoLHARD,  93,  152,  652. 
Voss,  398. 
VuLPius,  294. 

Wagner,  204,  364,  670. 
V.  Wahl,  538,  766. 
Walko,  110,  207,  208,  220. 
Wardell,  419. 
Warnecke,  Frz.,  220. 
Weber,  230. 
Wegner,  370,  530,  531. 
Weigert,  361,  364,  444. 
Weil,  338,  339,  548. 
Weinberger,  96. 
Weintraud,  316,  369,  378. 
Weir,  214. 
Weisker,  408. 


796 


INDEX  OF  AUTHORS 


Weiss,  M.,  22a 
Wernich,  677. 
Wertheimer,  305. 
West,  183. 

Westphalen,  108,  709. 
Wharton,  185. 
White,  414. 
Whiteford    H.,  214. 
Whitehead,  677. 
Wiedemann,  397. 
WiEGERT,  Karl,  689. 
Wieland,  E.,  531. 

WlJNHOFF,  402. 
WiLKENS,   116. 
WiLLE,  310. 
WiLLIGK,   199,  400. 

Wilson,  407,  408. 

WiNCKLER,  440. 

V.  Winiwarter,  404. 


WiNTERNITZ,  280. 
WiTTE,  176. 

WiTZEL,  29,  407,  440. 

WOLFFLER,  260,  506. 

WoLKow,  283. 

WOLKOWITSCH,  152. 
WUNDERLICH,  238,  263. 
Wyman,  37. 
Wyss,  408,  417,  419. 

Zawadzki,  167,  218. 

Zenker,  H.,  397,  400. 

ZiEGLER,  371,  444,  689  690. 

V.  ZiEMssEN,  37,  41,  42,  200,  201. 

ZlERKO,  201. 

ZoJA,  314,  316. 

Zondek,  M.,  283, 

ZUBER,  504. 

ZUCKERKANDL,  304. 


INDEX   OF   SUBJECTS 


Abdomen,  inspection  of,  224. 

pendulous,  271,  274,  277,  279,  292. 

prominence  in,  224,  226. 
Abdominal  bandage,  277. 
Abdominal  operations,  followed  by  gastric 

hemorrhage,  180. 
Abdominal  supporter,  278. 
Abdominal  viscera,  displacements  of,  263. 
Abdominal  wall,  flaccidity  of,  156. 

support  of,  289. 
Abie's  binder,  300. 
Abscess,  peri-esophageal,  2. 

psoas,  533. 
Abscesses,  encapsulated,  183. 

in  abdomen,  183. 
Absorption  of  bile,  causes  of,  334. 
Absorption  of  food,  635. 
Acetone,  9,  239,  252. 
Achlorhydria,  93,  94. 
Acholia,  341. 

intestinal,  without  jaundice,  497. 
Achylia,  64,  128,  643. 

chronic,  233. 

diagnosis  of,  76. 
Achylia  gastrica,  76,  231,  255,  653. 
Acid,  acetic,  636. 

aceto-acetic,  9. 

butyric,  636. 

caproic,  636. 

caprylic,  636. 

ethyl  sulphuric,  638. 

formic,  636. 

lactic,  in  intestinal  canal,  636. 

nucleinic,  639. 

propionic,  636. 

salicylic,  640. 

in  cholelithiasis,  505. 

succinic,  636. 

sulphuric,  in  urine,  503, 

tanrocholic,  640. 

valerianic,  636. 
Acidity  of  stomach,  172. 
Acidobutyrometric  test,  93. 
Acidosis  in  acute  yellow  atrophy,  352. 
Acids,  biliary,  640. 

organic,  in  intestinal  canal,  636. 

volatile  fatty,  67. 
Acute  yellow  atrophy  of  liver,  342. 
Adenocarcinoma,  196,  237,  260. 
Adhesions,  causing  fatal  intestinal  occlu- 
sion, 183. 

perigastric,  197. 

due  to  gall-stones,  505. 


Adrenalin  in  gastric  ulcer,  210. 
Air  in  peritoneal  sac,  536. 

in  stomach,  133. 
Air-pump,  39. 
Alanin,  352. 

Albumin  decomposition,  9. 
Albumin  digestion  in  pancreatic  disease, 

315. 
Albumin  fat  diet,  152. 
Albumin  in  the  diet,  110,  118. 
Albuminuria,  286. 

Albumoses  in  acute  yellow  atrophy,  352. 
Alcohol,  as  cause  of  hematemesis,  177. 

as  gastric  stimulant,  102. 

effect  of,  on  stomach,  130. 

forbidden  in  dilatation,  153. 

use  of,  in  gastroptosis,  279. 
Alcoholism,  chronic,  97. 
Algesimeter,  use  of,  169. 
Alkalies,  beneficial  effects  of,  206. 

for  gastric  dilatation,  156. 

for  hypersecretion,  118, 

in  hyperacidity.  111. 
Alkaline  intestinal  digestion,  129. 
Alkaline  waters  for  washing  of  stomach,  38. 
Alkaloids,  cadaveral,  643. 
Almond  milk  in  gastric  ulcer,  208. 
Aloin  test,  174. 

Amaurosis  from  hemorrhage,  177. 
Amyloidosis,  312. 

Amylolysis,  37,  89,  99,  105,  112,  652. 
Amylorrhea,  652. 
Amylorrhexis,  89,  105. 
Anacidity  of  stomach,  93. 
Anastomosis,  production  of,  in  stomach, 

213. 
Anemia,  as  cause  of  gastric  atony,  127. 

as  cause  of  gastric  ulcer,  161. 

extreme,  in  gastric  ulcer,  200. 

from  gastric  hemorrhage,  177. 

producing  atony  of  stomach,  73. 

neuroses  of  secretion  in,  76. 

treatment  of,  by  gastric  lavage,  44. 

with  stenosis  of  esophagus,  75. 

without  cachexia,  97. 
Anesthesia,  examination  under,  235. 

followed  by  gastric  dilatation,  145. 

in  esophageal  disease,  22. 

in  esophageal  sounding,  30. 
Aneurysm,  9. 

aortic,  2,  18,  49. 
perforation  of,  42. 

in  gall-stone  disease,  487. 
797 


798 


INDEX  OF  SUBJECTS 


Angina  pectoris  in  gastric  ulcer,  170. 
Angina  pectoris,  simulated  by  esophageal 

pain,  5. 
Angiomata  in  carcinoma,  224. 
Anorexia,  71. 

in  gastrectasis,  152. 
treatment  of,  48. 
Antibodies  to  intestinal  bacteria,  637. 
Antifat  cure,  corset  for,  277. 
Antifat  treatment,  271. 
Antisepsis  and  asepsis,  236. 
Antrum  of  stomach,  marked  development 

of,  56. 
Anus,  artificial,  262. 
Aorta,  abdominal,  pulsation  of,  292. 
dilatation  of,  8. 
perforating  aneurysm  of,  177. 
Apepsia,  643,  653. 

Apepsia  gastrica,  89,  91, 92, 94,95;  see  also 
Subacidity. 
diagnosis  of,  120. 
Aperients,  physiologic,  254. 
Appendicitis,  513. 

changes  in  the  serosa  in,  542. 
chronic,  causing  relapse,  555. 
diagnosis  of,  .564. 
recurrent,  574. 
relapsing  form  of,  574. 
without  fecal  calculus,  course  of,  555. 
congestive  hyperemia  following  opera- 
tion for,  545. 
due  to  fecal  impaction,  541. 
fecal  calculus  in,  treatment  of,  570. 
from  "relapses"  of  wall  of  appendix, 

541. 
modifications  in  the  course  of,  543. 
operation  for,  272. 
opium,  use  of,  in,  570. 
pathological        conditions        producing 

symptoms  of,  549. 
perforation,  symptoms  of,  in,  553^. 
purgation  in,  570. 
pus,  absorption  of,  after  operation  for, 

545. 
relation  of  mild  and  severe  changes  in 

the  appendix  in,  543. 
septic  thromboses  of  venous  trunks  in, 

545. 
suppuration  in,  543. 
Appendicitis  granulosa,  542,  543,  554. 
Appendicitis  simplex,  symptoms  of,  553. 
Appendicular  colic,  584. 

cause  of,  584. 
Apt)endix,  acute  distributed  gangrene  of, 
541. 
angina  of,  542, 
changes    of,    in    chronic    perityphlitis, 

.577. 
diseases  of,  dvie  to  bacteria,  541. 

with  gradual  onset,  541. 
empyema  of,  547. 
gangrene  of,  181,  541. 
inflammation  of,  528,  533. 
mesenteriolum,  implication  of,  in,  542. 
normal  contents  of,  577. 
normal  position  of,  576. 
palpation  of,  287. 


Appendix,  position  of,  in  relation  to  peri- 
tonitis, 540. 

relation  of,  to  neighboring  organs,  577. 

serosa  of,  changes  in,  542. 

shape  of,  577. 

the  seat  of  "chronic  catarrh"  of  the 
mucous  membrane,  542. 
Appetite,  capricious,  134. 

in  esophageal  diseases,  5. 

loss  of,  255. 

stimulation  of,  253. 
Appetizers,  value  of,  101. 
Arsenic  in  gastric  ulcer,  204. 
Arteries,  atheromatous,  48. 

mesenteric,  thrombosis  of,  192. 
Arteriosclerosis,  179. 
Artery,  coronary,  aneurysm  of,  177. 
Aspiration  of  gastric  contents,  106. 
Asthenia,  cardiac,  298. 
Asthma,  as  cause  of  floating  kidney,  264. 

bronchial,  508. 

catarrhal,  of  biliary  passages,  509. 

of  biliary  passages,  spasm  of  bronchial 
muscle  in,  509. 
Asthma  dyspepticum,  75. 
Atheroma,  49. 
Atonic-ectatic  conditions,  3. 
Atony,  gastric,  143. 

from  hurried  eating,  126. 

intestinal,  642. 

of  esophagus,  10. 

of  muscularis,  35. 

of  stomach,  83. 
Atrophy,  diabetic,  309. 

gastric,  232. 

of  liver,  acute  yellow,  342. 
Atropin  for  gastric  dilatation,  156. 

for  hyperacidity.  111. 

in  hypersecretion,  118. 

Bacilli,  lactic  acid,  231. 
Bacillus  proteus  fluorescens  in  Weil's  dis- 
ease, 339. 
Bacteria,  attenuation  of,  98. 

destruction  of,  in  small  intestine,  103. 

emigration  of,  from  one  organ  to  another, 
287. 

in  feces,  628. 

intestinal,  637. 

long,  120. 

number  of,  in  intestine,  639. 
Bakers,  hyperacidity  among,  108. 
Balls,  silver,  swallowing  of,  29. 
Balneotherapy  for  subacidity,  101. 
Baltic  Sea,  bathing  in,  280. 
Bandage,  as  support  to  stomach,  156. 

hypogastric,  36. 
Bard-Pic  syndrome,  320. 
Belladonna  for  gastric  dilatation,  156. 
Bellows,  distention  of  stomach  by,  137. 
Belt,  injurious  effects  of  wearing,  266. 
Bile,  mechanical  obstruction  of,  335. 

occurrence  of,  in  gastric  contents,  66. 
in  stomach,  144. 

parapedesis  of,  332. 

production  of,  quantitative  and  qualita- 
tive changes  in,  340. 


INDEX  OF  SUBJECTS 


799 


Bile,  regurgitation  of,  144-213. 

Bile  duct,  pathogenic  microbes  in,  337. 

Biliary  passages,  neoplasms  of,  396. 

Biliary  stasis,  192. 

Biliary  thrombi,  334. 

Bilious  typhoid,  347. 

Biliousness,  341. 

Bismuth  for  gastric  ulcer,  201,  203,  205, 

207. 
Bismuth   subnitrate,   use  of,   for  gastric 

ulcer,  60. 
Bismutose,  207. 

Bitter  tonics,  effect  of,  as  gastric  sprays,  59. 
Biuret  test  of  gastric  juice,  114. 
Blood,  composition  of,  in  gastric  hemor- 
rhage, 181. 
in  gastric  ulcer,  210. 
constituents  of ,  after  gastric  hemorrhage, 

176. 
from  esophagus,  11. 
in  stomach,  test  for,  230. 
in  stomach  contents,  66-96. 
in  the  feces,  174. 
in  vomitus,  135. 
inspissation  of,  36. 
vomiting  of,  190. 
Blood-mixture,  abnormal,  47. 
Blood  pressure,  increase  of,  210, 

by  gastric  lavage,  48. 
Blood-vessels,  erosion  of,  187. 
special  permeability  of,  179. 
Body,  constrained  position  of,  a  cause  of 

disease,  130. 
Bolus,  arrest  of,  in  esophageal  disease,  4. 
Borax  solutions,  irrigation  with,  38. 
Bougie,  esophageal,  passage  of,  9,  10. 

resistance  to  passage  of,  3,  11-15,  28. 
use  of,  15-17,  29. 
varieties  of,  23. 
Bowel  training,  706. 
Bowels,  state  of,  in  ectasis,  135. 
Brachial  plexus,  neuralgia  of,  170. 
Bread,  aleuronat,  roborat,  or  casein,  110. 
Breath,  offensive,  4. 
Bronzing  of  skin  in  pancreatic  disease,  317, 

318 
Bulimia,  71,  74-77. 
in  gastrosis,  81. 
therapy  of,  72. 

Cachexia,  carcinomatous,  252. 
in  esophageal  disease,  5-10. 
in  malignant  stenosis,  147. 
of  gastroptosis,  281 . 
Calculi,  hepatic.     See  Gall-stones. 

pancreatic.  72.  306. 
Cancer,  decomposition  of,  26. 
of  esophagus,  1. 

extirpation  of,  27. 

in  different  countries,  2. 

symptoms  of,  2. 

treatment  of,  27. 
of  gall-bladder,  489. 
of  stomach,  age  most  liable  to,  168. 
of  various  organs,  18. 
relation  of  trauma  to,  163. 
ulcer  as  cause  of,  10. 


Cancer  cell  nests,  6. 
Canine  gastric  juice,  102. 
Cannabis  indica,  207. 
Cannula,  permanent  use  of,  24,  26. 
Caput  Medusae,  376. 

Carbohydrates,  limitation  of,  in  dilatation, 
153. 
use  of,  in  gastric  disease,  152. 
Carbonic  acid,  inflation  of  stomach  with, 

137. 
Carcinoma,  annular  and  flat,  3. 
bloody  vomiting  in,  134. 
cicatrices  of,  131. 
colloid,  238. 

dropsical  symptoms  of,  239. 
gastric,  84,  123. 
proof  of,  233. 
removal  of,  157. 
gastric  and  intestinal,  221. 
diagnosis  of,  221. 
etiology  of,  222. 
incurability  of,  251. 
localization  of,  221. 
sudden  onset  of,  222. 
treatment  of,  251. 
lactic  acid  in,  98. 
medullary,  237. 

mortality  m  operations  for,  260. 
of  esophagus,  1. 
diagnosis  of,  8,  10. 
therapy  of,  22. 
of  gall-bladder,  489. 
of  intestine,  762. 
of  larynx,  17. 
of  pylorus,  134. 
of  rectum,  239,  245. 
of  small  intestine,  247. 

diagnosis  of,  249. 
of  stomach,  96. 

of  stomach  and  intestines,  drug  treat- 
ment of,  254. 
mortality  in,  258. 
operative  treatment  of,  256. 
of  vertebral  column,  17,  18. 
papillary,  247. 
stenotic,  250. 
umbilical,  228. 
visceral,  222. , 

objective  examination  for,  224. 
without  stenosis,  97. 
Carcinoma  ex  ulcere,  237. 
Cardia,  determination  of  position  of,  51. 
hypertrophic  stenosis  of,  24. 
insufficiency  of,  73. 
sounding  of,  30. 
spasm  of,  75. 
stenotic  ulcer  at,  194. 
tumor  in,  3. 
ulcer  of,  75. 

union  of,  with  upper  duodenum,  257. 
Cardialgia,  72. 
Cardiospasm,  24,  74. 
Carlsbad,  treatment  at,  215. 
Carisbad  cure,  112,  505. 

for  gall-stones,  505. 
Carisbad  waters  for  gastric  ulcer,  202. 
Casein  flocculi,  115. 


800 


INDEX  OF  SUBJECTS 


Catarrh,  acute  intestinal,  654. 
calomel  in,  665. 
course  of,  660. 
diagnosis  of,  661. 
etiology  of,  654. 
in  dyscrasias,  655. 
in  infectious  diseases,  655. 
pathology  of,  656. 
symptoms  of,  657. 
treatment  of,  663. 
by  drugs  in,  666. 
diet  in,  666. 
laxatives  in,  665. 
chronic  intestinal,  668. 
anemic  conditions  in,  674. 
diagnosis  of,  675. 
etiology  of,  668. 
gastric  digestion  in,  674. 
nervous  symptoms  in,  674. 
pathology  of,  669. 
symptoms  of,  670. 
treatment  of,  679. 

by  oil  enemata  in,  682. 
urine  in,  674. 
gastric,  171 ;  see  also  Gastric  Catarrh, 
intestinal,  635,  654. 

due  to  enemata,  656. 
membranous     intestinal    (see     Mucous 

Colic),  735. 
of  stomach,  chronic,  145. 
Caustics,  cicatrices  from,  131. 

esophageal  stenosis  from,  11,  13. 
Cauterization  of  esophagus,  22. 
Cecum,  carcinoma  of,  590. 

tuberculosis  of,  248. 
Cell  clumps,  intertubular,  308. 
Cell  nuclei,  digestion  of,  625. 
Cells,  hepatic,  functional  disturbance  of, 

335. 
Chalk  treatment  in  gastric  ulcer,  205. 
Charcot-Leyden  crystals,  510. 
Cheese  in  the  diet,  111. 
Chemical  findings  in  gastric  disease,  172. 
Chemical  processes  in  gastric  ulcer,  171. 
Chemism  of  stomach,  191. 
Cheyne-Stokes  respiration,  184. 
Childbirth  as  cause  of  pendulous  abdomen, 

277. 
Chlorin,  losses  of,  118. 

withdrawal  of,  87. 
Chloroform  narcosis,  127. 
Chloroform  test  for  hematin,  230. 
Chlorosis,  jis  cause  of  atony,  127. 
of  gastric  neuroses,  70. 
of  gastric  ulcer,  161. 
effect  of  marriage  upon,  274. 
gastric  lavage  in,  44. 
hyperacidity  in,  76. 
parorexia  in,  71. 
Cholangitis  catarrhalis,  329,  336. 
Cholangitis  due  to  gaU-stones,  505. 
Cholates,  640. 

Cholecystentero-anastomosis,  502. 
Cholecystitis,  etiology  of,  508. 
in  gall-stones,  471. 

simulating  chronic  perityphlitis,  595. 
Cholelithiasis,  98, 276 ;  see  also  Gall-stones. 


Cholelithiasis  as  symptom  of  pancreatitis, 
306. 
combined  with  cardiac  disease,  485. 

with  gastric  ulcer,  192. 
confounding  of,  with  chronic  perityph- 
htis,  595. 
with  gastralgia,  72,  192. 
difficulty  of  diagnosis  of  acute  enlarge- 
ment of  the  liver  in,  485. 
Cholelithiasis  intrahepatica,  499. 

jaundice  in,  468. 
Cholesterin  stones,  506,  509. 
Chyle,  mechanical  irritation  from,  197. 
Chyme  infection,  655. 
Cibophobia,  107. 
Cicatrices  in  esophagus,  12. 

in  stomach,  165. 
Cicatricial  distortion,  185. 
Cicatrization  in  gastric  ulcer,  200. 

of  esophagus,  12-13. 
Cicatrization,  tumor-like,  191. 
Circle,  vicious,  formation  of,  215,  271. 
Cirrhosis,  hepatic,  178,  179,  371. 
Cirrhosis  carcinomatosa,  445-448. 
Climate,  change  of,  benefits  of,  280. 
Cocain  for  relief  of  thirst,  26. 
Cochineal  test,  90. 
Coffee  in  the  diet,  111. 
Coins  in  esophagus,  31. 
Colic,  fecal,  647. 
flatulent,  241. 
intestinal,  710. 

stercoral,  710. 
mucous,  677,  735,  744. 

a  disease  of  middle  life,  738. 

astringents,  use  of,  in,  748. 

attacks  of  colic  in,  743. 

course  of,  740. 

diagnosis  of,  746. 

diet  in,  749. 

differentiation  of,  from  enteritis  mem- 

branacea,  745. 
due  to  peritoneal  adhesions,  737. 
etiology  and  pathogenesis  of,  736. 
influenced  by  mode  of  life,  737. 
intestinal   catarrh  of,   treatment  of, 

748. 
motor  disturbances  in,  treatment  of, 

748. 
mucous  masses  in,  740. 
bacteria  in,  742. 
basic  substance  found  in,  741. 
chemical  examination  of,  742. 
color  of,  740. 
crystals  found  in,  742. 
epithelia  included  in,  741, 
fat  in,  743. 

microscopic  examination  of,  741. 
round  cells  of,  742. 
nervous  symptoms  in,  treatment  of, 

750. 
passage  of  fecal  masses  of,  without 

colic,  744. 
pathologic  anatomy  of,  738. 
prognosis  of,  746. 

related  to  disease  of  genitalia,  736. 
structure  of  body  in  relation  to,  737. 


INDEX  OF  SUBJECTS 


801 


Colic,  mucous,  symptoms  and  course  of, 
739. 
synonyms  of,  735. 
treatment  of,  747. 
usual  in  nervous  individuals,  736. 
women  especially  predisposed  to,  736. 
wind,  647. 
Colica  mucosa,  735,  736. 
Colitis  membranacea,  735,  736. 
Colon,  catarrh  of,  656. 
chronic  catarrh  of,  588. 
displacement  of,  263,  294. 
mucus  in,  632. 

rupture  of,  from  gastric  ulcer,  183. 
spastic  contracture  of,  249. 
transverse,  dilatation  of,  44. 
solidification  of  feces  in,  294. 
surgery  of,  295. 
Coloptosis,  causes  of,  294. 
Color  reactions  in  examination  of  stomach, 

36. 
Colostomy,  239,  260,  262. 
Coma,  diabetic,  239. 

in  gastric  dilatation,  142. 
Coma  carcinomatosum,  239,  250. 
Common  gall-duct,  chronic  obstruction  of, 
by  stone,  407. 
by  tumors,  406. 
clinical  forms  of,  406-^15. 
diagnosis  of,  424. 
differential  diagnosis  of,  436-^38. 
due  to  catarrhal  jaundice,  409. 
pathology  of,  415-423. 
Compresses,  hot,  in  gastric  ulcer,  201. 
Condiments,  benefits  from  use  of,  100. 
Condurango  as  gastric  spray,  59. 
Condylomata,  7. 
Congenital  predisposition  from  habits  of 

ancestors,  108. 
Congestion  hepatique,  486. 
Congo  paper  and  reaction,  90,  91,  120. 
Constipating  diarrhea,  672. 
Constipation,  704. 
alimentary,  706. 
as  cause  of  hyperacidity,  112. 
causes  of,  286,  294. 
chronic,  107-108,  705. 
diet  in,  279. 
due  to  adhesions,  704. 

to  dilatation  of  colon,  706. 
to  drugs,  706. 
to  lack  of  exercise,  707. 
to  limited  ingestion  of  food,  707. 
to  sphincter  spasm,  708. 
flatulency  of,  710. 
habitual,  705. 

astringents  in,  avoidance  of,  721. 
atonic  spastic  form  of,  709. 
autointoxication  in,  711. 
bowel  movement  in,  714. 
cure  of,  717,  722. 
diagnosis  of,  713. 
diet  in,  717,  729. 
diet  list  for,  722. 

due  to  carcinoma  of  intestine,  714. 
to  colitis,  714. 
to  stenosis  of  pylorus,  714. 


Constipation,  habitual,  duration  of,  716. 
effect  of  curative  measures  on,  716. 
etiology  of,  705. 
exercise  in,  importance  of,  718. 
exploratory  irrigation  of  intestine  in, 

714. 
feces  in,  examination  of,  714. 
flatulency  in,  723. 
food  in,  absorbability  of,  720. 

mechanical  effects  of,  719. 
foods  stimulating  the  intestine  in,  718. 
fragmentary  bowel  movement  in,  710. 
intestinal  atony  in,  714. 
intestines  in,  examination  of,  714. 
kidneys  in,  711. 
laxative  remedies  in,  721. 
mineral  waters  of  use  in,  726. 
muscular  activity  of  large  intestine  in, 

709. 
neurasthenia  combined  with,  711. 
prophylaxis  of,  717. 
propulsion  of   intestinal  contents  in, 

709. 
rectal  examination  in,  714. 
rest  cure  for,  729. 
spastic  form  of,  709. 
sports  useful  in,  725. 
stercoral  diarrheic  form  of,  710. 
subcutaneous  injections  in,  729. 
symptoms  of,  709. 
treatment  of,  716. 
electricity  in,  724. 
enemata  of  oil  in,  727. 
glycerin  in,  728. 
gymnastics  in,  724. 
hydrotherapeutic,  725. 
injections  per  rectum  in,  727. 
laxative  teas  in,  726. 
massage  of  abdomen  in,  724. 
purgatives  in,  725,  730. 
hereditary,  706. 
in  esophageal  disease,  5. 
in  pancreatic  disease,  320. 
intestinal  colic  of,  710. 
physiologic,  704. 
psychogenous,  707. 
relief  of,  by  gastric  lavage,  43. 
spastic,  677. 
Constipation  tint,  673. 
Convalescence  from  gastric  ulcer,  204. 
Coprology,  651. 
Copropoesis,  641. 
Coproscopy,  651. 
Coprostasis,  240. 
Cor  bovinum,  18. 

Cor  mobile,  295;  see  also  Heart,  displace- 
ment of. 
Corde  colique,  275. 

Corset,  as  cause  of  gastroptoais,  266,  270, 
273,  276. 
for  floating  kidney,  289. 
improved  form  of,  277. 
Coryza  vasomotoria,  508. 
Cough,  shock  produced  by,  273. 
Cough  in  disease  of  esophagus,  4. 
Coughing  as  cause  of  displacement  of  ab- 
dominal viscera,  264. 


CCLLlieiE  01 


802 


INDEX  OF  SUBJECTS 


Cranberry  test,  140. 

Cream,  use  of,  in  gastric  disease,  152. 

Cream  in  the  diet,  152. 

Creosote  for  gastric  dilatation,  156. 

Cricoid  cartilage,  neoplasm  of,  5. 

Crises,  gastric,  72,  222. 

of  spinal  origin,  58. 
Cruveilhier's  description  of  gastric  rigidity, 

225. 
Currant  test,  106,  115,  116,  140. 
Curvature,  small,  tumor  of,  227. 
Cyanosis,  48. 

Cystic  tumor  in  pancreatic  disease,  320. 
Cystinuria,  644. 

Debility,  motor  gastric,  122. 
Decomposition,  products  of,  in  esophagus, 

11. 
Decomposition  of  food  in  esophagus,  4. 
Defecation  as  cause  of  gastric  perforation, 

184. 
Defense  musculaire,  517. 
Deficient   carbohydrate  digestion  in  dis- 
ease of  pancreas,  317. 
Deij;eneration  of  the  liver,  lactic  acid  in 

urine  of,  352. 
Deglutition,  difficulty  in,  75. 

lUsturbance  of,  1,  3-28. 

obstruction  to,  5. 

recurring  disturbances  of,  13. 
Dejecta,  offensive,  175. 

watery,  from  silver  nitrate,  206. 
Delirium  from  hemorrhage,  177. 
Depression,  influence  of,  on  stomach,  73. 

mental,  82. 
Dermatol,  207. 
Dextrin  in  feces,  612. 

in  subacidity,  102. 
Dextro-rotary  substance,  94. 
Diabete  bronz^,  318. 
Diubete  maigre,  306. 
Diabetes,  306. 

experimental  pancreatic,  309. 

experimentally    produced    in     animals, 
306. 
Diabetic  milk,  101. 
Diaphragm,  descent  of,  278. 

rupture  of  gastric  ulcer  into,  183. 
Diarrhea,  635;  see  also  Intestinal  Catarrh. 

acid,  641. 

a  symptom  of  intestinal  dyspepsia,  635. 

chronic,  varices  in,  708. 

chronic  intermittent,  97. 

diagnosis  of,  650. 

due  to  cold,  646. 

to  organic  acids,  636. 

etiolog\'  of,  644. 
laxatives  in,  645. 

fat,  652. 

fetid,  641. 

from  secretory  disturbance,  87. 

intercurrent,  671. 

jejunal,  627. 

nervous  influences  in,  645. 

nnctiirn;il,  (>64. 

•  irisr'm  of  term  of,  635. 

prolonged.  196,  671. 


Diarrhea,  reaction  of,  upon  nervous  eys- 
tem,  649. 

reflex,  646. 

relation  of,  to  subacidity,  103. 

relief  in,  by  gastric  lavage,  44. 

stercoral,  710. 

symptoms  of,  647. 

tendency  to,  97. 

true,  636. 
Diathesis,  uric  acid,  594. 
Diet,  albuminous,  78. 

bland,  in  esophageal  disease,  21. 

concentrated,  in  gastric  ulcer,  203. 

in  carcinoma,  252. 

in  constipation,  722. 

in  gastric  dilatation,  150. 

in  gastroptosis,  274,  278. 

in  subacidity,  99. 

in  ulcerative  carcinomata,  254. 

meat,  78. 

mixed,  results  of,  173. 

monotonous,  causing  repugnance,  85. 
injurious  effects  of,  128. 

regulation  of,  in  nervous  dyspepsia,  86. 

vagaries  of,  85. 

vegetable  or  lacto-vegetable,  110. 
Diet  schemes,  44. 
Dietetics  in  diseases  of  «6tomach,  38. 

in  esophageal  diseases,  19. 
Digestion,  condition  of,  during  menstrua- 
tion, 49. 

in  oral  cavity,  94. 

in  small  intestine,  129. 

insufficient,  of  food,  635. 

processes  of,  635. 

prolonged,  146. 

rapid,  106. 

time  necessary  for,  64. 
Dilatation,  atonic,  145. 

atonic  and  mechanical,  143,  147. 

gastric,  35,  64. 
diagnosis  of,  44. 

from  central  nervous  influences,  130. 
loss  of  fluids  in,  36. 

of  stomach,  122. 
Dilation  of  esophagus  by  silver  balls,  29. 
Dimethylamidoazobenzol,  120. 
Dimethylamidoazobenzol  paper,  90. 
Discharge,    muco-purulent,    from    esoph- 
agus, 8. 
Dittl's  crises,  286. 
Diversion,  beneficial  effects  of,  83. 
Diverticula,  2. 

Diverticulum  of  esophagus,  10,  13,  30. 
Dogs,  experiments  in,  108,  109. 

gastric  experiments  in,  161,  162. 
Dorsal  decubitus  after  operations,  effects 

of,  127. 
Douche,  internal,  of  stomach,  43. 

Scotch,  154. 

varieties  of,  154. 
Douches,  use  of,  154. 
Dress  reform,  276. 
Dropsy  of  gall-bladder,  488. 
Drugs,  inhibition  of  secretion  by,  111. 
Drjing  of  nerve  and  muscle,  36. 
Duct,  pancreatic,  occlusion  of,  311,  314. 


INDEX  OF  SUBJECTS 


803 


Ductus  choledochus,  304. 
Ductus  Santorini,  304. 
Ductus  Wirsungianus,  304. 
Duodenojejunal  boundary,  127. 
Duodenum,    arterio-mesenteric   invagina- 
tion of,  126. 
cancer  of,  247. 
chronic  stenosis  of,  759. 
compression  of,  127. 
dislocation  of,  127. 
ulcer  of,  175,  198. 
Dyspepsia,  69. 

as  symptom  of  nephroptosis,  285. 
gastric,  643. 
intestinal,  635. 

differentiation  of,  from  intestinal  dis- 
eases, 635. 
intestinal  fermentative,  619,  653. 

symptoms  of,  620. 
nervous,  79,  145,  185;  see  also  Gastrosis. 
confounded  with  gastric  carcinoma, 

84. 
diagnosis  of,  82. 
prognosis  of,  85. 
symptoms  of,  81. 
therapy  of,  85. 
tonic  measures  for,  86. 
Dysphagia,  10,  11,  14,  18. 
from  carcinoma,  21. 
in  esophageal  disease,  2,  27. 
intermittence  of,  15. 
sudden  appearance  of,  15. 
with  fluid  food,  15. 
Dyspnea  in  esophageal  disease,  5. 
Dyspnea  on  taking  food,  5. 
Dystopia,  renal,  288. 

Ectasis,  122;  see  also  Gastric  dilatation. 

chronic,  129. 

combined  with  hypersecretion,  128. 

diagnosis  of,  143. 

from  mechanical  hindrance,  130. 
Edema  of  extremities,  177. 
Effervescing  mixture,  137. 
Eggs,  use  of,  in  gastric  disease,  151. 
Electricity,    application   of,    to   stomach, 
154. 

in  gastroptosis,  280. 

in  neuralgia,  72. 
Emaciation,  33. 

as  cause  of  cor  mobile,  296. 
of  nephroptosis,  284. 

as  symptom  of  visceral  cancer,  222. 

from  gastric  neurosis,  82. 

in  ectasis,  135. 

in  esophageal  diseases,  19,  26. 

in  gastric  disease,  197. 

in  pancreatic  disease,  320. 

leading  to  intestinal  immobility,  127. 

rectal  nourishment  in,  152. 
Emboli,  bacterial,  161. 
Embolism  of  mesenteric  arteries,  192. 
Emetic  for  removal  of  foreign  body,  31. 
Emphysema  as  cause  of  floating  kidney, 

264. 
Empyema  from  gastric  ulcer,  183. 
Empyema  of  the  appendix,  547. 


Enemata,  nutritive,  152,  254. 
in  gastric  ulcer,  201. 
of  urine,  36. 

value  of,  in  esophageal  disease,  26. 
Enteritis  membranacea,  735,  736,  745. 

diet  in,  749. 
Entero-anastomosis,  260. 
Enteroptosis,  127,  263. 

combined  with  displaced  spleen,  292. 
Enterostomy,  213,  215. 
Enzymes,  absence  of,  from  gastric  con- 
tents, 230. 
of  gastric  juice,  36. 
Eosinophilic  cells  in  vomitus,  495. 
Epithelial  cells  in  gastric  contents,  67,  70. 
Epithelial  thickening,  7. 
Ergot  in  gastric  ulcer,  209. 
Erosion,  hemorrhagic,  160,  185. 
in  stomach,  97. 
of  esophagus,  16. 
Eructations,  81-85. 
acid,  77-78. 
of  gas,  73,  134. 
treatment  of,  27. 
Eruptions  due  to  diarrhea,  650. 
Erythrodextrin,  99. 
Esophageal  disease,  malignancy  of,  2. 
Esophagismus  in  various  diseases,  14. 
Esophagoscope,  use  of,  7,  9,  11,  12,  14,  15, 

19,  23,  26,  27,  28. 
Esophagoscopy,  1,  17,  31. 
Esophagotomy,  28,  30. 
Esophagus,  affections  of,  1. 
annular  narrowing  of,  7. 
atony  of,  18,  21. 
auscultation  of,  9. 
benign  dilatation  of,  10. 
cancer  of,  18,  19. 
carcinoma  of,  6,  21. 
cicatrices  of,  28. 
cicatricial  stricture  of,  27. 
combination  of  diseases  of,  16. 
compression  of,  8,  17. 

from  disease  of  neighboring  organs,18 
symptoms  of,  18. 
congenital  stenoses  of,  16. 
constriction  of,  3,  11,  15. 
deviation  of,  17. 

dilatation  of,  4,  12,  24,  25,  28,  75. 
diseases  of,  diagnosis  of,  11. 
capillary  hemorrhage  in,  8. 
nutrition  in,  20. 
diverticulum  of,  18. 
erosion  of,  31. 
examination  of,  6,  8,  15. 
fissure  of,  31. 
forced  probing  of,  19. 
foreign  bodies  in,  16,  17,  31. 
hemorrhage  from,  178. 
hyperesthesia  of,  18,  21. 
hypertrophy  of,  4. 
impermeability  of,  14,  15,  17,  27, 
induration  of  wall  of,  7. 
infiltration  of,  7,  8,  18,  19. 
inflammation  of,  3,  41. 
inflammatory  ulceration  of,  11. 
injection  of,  13. 


804 


INDEX  OF  SUBJECTS 


Esophagus,  inspection  of,  8. 
irrigation  of,  27,  31. 
laceration  of,  29. 
lavage  of,  22. 
local  irritation  of,  21. 
mechanical  obstruction  of,  3,  21. 
muscular    and   nervous  apparatus    of, 

21. 
narrowing  of,  7. 
nervous  disturbances  of,  10. 
nodules  in,  7. 
obstruction  of,  30. 
occlusion  stenosis  of,  16. 
organic  stricture  of,  24. 
paralysis  of,  18. 
passage  of  sound  in,  6. 
perforation  of,  5. 

by  aneurysmal  rupture,  177. 
permeability  of,  29. 
probing  of,  3,  22. 

results  of,  18. 
pulsation  of,  8. 

respiratory  displacement  of,  8. 
rupture  of,  177. 
sounding  of,  75. 
spasm  of,  10,  11,  14,  21. 
spastic  contracture  of,  30. 
stenosis  of,  1,  10,  11,  27,  75. 

causing  regurgitation  of  food,  74. 
from  foreign  bodies,   16. 
stenosis  of  lumen  of,  1. 
stricture  of,  26. 
dilatation  of,  22. 

following  scarlatinal  diphtheria,  13. 
ulcer  in,  13. 
ulceration  of,  28. 
use  of  cannula  in,  24. 
weakness  of,  21. 
Eucain  in  esophageal  disease,  22. 
Eucain  to  produce  anesthesia,  31. 
Examination,  physical,  in  esophageal  dis- 
ease, 0. 
in  gastric  disease,  133. 
Excrescences,  papillary,  7. 
Expiratory  immovability  of  pyloric  tumors, 

227. 
Eyes,  specks  before,  71. 

Fades  hippocratica,  183. 

Family  cholemia,  348. 

Fan-douche,  154. 

Faradic  current  applied  to  stomach,  154. 

Fat,  abdominal,  disappearance  of,  264. 

administration    of,    in    esophageal    dis- 
ease, 20. 

as  inhibiting  gastric  juice,  109. 

deficient  splitting  of,  624. 

in  the  diet,  110,  117,  206,  279. 

in  the  feces,  312. 
Fat  digestion,  311. 

disturbance  of,  314. 
Fat-splitting,  305,  311. 

diminished  in  disease  of  pancreas,  313, 
315.  317. 
Fats,  use  of,  in  gastric  disease,  151. 
Fattening  cure,  279. 
Fecal  masses,  removal  of,  43. 


Fecal  vomiting,  manner  of  occurrence  of, 

768. 
Feces,  acid  reaction  of,  653. 

admixture  of,  with  blood,  mucus,  and 

pus,  244. 
albumin   in,    decreased   absorption   of, 

625. 
altered  blood  in,  632. 
apparatus  for  fermentation  test  of,  620. 
biliary  coloring  matter  in,  demonstra- 
tion of,  624. 
blood  in,  190,  232. 
carbohydrates  in,  619. 
cells  from  asparagus  fibers  in,  614. 
cells  of  beans,  peas,  and  lentils  in,  612. 
chemical  examination  of,  174. 
connective  tissue  in,  616. 
containing  bismuth,  confusion  of,  with 

hemoglobin,  633. 
containing  elastic  fibers  in  remains  of 

animal  food,  615. 
corrosive  sublimate  test  of,  for  biliary 

coloring  matter,  626. 
decomposition  of,  619. 
dissolved    albumin  in,   importance  of, 
625. 
test  for,  626. 
examination  of,  244,  246,  605. 
after  administration  of  pankreon,  625. 
chemical,  necessity  of,  623. 
diet  in,  606. 
duration  of  ingesta  in  gastrointestinal 

tract,  608. 
duration  of  restricted  diet  in,  608. 
food  remains  commonly  found  in,  611. 
for  pyogenic  cocci,  498. 
importance  of,  605. 
important  considerations  in,  609. 
in  nurslings,  605. 
indication    of    digestive    disturbance 

in,  616. 
intestinal  fermentative  dyspepsia,  in, 

indication  of,  619. 
macroscopic,  609. 

coarse  particles  in,  610. 
undigested  constituents  in,  610. 
methods  of,  for  determining  amount 

of  digested  meat,  618. 
microscopical,  175. 

of  muscle  fibers  in,  617. 
obtaining  specimen  for,  606. 
rapidity  of   intestinal  passage  ascer- 
tained by,  608. 
showing  gastric  affection,  616. 
Teichmann's  hemin  test  in,  633. 
test  diet  in,  607. 
modification  of,  608. 
Weber-van  Deen,  633. 
fat  in,  312,  622,  624. 

causes  of  abnormal  amount  of,  623 
fermentation  of,  619. 
fermentation  test  of,  620. 
for  starch  in,  618,  619. 
positive  reaction  of,  621 
food  constituents  in,  635. 
food  in,  remains  of.  628. 
Gmelin's  test  in,  628. 


INDEX  OF  SUBJECTS 


805 


Feces,  hydrobilirubin  in,  624. 
in  cholelithiasis,  496. 
in  jaundice,  326. 

incubation  oven  test  for  starch  in,  618. 
leukourobilin  in,  624. 
mucus  and  connective  tissue  in,  differ- 
entiation of,  629. 
mucus  in,  confusion  of,  with  other  ab- 
normalities, 629,  630. 
diagnostic  importance  of,  631. 
microscopical  examination  of,  630. 
of  nurslings,  631. 

origin  of,  in  intestinal  catarrh,  631. 
muscle  fibers  in,  625. 

stages  of  digestion  of,  617. 
nucleo-proteid  of,  625. 
occult  blood  in,  test  for,  633. 
particles  of  carrot  in,  613. 
potato  cells  in,  612. 
pure  blood  upon,  632. 
pus  cells  in,  633. 
relation  of,    to   intestinal    fermentative 

dyspepsia,  620. 
remains  of  grain  from  bread  in,  612. 
of  leaf  vegetables  in,  613. 
of  meat  in,  significance  of,  617. 
shape  of,  244,  245. 

shreds  of  tissue  desquamated  in,  634. 
soaps  in,  312. 

spores  of  lycopodium  seeds  in,  614. 
starch  in,  618. 
stone  cells  of  pears  in,  615. 
tissue  shreds  in,  634. 
truffle  spores  in,  614. 
tubules  of  oranges  simulating  parasites 

in,  615. 
ustilagineous  spores,  resemblance  of,  to 
intestinal  parasites  in,  614. 
Ferment,  diastatic,  308. 
diastatic  salivary,  67. 
digestive,  69. 
glycolithic,  307. 
lab,  69. 
Fermentation,  gastric,  70. 
lactic  acid,  98. 
of  stomach  contents,  139. 
Fever,  carcinomatous,  238. 
in  pancreatic  disease,  320. 
intermittent  hepatic,  479. 
Fingers,  drumstick  changes  in,  142. 
Fissure  and  ulcer  confounded,  186. 
Fissures,  anal,  186. 
of  esophagus,  16. 
of  mucous  membrane,  186. 
Fistula,  broncho-esophageal,  27. 
gastric,  27,  29,  30. 
gastrocutaneous,  185. 
of  esophagus,  trachea,  or  bronchi,  5. 
operation  for,  257. 
Fluid,  abstention  from,  at  meals,  278. 
foamy  and  mucoid,  ejection  of,  4. 
in  stomach,  133. 

propulsion  of,  134. 
insufficient  absorption  of,  635. 
introduction  of,  into  system,  36. 
Foetor  ex  ore,  513. 
Follicular  hemorrhage,  160. 
52 


Food,  absorbability  of,  720. 

advantages  of  frequent  ingestion  of,  81. 

animal,  78. 

proper  cooking  of,  100. 

animal  and  starchy,  78. 

appetizing  preparation  of,  100. 

arrest  of,  in  esophagus,  13. 

artificial  preparations  of,  253. 

coarse,  irritation  from,  98. 

decomposition  of,  in  stomach,  63. 

deleterious  residue  of,  641. 

ejection  of,  by  coughing,  183. 

equicaloric  proportions  of,  109. 

fluid  and  pappy,  151. 

gastric  digestibility  of,  44. 

gastric  stimulation  from,  103. 

gelatinous,  100. 

indigestible  residue  of,  254. 

ingestion  of,  causing  dyspnea,  5. 

mechanical  effects  of,  719. 

percentage  of  non-absorption  of,  720. 

proper  cooking  of,  215. 

regurgitation  of,  4,  22,  73,  74. 

retention  and  decomposition  of,  34. 

spiced,  irritation  from,  20. 

stagnation  of,  in  stomach,  66,  84. 

tainted,  63. 

temperature  of,  20. 

which  stimulates  appetite,  100; 
Food  residua,  nature  of,  9.  * 

Foreign  bodies  in  esophagus,  16,  17,  31. 

obstructing  pylorus,  131. 
Freiburg  pro-rector  oration,  35. 
Fruits  in  the  diet.  111. 
Fulness,  sense  of,  after  meals,  133. 
Function,  digestive,  destruction  of,  310. 

gastric,  9,  63,  229. 

Gait  of  tabes  dorsalis,  133. 
Galante's  stomach-tube,  40. 
Gall-bladder,  dropsy  of,  509. 
inflammation  of,  533. 
neoplasms  of,  397,  398,  399. 
diagnosis  of,  403. 
duration  of,  403. 

etiology  and  pathogenesis  of,  399, 400. 
prognosis  of,  403. 
radical  treatment  of,  404,  406. 
symptoms  of,  401. 

uncertain  and  inconstant,  401. 
treatment  of,  404. 
palpable,  192. 
Gall-bladder,  stones  in,  235,  242. 
Gall-stone  colic  among  women,  192. 
Gall-stone  incarcerated  in  pylorus,  196. 
Gall-stones,  464. 

a  surgical  disease,  505. 

abscess  of  liver  in,  486. 

absence  of,  in  alcoholic  cirrhosis,  508. 

adhesions  of  the  gall-bladder  in,  474. 

albuminuria  observed  in,  501. 

alcohol  in,  abuse  of,  490. 

aneurysm  in,  487. 

ascites  in,  485. 

attack  effective  of,  472. 

attack  ineffective  of,  472. 

bacteria  in,  479. 


806 


INDEX  OF  SUBJECTS 


Gall-stones,  biliary  passages  in,  surgery  of, 
506. 

blood  in,  examination  of,  503. 

carcinoma  at  the  porta  hepatis  in,  485. 

carcinoma  of  gall-bladder  in,  486. 
differentiation   of,   from  lithiasis  in, 
489. 

Carlsbad  cure  in,  value  of,  505. 

chemical  examination  of  blood  in,  507. 

chills  in,  477. 

cholesterin  in,  507,  508,  509,  510. 

choluria  in,  presence  of,  501. 

composition  of,  501. 

constipation  usual  in  colic  of,  498. 

contraction   of  abdominal   muscles  in, 
485. 

cystic  duct  in,  closure  of,  488. 

occlusion  of,  due  to  lymph-gland,  488. 

defense  musculaire  accompanying  colic 
in,  485. 

diagnosis    of,   from    pancreatic   stones, 
477. 

diarrhea  a  symptom  of,  498. 

diet  in,  504. 

differential  diagnosis  of,  478. 

differentiation    of,    from    gastric    car- 
cinoma, 494. 

dilatation    from    cicatricial    closure    of 
choledochus  in,  495. 

dyspnea  a  symptom  of,  483. 

early  operation  in,  indications  for,  505. 

echinococci  in  incisura  hepatis  in,  489. 

echinococcus  of  the  liver  in,  484. 

enlargement  of  liver  in,  486. 

eosinophilic  cells  in  vomitus  of,  495. 

epistaxis  in,  482. 

etiology  of,  506. 

examination  of  abdomen  in,  485. 

examination  of  feces  in,  496. 

examination  of,  in  the  feces,  499. 

fate  of,  in  intestine,  500. 

fibrin  in  blood  in,  increase  of,  503. 

gall-bladder  in,  487. 

adhesion  of,  to  large  omentum,  490. 
contraction  and  displacement  of,  490. 
displacement  of,  487. 
distention  of,  a  cause  of  permanent 

jaundice,  488. 
dropsy  of,  488. 

excessive  hardness  a  symptom  of  car- 
cinoma of,  48i/. 
method  of  examination  in  tumor  of, 

489. 
tumor  of,  487. 

gastric  and  intestinal  ulcers  in,  490. 

gastric  lavage  in  treatment  of,  504. 

gastric  symptoms  in,  490. 

headache  in,  470. 

heart  in,  484. 

hematemesis  a  symptom  of,  494. 

hemorrhagic  admixture  of  feces  in,  499. 

hemorrhagic  diathesis  m,  482. 

hepatic  region  in.  auscultation  of,  487. 

humeral  theory  in  etiology  of,  507. 

hyperemia  of  the  lungs  m,  of  the  aged, 
484. 

hypothermia  in,  482. 


Gall-stones,  immotility  of  diaphragmatic 
respiration  in,  483. 

immunity  from,  in  tuberculosis,  483. 

impacted  in  the  duodenum,  492. 
near  the  ileo-cecal  valve,  493. 

in  animals,  507. 

in  cystic    and    hepatic    ducts    simulta- 
neously, 499. 

in  intestinal  mucous  membrane  a  cause 
of  diarrhea,  498. 

in  sigmoid  flexure,  493. 

in  the  aged,  477. 

indican  in  urine  of,  501. 

indigo  reaction  in,  value  of,  502. 

indolent  forms  of,  477. 

infectious  theory  in  etiology  of,  508. 

inflammatory  dropsy  of  gall-bladder  in, 
471. 

intestinal  acholia  without  jaundice  in, 
497. 

intestinal  occlusion  in,  diagnosis  of,  493. 
from  contraction  around  stone,  492. 

invaginated,  131. 

jaundice  in,  465. 

jugular  glands  in,  483. 

large,  a  contra-indication  to  operation, 
500. 
in  cecum,  492. 
in  intestines,  492. 

leucin  in  urine  of,  501. 

leukocytosis  in,  503. 

lithogenous  carcinoma  with  hemateme- 
sis and  melena  in,  494. 

lithogenous  occlusion  of  common  duct 
in,  488. 

liver  in,  485. 

local  rise  of  temperature  in  right  hypo- 
chrondrium  in,  485. 

location  of,  499. 

lungs  in,  483,  484. 

melena  a  symptom  of,  499. 

meteorism  in,  485. 

extensive,    in    volvulus    of    sigmoid 

flexure,  493. 
slight,  in  intestinal  obstruction  from, 
493. 

nervous  symptoms  in,  469. 

nocturnal  exacerbation  of  pain  in,  475. 

nucleus  of,  501. 

operation  in,  method  of,  504. 

pain  in,  471. 

treatment  of,  504. 

palpation  of,  in  intestine,  493. 

panniculus  adiposis  in,  marked  develop- 
ment of,  485. 

paroxysmal  cough  in,  483. 

passage  of,  a  sign  of  perforation,  500. 

perihepatitis  in,  486. 

peritonitis  in,  476. 

posture  of   patient    during   attack  of, 
470. 

prognosis  of,  503. 

pruritis  in,  469. 

pulse  in,  484. 

radiation  of  pain  in,  472. 

rarity  of,  in  children,  483. 

reflex  paralysis  in,  470. 


INDEX  OF  SUBJECTS 


807 


Gall-stones,  relapsing  intestinal  occlusion 
in  the  aged  in,  493. 
Riedel's  lobe  in,  489. 
rupture  of  the  diaphragm  and  pleura 

rare  in,  484. 
saUcylic  acid  of  value  in  treatment  of, 

505. 
size  of,  in  the  feces,  500. 
sodium  urate  in,  excretion  of,  501. 
spleen  in,  enlargement  of,  496. 
stercobilious  vomiting  in,  491,  493. 
subphrenic  abscess  rare  in,  484. 
sulphuric  acid  in  urine  preceding  colic 

of,  503. 
suppurative  cholangitis  in,  486. 
symptomatology  of,  464-503. 
temperature  in,  rise  of,  corresponding 

to  decrease  of  urea,  502. 
transitory  jaundice  in,  466. 
treatment  of,  504. 
tyrosin  in  urine  of,  501. 
uric  acid  in,  excretion  of,  501. 
urine  in,  amount  of,  501. 

exact  quantitative  analysis  of,  valu- 
able in,  502,  503. 
vomiting  a  symptom  of,  490. 
vomiting  of  uncontrollable  nature  in, 

491. 
vomitus  matutinus  in,  490. 
wandering  liver  in,  486. 
xanthoma  in,  469. 
Gangrene,  pulmonary,  5. 
Gas,  carbonic  acid,  as  cause  of  gastrop- 
tosis,  267. 
in  stomach,  139. 
Gastralgia,  72,  169. 

combined  with  gastric  ulcer,  192. 
nervous,     differentiated    from    gastric 

ulcer,  188. 
showing  a  family  tendency,  197. 
treatment  of,  43. 
with  mild  jaundice,  192. 
Gastrectasis,  73,  84,  122,  276. 
combined  with  tetany,  170. 
from  single  trauma,  130. 
hyperacidity  in,  76. 
Gastric  activity,  disturbance  of,  70. 
Gastric  and  intestinal  carcinomata,  me- 
chanical treatment  of,  255. 
Gastric  atony,  from  psychical  influence,  129. 
from  trauma,  130. 
hereditary,  127. 
Gastric  cancer,  independent  of  ulcer,  167. 
proportional  affection  of  sexes  in,  168. 
rupture  of,  192. 
Gastric  carcinoma,  84. 
acute,  238. 

chemical  findings  in,  236. 
complications  and  sequels  of,  238. 
course  of,  237. 
diagnosis  of,  234. 

distinguished  from  gastric  ulcer,  188, 
extirpation  of,  257. 
fever  in,  238. 

internal  treatment  of,  252. 
latent,  237. 
operation  for,  236. 


I  Gastric  carcinoma,  perforation  of,  191. 
prognosis  of,  239. 
seat  of,  238. 

topical  diagnosis  of,  120. 
Gastric  catarrh,  171,  270. 

as  cause  of  gastroptosis,  267. 
Gastric  contents,  acidity  of,  35. 
acids  in,  67. 

admixture  of  blood  in;  174. 
analysis  of,  36. 
anomalies  of,  63. 
characteristic  layers  of,  139. 
chymification  of,  99. 
coffee  ground,  256. 
constituents  of,  233. 
decomposition  of,  65. 
delayed  expulsion  of,  128. 
dextro-rotary  substance  in,  93. 
digestion  test  of,  ^7. 
evacuation  of,  119,  229,  230. 
examination  of,  54,  64,  66,  77,  96,  139. 

bacteriologic,  36. 

chemical,  67,  119. 

chemical  and  microscopical,  47. 

microscopical,  115,  119,  231,  233. 
expulsion  of,  153. 
extreme  subacidity  of,  93. 
hydrochloric  acid  in,  67,  78. 
hyperacid,  peculiarities  of,  105. 
inflow  and  outflow  of,  144. 
methods  of  testing,  140. 
microorganisms  in,  67. 
osmotic  concentration  of,  93. 
propulsion  of,  128. 
qualitative  tests  of,  67,  68. 
reaction  of,  67. 
removal  of,  61,  64. 
specific  gravity  of,  93. 
stagnation  of,  91,  99,  129,  139. 
subacidity  of,  89. 
sudden  discharge  of,  56. 
test  of,  52. 

total  acidity  of,  68,  91. 
Gastric  crises,  117. 
Gastric  digestion,  94. 

amylolytic  and  proteolytic  stage  of,  37. 
marked  disturbance  of,  278. 
Gastric  dilatation,  57,  122,  163. 
acute,  126. 

acute  and  chronic,  145,  150. 
causes  of,  125,  149. 
chronic,  145. 
clinical  forms  of,  122. 
course  of,  144. 

diagnosis  of,  122,  132,  133,  146. 
diet  in,  150. 
differentiation  of,  from  other  affections, 

143. 
general  condition  and  nutrition  in,  135. 
in  children,  126. 
nervous  symptoms  of,  141. 
objective  symptoms  of,  135,  141. 
pro^osis  of,  149. 
subjective  symptoms  of,  133. 
surgical  treatment  of,  156. 
symptoms  of,  132. 
treatment  of,  35,  144,  149,  150. 


808 


INDEX  OF  SUBJECTS 


Gastric    disease,    advantages    of    institu- 
tional treatment  in,  61. 

malignant,  236. 

physical  examination  in,  136. 

treatment  of,  32. 
(Jastric  douche,  59. 
(Jastric  fistula,  formation  of,  45. 

in  dogs,  102,  109. 

in  man,  109. 
Gaatric  hemorrhage,  178. 

causes  of,  175. 

composition  of  blood  in,  181. 

fatality  of,  177. 

indications  for  operation  in,  211. 

menstrual,  179. 

occult,  232. 

parenchymatous,  179. 

repetitions  of,  176. 

vicarious,  179. 
Gastric  insufficiency,  271. 
Gastric  juice,  acidity  of,  104. 

changes  in,  36. 

characteristics  of,  113. 

r^omposition  of,  65. 

continuous  flow  of,  113. 

diminution  of,  109. 

during  menstruation,  49. 

hyperacidity  of,  71. 

hypersecretion  of,  60,  87. 

influence  of  sweating  on,  111. 

inhibiting  of,  by  drugs,  111. 

irregular  outpour  of,  173. 

layer  quotient  of,  105. 

microscopic  examination  of,  67. 

peptonizing  action  of,  77. 

residue  of,  estimation  of,  106. 
Gastric  lavage,  101,  118,  136,  139,  140. 

apparatus  for,  53. 

at  evening,  61,  155. 

benefits  of,  34,  46. 

Biedert's  method  of,  41. 

by  patients  themselves,  37. 

clinical  use  of,  46. 

contraindications  of,  48. 

effect  of,  in  the  debilitated,  59. 

findings  of,  114, 

for  eructation  of  gas,  73. 

former  methods  of,  39. 

hemorrhage  during,  57. 

history  of,  32. 

Hodgen's  method  of,  40. 

in  cancer  of  stomach  and  intestine,  255. 

in  dilatation,  145,  146,  154. 

in  diseases  of  liver  and  gall-bladder,  44. 

in  mucous  membrane  erosions,   180. 

in  recumbent  posture,  56. 

in  the  debilitated,  55. 

individualization  of,  56. 

interruption  of,  56. 

.liirgensen's  method  of,  39. 

Kussmaul's  directions  for,  43.     " 

rebound  in,  40. 

solutions  used  for,  59. 

suitable  cases  for,  48. 

suitable  time  of  day  for,  60. 

techiiio  of,  41,  46. 

Uffelmann's  process  of,  119. 


Gastric  lavage,  with  ice  water,  209. 

with  iron  chlorid  solution,  202. 

with  silver  nitrate  solution,  186. 
Gastric  motility,  disturbance  of,  94,  226. 
Gastric  mucous  membrane,  excoriation  of, 
57. 

fissures  of,  186. 

hj^persensitiveness  of,  186. 

injuries  of,  42,  56. 

irritability  of,  57, 
Gastric  musculature,  atony  of,  35. 

fatty  and  choroid  degeneration  of,  35. 

paresis  of,  35, 
Gastric  necrosis,  160. 

Gastric  perforation,   act  of  defecation  a 
cause  of,  184, 

percentage  of,  185. 

poisoning  simulated  by,  185. 

self-induced  vomiting  a  cause  of,  184. 
Gastric  rigidity,  225, 

detection  of,  226. 
Gastric  secretion,  88. 

absence  of  acid  in,  76. 

discharge  of,  118, 

disturbances  of,  128, 

independent  of  food,  103. 

insufficiency  of,  89. 

retention  of,  116,  173. 

substitution  for,  76. 

variations  of,  in  health,  88. 
Gastric  tetany,  142, 
Gastric  tumor,  position  of,  193. 
Gastric  ulcer,  83,  117,  159,  276. 

acute  and  chronic  forms  of,  159. 

age  of  occurrence  of,  168. 

ambulatory  cases  of,  206. 

at  fundus,  194. 

bismuth  treatment  of,  43,  201,  205. 

carcinomatous,  237. 

carcinomatous  degeneration  of,  191. 

carcinomatous  transition  of,  173. 

chronic  diagnosis  of,  188. 

cicatrization  of,  165,  185. 

combination  of,  with  gastrectasis,  184. 
with  gumma,  187. 

confounding  of,  with  gastralgia,  72. 

diet  in,  202. 

differentiation  of,  from  hyperacidity,  77, 
112, 
from  gastralgia  and  carcinoma,  188. 

emaciation  in,    198. 

etiology  of,  159, 
bacteria,  161. 

circulatory  disturbance,  160. 
endarteritis  of  smallest  vessels,  160. 
hemorrhagic   erosions,  160. 
trauma,  162. 
vascular  lesions,  160. 

frequency  of  hemorrhages  in,  176. 

healing  processes  of,  215. 

hemorrhage  from,  58. 

hydrochloric  acid  in,  172. 

indications  for  operation  in,  215, 

in  Finland,  163. 

irritative  symptoms  of,  168. 

latent,  174,  179,  234. 

literature  of,  216. 


INDEX  OF  SUBJECTS 


809 


Gastric  ulcer,  localization  of,  164, 193, 194. 

malignant  degeneration  of,  223. 

microscopic  section  of,  164. 

mineral  spring  treatment  of,  202,  215. 

mortality  in,  211,  212. 

normal  type  of,  168. 

obscure  development  of,  163. 

oil  treatment  of,  207. 

operation  for,  194. 

operative  statistics  of,  214. 

pain  in,  81,  169. 

pathological  anatomy  of,  163. 

perforation  of,  165,  167,  214. 
while  dancing,  184. 

perigastric  adhesions  of,  211. 

prognosis  of,  199. 

proportional  affection  of  the  sexes  in,168. 

pure,  uncomplicated,  214. 

rectal  nutrition  in,  201. 

relapses  of,  200. 

relation  of  nervous  system  to,  162. 

relation  of,  to  cancer,  167. 

round,  161. 

rupture  of,  177,  182. 

sequelae  of,  168. 

size  of,  164. 

solitary,  161. 

statistics  of,  200. 

surgical  results  in,  211. 

surgical  treatment  of,  210. 

symptoms  of,  168. 

syphilitic,  167. 

the  lesion  in,  184. 

transition  of,  into  carcinoma,  180. 

treatment  of,  60,  84,  201. 

triad  of*  symptoms  of,  169. 

tubercular,  166. 

vomiting  in,  181. 

with  latent  course,  168. 
Gastric  ulcers,  isolated,  simultaneous  rup- 
ture of,  185. 

usual  number  of,  164. 
Gastric  wall,  atony  of,  84. 

degeneration  of,  43,  45. 

necrosis  of,  162. 

torsion  of  ner%'es  of,  185. 
Gastritis,  acid,  76,  77,  85,  108. 

acute  phlegmonous,  165. 

chronic,  83,  84,  146. 

denoting  of,  by  mucus  coagula,  66. 

differentiation  of,  from  dyspepsia,  70. 

proof  of,  65. 
Gastritis  graAds,  232. 
Gastritis  phlegmonosa,  233. 
Gastroanastomosis,  sequels  of,  212. 
Gastrodynia,  72. 

differentiation   of,    from   gastric   ulcer, 
188. 
Gastroenterostomy,    128,    157,    191,    195, 
196,  215,  257,  258,  259. 

antecolica  and  retrocolica,  212. 

indication  for,  118. 
Gastrogenous  phosphaturia,  115. 
Gastrohepatic    ligament,    shortening    of, 

281. 
Gastrointestinal  canal,  malignant  disease 
of,  276. 


Gastrohth,  235. 
Gastroneurosis,  combined,  80. 
Gastroptosis,  107,  118,  127,  146,  265. 

boundaries  of  stomach  in,  1.36. 

combination  of,  with  enteroptosis,  143. 

confounding  of,  with  gastrectasis,  147. 

diagnosis  of,  276. 

diet  in,  274. 

drug  treatment  of,  280. 

gastrectasis  a  cause  of,  268. 


hyperacidity  in,  76. 
in  hypersecretion,  117. 


m  women,  83. 

proof  of,  275. 

prophylaxis  of,  276. 

relation  of,  to  chlorosis,  274, 

statistics  of,  265. 

surgical  treatment  of,  281. 

symptoms  of,  273. 

treatment  of,  276. 
Gastrorrhcpa  acida,  76,  78.  ' 

Gastroscope,  194. 
Gastroscopy,  235,  237. 
Gastrosis,  79. 

causes  of,  80. 

infrequency  of  meals,  80. 

diagnosis  of,  82. 

of  reflex  sexual  origin,  80. 

symptoms  of,  81. 
Gastrostomy,  27,  28,  29,  45. 
Gastrosuccorrhea,  94,  104,  113,  173,  190. 
Gastroxynsis,  76. 

Gelatin  in  treatment  of  gastric  ulcer,  210. 
Genital  organs  (female),  diseases  of,  588. 
Girdle  sensation,  275. 
Glands,  para-umbUical,  228. 

peri-umbilical,  228. 

supraclavicular,    enlargement    of,    198, 
228. 
Glandular  parenchyma,    proliferation    of, 

108. 
Gluczinsky's  test,  191. 
Glycosuria,  alimentary,  306,  309. 
constant,  310. 

occurrence  of,  after  use  of  suprarenal 
extract,  210. 
statistics  of,  310. 

transitory,  307,  309. 
Gmelin's  test,  325. 
Gnawing  sensation,  114. 
Goiter,  2,  17. 
Grape  cure,  732. 

Grating  sensation  in  gastric  region,  223. 
Growths,  esophageal,  7. 
Guaiac  test,  174,  244. 
Gumma,  syphUitic,  167. 
Giinzburg  reagent,  67,  90. 
Giinzburg's  test,  85. 
Gurgling,  intestinal,  273,  277. 
Gurgling  sound  in  esophagus,  9. 
Gymnastics,  Schreber  s  curative,  724. 

Swedish  curative,  724. 

Hamamelis  virginica,  209. 
Hammerschlag's  test,  92,  95. 
Head,  numbness  in,  82,  135. 
Headache  in  gastric  dilatation,  142. 


810 


INDEX  OF  SUBJECTS 


Heart,  amyloid  degeneration  of,  179. 

corrosion  of,  from  gastric  ulcer,  177. 

dilatation  of,  123. 

displacement  of,  263,  264,  295. 
causes  of,  296. 
symptoms  of,  298. 

in  women,  greater  movability  of,  296. 

neuroses  of,  79. 

normal  position  of,  295. 

rupture  of,  from  gastric  ulcer,  183. 

slow  action  of,  141. 

valvular  disease  of,  48. 

wandering,  295. 
Heart  brace,  300. 
Heat,  application  of.  111. 
Heels,  high,  effect  of,  273. 
Helminthiasis,  bulimia  in,  72. 
Hematemesis,  172,  203,  234. 

as  symptom  of  carcinomata,  223. 

fatal,  187. 

frequency  of,  176. 

in  gastric  ulcer,  169. 

in  jaundice,  494. 
Heniatin  in  gastric  contents,  230. 
Hematuria,  286. 
Hemicrania  dyspeptica,  650. 
Hemicrania  intestinalis,  650. 
Hemoglobin  in  gastric  contents,  230. 
Hemorrhage,  capillary,  8,  49,  233. 

from  mucous  membrane,  13. 

from  old  gastric  ulcers,  58. 

from  stomach,  159,  174;  see  also  Gastric 
Hemorrhage. 

gastric,  57,  143,  162,  208. 
controlled  by  lavage,  58. 
recuperation  after,  211. 
treatment  of,  210. 
by  bismuth,  60. 
by  ice  water,  209. 

internal,  5. 

intestinal,  244. 

occult,  174,  179,  633. 

punctiform,  in  esophagus,  7. 

tendency  to,  48. 

vicarious,  179. 

vicarious  gastric,  713. 
Hemorrhagic  pancreatitis,  321. 
Hemorrhagic  stools  in  pancreatic  disease, 

320. 
Hemorrhoidal  pessaries,  734. 
Hemorrhoidal  prolapse,  716. 
Hemorrhoids,  704. 

catarrh  of  rectum  a  complication  of,  715. 

cholelithiasis  a  factor  of,  708. 

cold  applications  to,  732. 

complication  of,  715. 
treatment  of,  732. 

diagnosis  of,  715. 

diet  in,  731. 

differential  diagnosis  of,  715. 

digital  examination  of  rectum  in,  715. 

due  to  circulatory  disturbance,  708. 

elevation  of  buttocks  in,  731. 

etiology  of,  708. 

external,  715. 

grape  c\ire  of,  732. 

hemorrhages  of,  712. 


Hemorrhoids,  hepatic  congestion  in,  712. 

hereditary  predisposition  to,  708. 

in  childhood,  709. 

in  pregnancy,  708. 

internal,  715. 

itching  and  burning  in,  712. 

mineral  water  cures  for,  731. 

mixed,  715. 

prolapse  of,  treatment  of,  734. 

symptoms  of,  711. 

treatment  of,  730. 

combined  with  constipation,  731. 

enemata  in,  731. 

exercise  in,  731. 

incarceration  of,  734. 

laxative,  730. 

suppositories  in,  732. 

ulceration  of,  712,  716. 

vicarious  gastric  hemorrhage  in,  713. 

with  incontinence  of  rectal  sphincters, 
716. 
Hepatargy,  341. 

Hepatic  abscess  due  to  gall-stones,  505. 
Hepatic  artery,  compression  of,  487. 
Hepatic  colic  due  to  simple  adhesions,  475. 
Hepatic  duct,  sympathetic  spasm  of,  192. 
Hepatic  dyspepsia,  341. 
Hepatic  insufficiency,  340. 

hemorrhagic  diathesis  in,  341. 

symptoms  of,  341. 
Hepatic  region,  auscultation  of,  487. 
Hepatoptosis,  290. 

distinguished  from  other  diseases,  291. 

symptoms  of,  291,  292. 
Hereditary  jaundice,  348. 
Hernia  epigastrica,  107. 
Hernia  of  the  linea  alba,  198. 
Hernia,  strangvdated,  180. 
Heterochylia,  94. 
Hop  tea  as  gastric  spray,  59. 
Hiihnerfeld's  reagent,  175. 
Hunger,  anomalous,  71. 

artificial  relief  of,  26. 
Hunger  center  in  brain,  71. 
Hydrastis  canadensis,  209. 
Hydrochloric  acid,  absence  of,  140. 
from  stomach  contents,  76. 

cessation  of,  98. 

combined,  90,  114. 

deficiency  of,  84,  91. 

experiments  in  dogs,  108. 

free,  quantitative  estimation  of,  120. 

increase  of,  in  stomach,  169. 

in  gastric  contents,  68,  231. 

in  gastric  juice,  65. 

in  stomach,  36. 

qualitative  estimation  of,  53. 

secretion  of,  9,  88. 

test  for,  90. 
Hydronephrosis,  286. 
Hydroparacumaric  acid,  352. 
Hydropathy,  154. 

for  diseases  of  stomach,  154. 
Hydrorrhoea  gastrica,  106. 
Hydrotherapy  in  gastroptosis,  280. 
Hygiene  in  esophageal  disease,  19. 
Hyperaciditas  anorganica,  93. 


INDEX  OF  SUBJECTS 


811 


Hyperaciditas  hydrochlorica,  104. 
Hyperaciditas  larvata,  105. 
Hyperaciditas  occulta,  105. 
Hyperacidity,  76,  89,  93,  103. 

as  cause  of  gastric  ulcer,  160. 

as  sign  of  gastric  ulcer,  173. 

chemical  conception  of,  104. 

drug  treatment  of,  111. 

etiology  of,  108. 

functional,  77. 

gastric,  64. 

in  different  countries,  107. 

in  gastric  ulcer,  171. 

of  stomach,  67,  75. 

persistent,  212. 

suitable  diet  for,  78. 

symptoms  of,  107. 

treatment  of,  78,  109. 
Hyperchlorhydria,  60,  76,  93,   172,   173, 
190,  192. 

diet  in,  203. 

treatment  of,  43. 
Hyperchylia,  94. 
Hyperesthesia  gastrica,  112. 
Hyperesthesia  of  gastric  walls,  72. 
Hyperglycemia,  307. 
Hypermotility,  gastric,  53. 

of  stomach,  71,  74. 
Hypernutrition,  279. 
Hypersecretion,  76,  78,  113,  128,  129, 173. 

chronic,  116. 

combined  with  dilatation,  143. 

diagnosis  of,  115. 

gastric,  60,  61,  64. 

neurogenous,  117. 

pathogenesis  of,  116. 

symptoms  of,  114. 

treatment  of,  117. 
Hypertrophic  pyloric  stenosis,  232. 
Hypertrophy,  stenosing  pyloric,  98. 
Hypochlorhydria,  94. 
Hypocholia,  340. 
Hypochondriasis,  82. 

Hypochondrium,  peculiar  phenomenon  in, 
225. 

right,  pain  in,  192. 
Hypochylia,  94. 
Hypopepsia,  94. 
Hysteria,  as  cause  of  eructations,  73. 

as  cause  of  gastric  neuroses,  70,  74. 

combined  with  gastrosis,  82. 

gastric  hemorrhage  in,  58. 

painful  pressure  areas  in,  84. 

significant  of  floating  kidney,  288. 

with  esophagismus,  14. 

Ice,  application  of,  in  gastric  ulcer,  207. 

in  esophageal  disease,  20. 

use  of,  in  gastric  ulcer,  209. 
Ice  cold  fluids,  effect  of,  108. 
Ichochymia,  122. 
Ictere  hemaph6ique,  341,  410. 
Icterus.    See  Jaundice. 
Icterus  gravis,  341. 
Icterus  neonatorum,  331. 
Ileum,  carcinoma  of,  247. 
Ileus,  dynamic,  765. 


Ileus,  mechanical,  765. 

paralytic,  517,  765. 

treatment  of,  by  gastric  lavage,  43,  47. 
Iliac  fossa,  sensitiveness  in,  28.5. 
Inanition,  14. 

in  esophageal  disease,  5. 

prevention  of,  30. 
Indican  in  urine,  9. 

Indican  excretion  insufficient  in  pancre- 
atic disease,  321. 
Indigo  reaction,  502. 
Indol,  636. 

Infarct,  hemorrhagic,  160. 
Infiltration  ligneuse,  489. 
Infiltration,  small  cell,  165. 
Infusions,  subcutaneous,  in  gastric  ulcer, 

210. 
Ingesta,  abnormal  decomposition  of,  171. 

expulsion  of,  from  stomach,  125. 

hot  or  cold,  as  cause  of  pain,  170. 

permanent  retention  of,  in  stomach,  125. 

propulsion  of,  73. 

stagnation  of,  75. 
Innervation,  disturbances  of,  1,  15. 
Inspection  in  gastric  disease,  135. 
Inspection  of  esophagus,  6. 
Intestinal  activity,  disturbance  of,  141. 
Intestinal  canal,  tuberculosis  of,  187. 
Intestinal  carcinoma,  240. 

complications  and  sequels  of,  250. 

diagnosis  of,  248. 

distinguished    from    other    conditions, 
242. 

movability  of,  242. 

prognosis  of,  251. 

symptoms  of,  240. 
Intestinal  constriction,  751. 

abdomen  in,  palpation  of,  760. 

alteration  of  fecal  movements  in,  751. 

anatomical  nature  of,  760. 

bowels  in,  regulation  of,  764. 

carcinoma  the  cause  of,  761. 

caution  in  diagnosis  of,  761. 

cicatricial  strictures  causing,  761. 

colon  the  seat  of,  758. 

constipation  in,  752. 

course  of,  762. 

diagnosis  of,  753,  761,  762. 

diarrhea  in,  752. 

diet  in,  764. 

digital  rectal  examination  in,  759,  760. 

due  to  benign  tumors,  756. 
to  carcinomata,  755. 
to  chronic  peritonitis,  757. 
to  internal  cicatricial  strictures,  756. 
to  pressure  of  tumor-like  masses,  757. 
to  sarcomata,  755. 
to  tuberculomata,  755. 

duodenum  in,  chronic  stenosis  of,  759. 

etiology  of,  754. 

external,  by  peritoneal  processes,  757. 

feces  in,  752. 

hernial  rings,  examination  of,  759,  760. 

insidious  onset  of,  762. 

intestinal  stiffening  of,  753. 
diagnostic  value  of,  754. 

Japarotomy  in,  762. 


812 


INDEX  OF  SUBJECTS 


Intestinal  constriction,  leading  to  occlu- 
sion, 763. 
pain  in,  752,  759. 
pelvic  peritonitis  preceding,  761. 
peristalsis  increased  in,  753. 
prognosis  of,  762. 
seat  of,  762. 

seat  of  obstruction  in,  758. 
small  intestine  seat  of,  759. 
stenosis  of  rectum  in,  760. 
symptomatology  of,  751. 
treatment  of,  763. 

by  operation,  763. 

non-surgical,  764. 

symptomatic,  764. 
treatment  of  colic  in,  764. 

of  occlusion  in,  764. 
tumors  in,  759,  760. 
vaginal  examination  in,  759,  760. 
Intestinal  immobility,  127. 
Intestinal  obstruction,  treated  by  gastric 

lavage,  43. 
Intestinal  occlusion,  751,  765. 
abdomen  in,  780. 
anatomical  changes  in,  765. 
arterio-mesenteric,  126. 
blood  in,  intoxication  theory  of,  772. 

reflex  theory  of,  772. 
bowels  in,  780. 
cardiac  activity  in,  782. 
causes  of,  773. 

obstruction,  774. 
circulatory  apparatus  in,  772. 
collapse  in,  780. 
course  of,  773. 
development  of,  766. 
diagnosis  of,  775. 
diarrhea  in,  772. 

differentiation  of,  from  peritonitis,  776. 
due  to  internal  incarceration,  779. 

to  invagination,  779. 

to  obstruction  by  foreign  bodies,  779. 

to  paralysis  of  intestine,  779. 

to  volvulus.  779. 
electrotherapy  in,  786. 
fecal  vomiting  in,  767,  775. 
feces  of,  778. 
gall-stones  in,  781. 
hernial  rings  in,  777,  779. 
impermeability  of  intestine  in,  775. 
in  pancreatic  disease,  320. 
indicanuria  in,  778. 
ingestion  of  food  in,  785. 
mitial  pain  of,  770. 
insidious,  778. 
meteorism  in,  769,  771,  775,  778. 

local,  766. 

stasis,  766. 
pain  in,  780. 

paralysis  of  intestine  in,  774, 
pathologic  anatomy  of,  779. 
pathology  of,  765. 
peristalsis  in,  772. 
rectal  examination  in,  777,  779. 
seat  ot,  777. 

s|K>n(aneous  cure  of,  781. 
strangulation  in,  766,  769,  778. 


Intestinal     occlusion,    strangulation    in, 
symptoms  of,  770. 
treatment  of,  781. 
non-operative,  782. 
symptoms  of,  766,  767. 
tetanic  intestinal  stiffening  in,  772. 
treatment  of,  780. 
by  atropin,  785. 
by  enemata,  783. 
by  gastric  lavage,  784. 
by  massage,  784. 
by  operation,  782. 
by  opium,  784. 
by   purgatives,  783. 
by  rectal  irrigation,  783. 
urine  in,  increased  constituents  of,  769. 
vaginal  examination  in,  777. 
volvulus  in,  771. 
vomiting  in,  771,  775,  778^  780. 
Intestinal  rumbling,  75. 
Intestinal  stagnation,  712. 
Intestinal  tract,  hemorrhage  from,  179. 
Intestine,  carcinoma  of,  240,  259,  755. 
catarrh  of,  631.    See  also  Diarrhea, 
constriction  of,  180. 
disorders  of  gastric  lavage  in,  43. 
foods  which  stimulate,  718. 
increased  activity  in,  635. 
irrigation  of,  714. 
irritability  of,  642. 

mucous  membrane  of,  increased  secre- 
tion of,  635. 
sarcomata  of,  755. 
small,  cancer  of,  247,  254. 
.traumatic  contusion  of,  533. 
Intoxication,  "septic,"  521. 
Inulin,  use  of,  in  subacidity,  103. 
lodipin  test,  140. 

Iron-preparations  in  gastric  ulcer,  204. 
Irrigation,  ice- water,  171. 
of  stomach,  38. 
therapeutic,  155. 
Ischuria  paradoxa,  33,  671. 

Jaques's  esophagus  tube,  49. 
Jaundice,  absence  of,  in  gall-stone  colic, 
192. 

acathectic,  332. 

amido-acids  in  urine  of,  351. 

anhepatogenous,  329. 

appearance  of  feces  in,  326. 

catarrhal,  328,  330,  336. 

causes  of,  328,  329,  331,  332,  333. 

composition  of  urine  in,  325. 

constipation  in,  327. 

cythemolytic,  330. 

epidemic,  338. 

flatulence  in,  327. 

Gmelin's  test  of  serum  in,  326. 

hematogenous,  329. 

hemolytic,  330,  331. 

hyaline  casts  in  urine  of,  326. 

in  disease  of  the  pancreas,  317,  320. 

in  duodenal  ulcer.  199. 

infectious,  331,  338. 

obstructive,  329. 

post-operative,  467. 


INDEX  OF  SUBJECTS 


813 


Jaundice,  prognosis  of,  353. 
simple,  diagnosis  of,  351. 
simple  essential,  328. 
symptom-complex   of,   in   various  dis- 
eases, 327. 
symptoms  of,  335,  336,  337. 
treatment  of,  354,  355. 
alkaline  waters  in,  356. 
by  drugs,  360. 

by  injection  of  water  into  colon  in,  3§7. 
cholagogues  in,  356. 
electricity  in,  356. 
food  in,  357,  358. 
lavage  in,  360. 
massage  in,  356. 
yellow  color  of  blood  serum  in,  326. 
Jaundice  and  hepatic  insufficiency,  325. 
Jejunostomy,  215,  257. 
Jejunum,  carcinoma  of,  247. 
Jennerization,  698. 

Kfilbersterbe,  637. 

Kidney,  examination  of,  while  in  warm 
bath,  287. 
extirpation  of,  290. 
floating,  diagnosis  of,  288. 

treatment  of,  289. 
lying  in  pelvis,  288. 
suture  of,  290. 

unilateral  movability  of,  263. 
wandering,  281.    See  also  Nephroptosis, 
predisposition  to,  285. 
Kidneys,  benefits  to,  from  gastric  lavage, 
44. 
change  of  form  in,  288. 
displacement  of,  281 .    See  also  Nephrop- 
tosis. 
Klemperer's  oil  test,  140. 
Knee-elbow  position  in  gastric  dilatation, 

150. 
Kussmaul's  treatment  of  gastric  diseases, 
32,  38. 
for  gastric  dilatation,  35. 
Kyphoscofiosis,  273. 
in  women,  288. 
vertebral  column,  265. 

Lab,  coagulation  of,  69. 
Lab  ferment,  69,  88,  94,  232. 

tests  for,  92. 
Lab-zymogen,  121. 

Labor,  displacement  of  heart  after,  299. 
Lacing,  tight,  a  cause  of  gastroptosis,  266, 
269,  270,  273,  276. 
a  cause  of  nephroptosis,  284. 
Lactic  acid,  absence  of,  90. 

in  gastric  contents,  68, 119, 140, 230, 232. 

in  the  stomach,  172. 

increase  of,  98. 
Lactic  acid  fermentation,  142,  232. 
Laennec's  cirrhosis,  371. 
Laminaria  tents,  24,  26,  28,  29. 
Langerhans'  islands,  degeneration  of,  309. 
Laparotomy,  exploratory,  235. 
Laryngitis,  8. 
Larynx,  carcinoma  of,  17. 

catarrh  of,  27. 


Lassitude  in  neurasthenia,  82. 
Laughter,  prolonged,  as  cause  of  nephrop- 
tosis, 284. 
Lavage,  control  of  hemorrhage  by,  58. 
gastric,  32,  185,  504. 

for  peristaltic  unrest,  75. 
of  esophagus,  22. 
with  ice-water,  181. 
"Layer  test"  of  hyperacidity,  106. 
Leeches,  in  gastric  iilcer,  207. 
Leo's  test  for  hydrochloric  acid,  90. 

for  total  acidity,  120. 
Leroy  curette,  31. 
Leube,  diet  schemes  of,  44. 
Leub's  digestion  test,  140. 
Leukocytes,  84. 

in  gastric  contents,  67,  70,  78,  97,  113. 
protoplasmic  ring  of,  89. 
Leukocytosis,  digestive,  233. 
Levulose  for  hyperacidity,  110. 
L'hepatisme,  265. 
Lientery,  183,  651. 

amylum,  652. 
Life,  prolongation  of,  in  carcinoma,  259.' 
Linossier's  reagent,  90. 
Linossier's  test,  120. 
Lipoma,  235. 
Liver,  abscess  of,  480. 

acute  yellow  atrophy  of,  342. 
course  of,  345. 

decrease  in  excretion  of  urea  in,  352. 
diagnosis  of,  351. 
etiology  of,  342,  343,  347. 
increased  excretion  of  ammonia  in,  352. 
leucin  and  tyrosin  in  urine  in,  345. 
pathology  of,  345,  349. 
profuse  diuresis  in,  345. 
symptoms  of,  343,  344. 
adenoma  of,  443. 
carcinoma  of,  443. 
nodulated,  447. 
chronic  inflammation  of,  361. 
etiology  of,  363-371. 
pathology  of ,  361-371. 
varieties  of,  363-371. 
cirrhosis  of,  371. 
ascites  in,  375. 
bihary,  388. 
etiology  of,  388. 
pathology  of,  388. 
symptoms  of,  389. 
treatment  of,  389. 
collateral  circulation  in,  375. 
complications  in,  379. 
diagnosis  of,  380. 
differential  diagnosis  of,  380. 
duration  of,  380. 
etiology  of,  371,  372. 
hypertrophic,  385. 

diagnosis  of,  387.  i 

etiology  of,  387. 
pathology  of,  385. 
prognosis  of,  387. 
symptoms  of,  386. 
treatment  of,  387. 
by  calomel.  387. 
levulosuria  in,  379. 


814 


INDEX  OF  SUBJECTS 


Liver,  cirrhosis  of,  metabolism  in,  377. 
pathology  of,  372,  373. 
peritoneal  tuberculosis  and,  379. 
primary  carcinoma  and,  379. 
prognosis  of,  381. 
pulse  in,  376. 
respiration  in,  376. 
symptoms  and  course  of,  374-379. 
treatment   of,  381-384. 

surgical,  384. 
urine  in,  378,  379. 
displaced  lobe  of,  242. 
displacement  of,  290.   See  also  Hepatop- 

tosis. 
downward  pressure  upon,  270. 
echinococcus  of,  454. 
alveolaris,  460. 
cystic,  diagnosis  of,  459. 
pathology  of,  455. 
perforation    of,    into    neighboring 

organs,  457-459. 
treatment  of,  459-460. 
multilocularis,  460. 
diagnosis  of,  462. 
prognosis  of,  463. 
symptoms  of,  462. 
treatment  of,  463. 
symptoms  of,  456-459. 
enlargement  of,  178. 

connected  with  rectal  carcinoma,  246. 
granular  atrophy  of,  371. 
melanosarcoma  of,  441. 

symptomatology  of,  441. 
metastases  of,  228,  236. 
neoplasms  of,  396,  438. 
clinical  forms  of,  438-447. 
diagnosis  of,  450-452. 
hemorrhages  in,  446. 
malignant,  440. 
massive  cancer  in,  447. 
treatment  of,  452,  453. 
non-parasitic  cysts  of,  440. 
syphilis  of,  389,  390. 
clinical  course  of,  391.  • 
diagnosis  of,  392. 
symptoms  of,  391. 
treatment  of,  392. 
topographical  changes  in,  192. 
wandering,  290,  486. 
Liver  dulness,  disappearance  of,  184. 
Lung,  cancer  of,  18. 
Lumbar  lardosis,  127. 
Luschka's  plates,  51. 
Luxury  consumption,  299. 
Lymph-glands,  cancer  of,  18. 
enlargement  of,  2,  6. 
peri-esophageal  processes  from,  13. 
peripheral,  198. 
I/ymphatic  follicles,  rupture  of,  161. 
Ly'uphomata,  syphilitic,  30. 
Lympho-sarcoma,  239. 

Maltosuria  in  pancreatic  disease,  321. 
Mandrin  in  stomach-tube,  use  of,  50. 
Massage  in  gastric  dilatation,  153. 

in  u;astroptosis,  278. 
of  stomach,  153. 


Massive  stools  in  pancreatic  disease,  317. 
Mastication,  importance  of,  100. 
Meals,  frequent,  value  of,  103. 

infrequency  of,  81. 

light,  benefits  from,  152. 

rational  arrangement  of,  110. 

small  and  frequent,  118. 
Meat,  aversion  to,  253. 

proper  cooking  of,  100. 

•use  of,  in  gastric  disease,  151. 
Meat  diet,  over-stimulation  from,  108. 
Meat  extracts,  use  of,  110. 
Mediastinum,  rupture  of  gastric  ulcer  into, 
183. 

tumors  of,  2. 
Megalogastria,  123,  124,  146. 
Melena,  173,  179,  234. 

as  svmptom  of  carcinomata,  223. 

in  cholelithiasis,  499. 
Menorrhagia,  bulimia  in,  72. 
Menstruation,  tendency  to  gastric  hemor- 
rhage in,  49. 
Menstruation  in  cases  of  gastric  ulcer,  207. 
Mental  disease,  association  of,  with  dis- 
placement of  the  colon,  263. 
Merycism,  73. 
Mesentery,  abnormal  length  of,  127. 

metastasis  of,  236. 
Metabolism,  investigations  in,  204. 

sugar,  308. 
Metastasis,  ovarian,  196. 
Meteorism,  243. 

local,  766. 

peritoneal,  536. 

stasis,  766. 
Methemoglobin,  174. 
Methylene  orange  test,  91. 
Mett's  test,  92,  95,  120. 
Microorganisms  in  stomach,  76. 
Microtome,  6. 
Migraine,  79. 

due  to  diarrhea,  650. 
Milk,  coagulation  of,  121. 

free  consumption  of,  279. 

free  from  sugar,  101. 

in  the  diet,  78,  101. 
effect  of,  78. 

in  gastric  disease,  151. 

salicylated,  101. 

use  of,  in  gastric  ulcer,  203. 
Milk  fat,  curative  powers  of,  109. 
Morphin  in  esophageal  disease,  22. 

in  gastric  ulcer,  207. 
Morphinism,  cause  of  intermittent  fever, 

482. 
Motility  of  stomach,  117. 
Motor  msufficiency,  146. 
Mucosa,  gastric  disease  of,  160. 
Mucous  membrane,  desquamation  of,  186. 

gastric,  atrophy  of,  76. 
erosions  of,  180. 
irritation  of,  35,  179. 
laceration  of,  42. 
nutrition  of,  159. 
toxin  infection  of,  181 
varices  of,  178. 
vulnerability  of,  97. 


INDEX  OF  SUBJECTS 


815 


Mucous  membrane,  in  esophageal  disease, 
7,  8. 

purulent,  8. 

vulnerability  of,  76. 
Mucus,  gastric,  78. 

in  gastric  contents,  55,  66,  77. 

in  stomach,  87. 

microscopic  examination  of,  67. 
Murmur,  abdominal,  225. 

pressing-through,  9. 
Murmurs,  deglutition,  9. 
Murphy's  button,  212. 
Musculature,    hypertrophic,   degeneration 

of,  143. 
Myasthenia  gastrica,  122. 
Myoparesis  of  stomach,  18. 

Nahrtoast,  110. 

Nails,  vasomotor  and  trophic  changes  in, 

4. 
Narcotics,  paralyzing  effect  of,  130. 
Necrosis  of  gastric  mucous  membrane,  160. 
Nematodes  in  pleural  cavity,  183. 
Neoplasm,  carcinomatous,  167. 

benign,  249. 

of  trachea,  5. 
Nephrolithiasis,  550. 
Nephroptosis,  281. 

age  hable  to,  282. 

combination  of,  with  gastroptosis,  285. 

diagnosis  of,  287. 

etiology  of,  283. 

operative  treatment  of,  290. 

slow  recovery  from,  287. 

statistics  of,  282. 

symptoms  of,  284. 
Nephrorrhaphy,  dangers  of,  290. 

results  of,  290. 
Nerves,  esophageal,  sensitiveness  of,  3. 

recurrent  laryngeal,  5. 
paralysis  of,  4. 
Nervous   disturbances   from  under-nutri- 

tion,  299. 
Nervous  hepatic  colic,  473. 
Nervous  system,  central,  diseases  of,  130. 

derangement  of,   from  gastric  disease, 
141. 

hyperirritation  of,  72. 
Neuralgia,  intercostal,  170. 
Neurasthenia,  a  cause  of  gastric  disease, 
79. 

accompanied  by  esophagismus,  14. 

predisposing  to  gastric  neuroses,  70. 
Neurasthenia  dyspeptica,  80. 
Neurasthenia,  gastrica,  80. 
Neuroses,  cardiac,  299. 

gastric,  70. 

predisposing  causes  of,  70. 
treatment  of,  74. 

motor,  of  stomach.  72. 

of  secretion,  76,  509. 

sensory,  of  the  stomach,  71. 
Niche,  paravertebral,  for  kidney,  283. 
Nicotin  as  cause  of  gastrosis,  80. 
Nitrogen    absorption    insufficiency   of,   in 

pancreatic  disease,  316. 
Nodules,  miliary,  in  stomach,  166. 


Nourishment  by  rectum,  62,  152. 
Nourishment  in  carcinoma,  252,  253. 
Nurslings,  fat-splitting  in,  313. 

feces  of,  605,  631. 

nephroptosis  in,  281. 

pyloric  stenosis  in,  131. 
Nutrition,  artificial,  20. 

artificial  or  extra-buccal,  254. 

disturbance  of,  from  gastroptosis,  276. 

faulty,  127. 

general,  damaged  by  diarrhea,  98. 

in  esophageal  disease,  20,  29,  30. 

Obesity  cure  as  cause  of  displacement  of 

heart,  299. 
Obstruction,  intestinal,  242. 
Occlusion,    arterio-mesenteric    intestinal. 
145. 

of  hepatic  circulation,  178. 

of  intestine,  492. 
Odor,  fetid,  from  decomposition  of  food, 
4. 
treatment  of,  27. 

of  gastric  contents,  66. 
Oil,  ingestion  of,  as  cause  of  hemorrhage, 
176. 

in  the  diet,  110. 
Oligocholia,  340. 
Olive  oil  for  gastric  ulcer,  207,  208. 

in  gastric  dilatation,  154. 

in  gastric  disease,  186. 
Operation  in  gastric  ulcer,  mortality  in, 

214. 
Operations  on  stomach,  results  of,  213. 
Opium  in  treatment  of  carcinoma,  255. 
Oral  cavity,  bacteria  in,  99. 

cleansing  of,  99. 

infection  from,  224. 
Orexin  for  gastric  dilatation,  156. 
Ovaries,  neoplasm  of,  196. 
Oxyacids,  352. 
Oxybutyric  acid,  9,  239. 
Oxymandelic  acid,  352. 

Pain,  distribution  of,  in  esophageal  dis- 
ease, 4. 

epigastric,  5. 

following  ingestion  of  food,  169. 

gastric,  77,  134,  163,  183. 

gastric  and  intestinal,  255. 

in  gastric  ulcer,  169. 

pyloric,  193. 

typical,  in  gastric  ulcer,  197. 
Palpation,  facilitating  of,  by  structure  of 
body,  283. 

of  esophagus,  6. 
Palpitation,  cardiac,  82. 
Pancreas,  absence  of  function  of,  306. 

anatomy  and  physiology  of,  304. 

atrophy  of,  312. 

chemistry  of,  315. 

destruction  of,  305. 

digestive  function  of,  305. 

disease  of,  301. 

combined  with  diabetes,  306. 
symptoms  of,  304,  625. 


816 


INDEX  OF  SUBJECTS 


Pancreas,  diseases  of,  histoiy  of,  303. 
obscure  knowledge  of,  303. 
surgery  in,  304. 

extirpation  of,  306,  310. 

head  of,  carcinoma  of,  312. 

induration  of,  312. 

innervation  of,  304. 

internal  secretion  of,  305,  307. 

nerve  apparatus  of,  305. 

of  dogs,  excision  of,  313. 
experiments  in,  308. 

relation  of,  to  fat-splitting,  313. 

secretion  of,  305. 

total  destruction  of,  without  diabetes, 
309. 

transplantation  of  portions  of,  307. 

two  ducts  of,  304. 

tying  of  ducts  of,  307. 
Pancreatic  apoplexy,  321. 
Pancreatic  artery,  corrosion  of,  177. 
Pancreatic  colic,  317,  318. 
PaiuTcatic  duct,  occlusion  of,  305. 
Pancreatic  juice,  increased  secretion  of,  128. 

regurgitation  of,  213. 
Pancreatic  necrosis,  321. 
Pancreatic  pain,  318,  319. 
Pancreatitis,  gall-stones  a  cause  of,  505. 

hemorrhagic,  321. 

interacinous,  308. 

interlobular,  308. 
Pankreon,  255. 

for  subacidity,  102. 
Panniculus  adiposus,  485. 

retention  of.  in  pernicious  anemia,  97. 
Papilloma,  235. 

rectal,  249. 
Paquelin  cautery,  25. 
Paracholia,  nervous,  469. 
Parasecretion,  104,  113,  173. 
Parenchyma,  secreting,  116. 
Paresis  of  gastric  musculature,  34. 
Parorexia,  71. 
Pastry,  hot,  effect  of,  108. 
Pathology,    gastric,    symptom-complexes 

of,  87. 
Pedatrophia,  673. 
Pedicles,  torsion  of,  192. 
Pentosuria  in  pancreatic  disease,  321. 
Penzoldt-Dehio    method,    of    evacuating 

stomach,  138. 
Pepsin,  94. 

absence  of,  98. 

for  subacidity,  102. 

in  gastric  contents,  232. 
estimation  of,  120. 

Mett's  test  for,  92. 

secretion  of,  88. 

tests  for,  69,  92. 
Peptic  ulcer,  159. 

Pejitones  in  acute  yellow  atrophy,  352. 
Peracidity,  104. 
Perforation,  gastric,  operation  after,  214. 

of  stomach  from  seli-induced  vomiting, 
184. 
Periai)]K'ndicitis,  533. 

purulent,  circumscribed,  symptoms  of, 
553. 


Pericarditis,  18. 
Pericholecystitis,  549. 
Peri-esophageal  processes,   13. 
Perigastritis,  98,  130,  165,  182,  235. 
Perihepatitis  in  gall-stones,  486. 
Peristalsis,  active,  143. 
disturbance  of,  21. 
due  to  gases,  636. 
gastric,  156. 
increased,  60,  636, 
Peristaltic  unrest,  75. 
Peristaltism,  225. 
Peritoneal  collapse,  515. 
Peritoneal  irritation,  534. 
Peritoneal  sepsis,  523. 
Peritoneum,  constriction  of,  762. 

inflammation  of,  bacteriological  findings 
is,  529,  530. 

pyogenic  organisms  in,  529. 
Peritonism,  539. 
Peritonitis,  acute  diffuse,  513. 

abscess  formation  in,  518. 

adhesions  in,  at  point  of  rupture,  519. 
formation  of,  532. 
rupture  of,  532,  533. 

air  in  peritoneal  sac  in,  536. 

albuminuria  in,  518. 

bacterial  infection  in,  520. 

bowels  in,  condition  of,  517. 

chemical  form  of,  519. 

clinical  history  of  a  case  of,  513-516 

coli  bacilli  in,  presence  of,  516. 

collapse  in,  535. 
treatment  of,  563. 

colon  in,  evacuation  of,  563. 

diagnosis  of,  538. 

diet  in,  561. 

differentiation    of,     from    gall-stone 
colic,  538. 
from  intestinal  obstruction,  538. 

exploratory  laparotomy  in,  560. 

exudation  in,  518. 

gas  in  abdominal  cavity  in,  537. 

indicanurit  in,  518. 

internal  treatment  of,  560,  561. 
indications  for,  561. 

laparotomy  in,  521. 

local  symptoms  of,  536. 

meteorism  a  symptom  of,  536. 

omentum  in,  525. 

operative  measures  in,  559. 

opium  in,  effect  of,  519. 

opium  in  treatment  of,  562. 

pain  in,  517. 

pain  upon  pressure  in,  537. 

pathology  of,  534. 

perforation  into  abdominal  cavity  in, 
522. 

peritoneal  meteorism  in,  537. 

peritoneum  in,  changes  in,  531. 

prophylaxis  of,  558. 

pus  foci  in  uterus  in,  523. 

recovery  after  operation  in,  560. 

rupture  of  pus  into  intestine  in,  516. 

septic  intoxication  in,  536. 

stomach  in,  rupture  of,  521. 

streptococci  in,  presence  of,  516. 


INDEX  OF  SUBJECTS 


817 


Peritonitis,  acute  diffuse,  surgical  treat- 
ment advisable  in,  560. 
symptoms  of,  535. 
in  course,  518,  519. 
in  onset,  517. 
temperature  in,  517. 
treatment  of,  536. 
unfavorable  for  operation.  560. 
urinary  complications  in,  537. 
vomiting  in,  517,  537. 
appendix,  position   of,  in   relation  to, 

540. 
attenuated  general,  525. 
bacterial  and  chemical,  discrimination 

of,  in  prophylaxis,  559. 
chemical,  531,  533,  534. 

from  circumscribed   periappendicular 

abscess,  533. 
plastic  exudates  of,  534. 
plastic  form  of,  533. 
circumscribed,  540. 
clinical  picture  of,  540. 
origin  of,  557. 
gastric  ulcer,  557. 
infection  of  biliary  passages,  557. 
perforating  typhoid  ulcer,  557. 
pathology  of,  540. 

purulent,  points  of  preference  for,  558. 
confounded  with  uremia,  538. 
diaphragmatic  respiration  in,  537. 
diffuse,  181. 

circumscribed  and,  513. 
due  to  piierperal    suppurative   proc- 
esses, 557. 
etiology  of,  528,  529,  530. 
general,   from  perforating,   gangrenous 

appendix,  181. 
in  acute  articular  rheumatism,  529. 
malarial,  529. 
origin  of,  537. 

from   neighboring  organs    in  perito- 
neum, 557. 
from  the  vessels,  528. 
pelvic,  761. 
perforative,  167,  183. 

spontaneous  cure  of,  184. 
symptoms  of,  553. 
periappendicular  abscesses  in,  558. 
progressing  rapidly  after  consolidation 
of  a  local  perityphlitis,   525. 
palpation  valuable  in,  525. 
progressive  purulent,  524,  525,  533,  554. 

plastic  inflammation  in,  525. 
puerperal  523. 

bacteriological  findings  in,  531. 
diarrhea  in,  523. 
early  collapse  in,  523. 
purulent,  bacteriological  findings  in,  530. 
sero-fibrinous,  533. 
severity  of,  534. 

simulated  by  fecal  accumulation,  538. 
simulating  cardialgia,  538. 
typhoid,  529. 
Perityphlitis,  513. 

abscesses  in  duration  of,  555. 
acute,  fecal  calculus  in,  576. 
inflammatory  process  in,  575. 


Perityphlitis,  adhesions  in,  causing  pain, 

556. 
indications  of,  554, 
chronic,  573. 

anatomical  and  histological  changes 

in,  575. 
anatomical  chmiges  in,  577. 
bath  cures  in,  600. 
catarrh  of  the  colon  in,  treatment  of. 

600. 
clinical  picture  of,  578. 
colitis  a  cause  of,  575. 
complications  of,  588. 
confounded  with  cholecystitis,  595. 

with  cholelithiasis,  595. 
constipation  a  cause  of,  575. 
diagnosis  of,  589. 
diet  in,  599. 
dislocation     of     kidney     resembling 

symptoms  of,  595. 
empyema  of  vermiform   process  in, 

578. 
etiology  of,  574. 

extirpation  of  appendix  in,  597. 
exudation  in,  598. 
Gerlach  valve  in,  577. 
habitual   constipation   in,   treatment 

of,  600. 
indigestion  a  factor  in,  599. 
internal  medicine  in,  573. 
intestinal  catarrh  a  cause  of,  575. 
laparotomy  in,  573,  575. 
mineral  spring  cures  in,  600. 
new  attacks  in,  prevention  of,  598. 
obstruction  of  vermiform  process  in, 

578. 
occurrence  of,  with  other  organic  dis- 
eases, 595. 
operation  at  puberty  in,  602. 

causes  of  failure  of,  603. 

dangers  of,  602. 

results  of,  602. 
origin  of,  574. 
prognosis  of,  595. 
prognosis  of  subsequent  attacks  of 

598. 
relapse  after  operation  in,  603. 
remissions  in,  597. 
simulated  by  hernia,  595. 
therapeutic  considerations  in,  597. 
traumatic  influences  in,  575. 
treatment  of,  597. 
uterine  adnexa,  disease  of,  a  cause  of, 

575. 
with  chronic  catarrh  of  colon,  588. 
with  diseases  of  right-sided  adnexa, 

588. 
chronic  relapsing,  574,  581. 
atypical  cases  of,  584. 
diagnostic  factors  in,  591. 
differentiation  of,  from  colitis,  593. 

from    disease    of    uterine    adnexa 
593,  594. 

from  renal  calculus,  594. 
McBumey's  point,  591. 

importance  of,  in  diagnosis  of,  583, 

pain  in  region  of,  583. 


818 


INDEX  OF  SUBJECTS 


Perityphlitis,  chronic  relapsing,  palpation 
of  vermiform  process  in,  591. 

prognosis  of,  596. 

removal  of  appendix  In,  601. 

symptoms  of,  582. 

temperature  in,  583. 

treatment  of,  599. 

typical  cases  of,  582. 

varieties  of,  581. 
circumscribed,  540. 

acute,  localization  of,  541. 

differential  diagnosis  of,  549. 

fever  in,  547. 

pain  a  symptom  of,  546. 

symptoms  of,  545. 

tumor  of,  548. 

urine  in,  549. 

vomiting  in,  548. 
confounded   with  tuberculosis  and  ac- 
tinomycosis of  cecum  and  appen- 
dix, 549. 
course  of,  554. 
dangers  of  non-operation  in,  567. 

of  operation  in,  567. 
diagnosis  of  form  of,  550. 
diet  in  treatment  of,  572. 
differentiation  between  true  and  pseu- 
do-,  594. 

of  from  acute  intestinal  occlusion,  549. 

from  fecal  tumor,  549. 

from  other  conditions,  549. 
due  to  chronic  appendicitis,  556. 

to  fecal  calculus,  556. 
empyema  of  appendix  in,  symptoms  of, 

553. 
fecal  calculi  in,  564. 
fecal  discharges  of,  572. 
latent,  581. 

transitions  from,  582. 
malignant  affections  in,  554. 
masked,  585. 

massage  in,  treatment  by,  573. 
moderate  circumscribed,  526. 

obliteration    of    appendix   following, 
527. 
non-operative  treatment  of,  569. 
operation  in,  absolute  indications  for, 
566. 

after  attack,  569. 

during  attack,  568. 
operative  considerations  in,  565. 
opium  in,  misuse  of,  571. 

use  of,  .570,  571. 
prognosis  of,  566. 
prophylaxis  of,  534. 
purgation  in  treatment  of,  573. 
pus  in,  significance  of,  551. 

symptoms  of,  553. 
relapses  in,  554,  572. 

due  to  pus,  556. 
resembling  neoplasms  of  cecum  or  colon, 

549. 
residual,  574,  578. 

diagnostic  factors  in,  589. 

differentiation  of,  from  carcinoma  of 
cecum,  590. 
from  cecal  tuberculosis,  590. 


Perityphlitis,  residual,  forms  of  develop- 
ment of,  578. 
McBurney's  point  in,  590. 
operative  treatment  of,  599. 
prognosis  of,  596. 
recovery  after  repeated  rupture  in, 

579. 
temperature  a  diagnostic  factor  in, 

591. 
vomito  nigro  in,  579. 
rupture  of  abscess  of,  545. 
suppurative,  541. 

surgical  indications  in  slowly  progres- 
sive cases  of,  569. 
treatment  of,  565. 
tumor  in,  palpation  of,  583. 
Perityphlitis  larvata,  585,  588. 
Pernicious  anemia,  97. 
Pettenkofer's  test,  326. 
Petruschky's  test,  193. 
Pharynx,  catarrh  of,  27. 
Phenol,  6.36,  640. 
Phenolphthalein,  90,  91,  98,  120. 
Phenyl  acid,  irrigations  with,  38. 
Phosphates,  acid,  in  gastric  contents,  91. 

influence  of,  95. 
Phosphaturia,  115. 
Phosphorus  poisoning,  346. 
Phthisis,  incipient,  gastric  lavage  in,  48. 

pulmonary,  166. 
Physical  therapy.  111. 
Physostigmin,  786. 
Pleiochromia,  331. 
Pleura,  cancer  of,  18. 
Pneumopericarditis,  183. 
Poisoning,  acute,  gastric  lavage  in,  47. 
by  atropin.  111. 
corrosive,  59. 
Polycholia,  331. 
Polypi,  pediculated,  131. 

rectal,  249. 
Portal  vein,  corrosion  of,  177. 

stasis  of,  223. 
Posture,  importance  of,  in  dilatation,  153. 
Potatoes  for  removal  of  foreign  body,  31. 
Poultice  to  abdomen,  287. 
Pregnancies,  repeated,  a  cause  of  hepatop- 
tosis,  290. 
as  cause  of  nephroptosis,  284. 
Pregnancy,  extrauterine,  196. 
parorexia  in,  71. 
relation  of,  to  chlorosis,  274. 
Prelum  abdominale,  48. 
Press,  abdominal,  271,  274. 
Pressure,  sensation  of,  in  stomach,  222. 
Pressure  in  gastric  region,  77. 
Pressure  of  fluid  in  gastric  lavage,  54. 
Pressure  point,  epigastric,  171. 

in  gastric  ulcer,  170. 
Probes,  metallic  spiral,  28. 
Processes  of  fermentation  and  decomposi- 
tion in  intestine,  640. 
Proctitis,  659. 

Proctitis  hspmorrhoidalis,  715. 
Proliferations,  cauliflower-like,  into  esoph- 
agus, 7,  8. 
Proteid  decomposition  in  colon,  638. 


INDEX  OF  SUBJECTS 


819 


Proteid  producing  peristalsis,  636. 

Proteolysis,  37,  89. 

Proteorrhea,  652. 

Pruritus,  79. 

Pseudo-ileus,  251.  ^ 

Pseudo-peritonitis,  539. 

clinical  picture  of,  539. 

diagnosis  of  point  of  origin  of,  539. 

hernial  rings  in,  examination  of,  539. 

rectal  examination  in,  539. 

rectal   temperature   of   importance    in, 
539. 

vaginal  examination  in,  539. 
Pseudo-perityphlitis,  593. 
Psychical  irritation,  76. 
Psychical  stimulation  during  gastric  lav- 
age, 48. 
Ptomains,  643. 
Ptyalin,  652. 
Pulmonary  phthisis,  197. 
Pulsation,  epigastric,  171,  275. 
Pulse  of  aortic  insufficiency,  133. 
Pupils,  inequality  of,  4. 
Purgatives,  223.  241. 

in  intestinal  carcinomata,  255. 
Purin  substances  in  acute  yellow  atrophy, 

352. 
Purulent  processes  with  hemorrhage,  180. 
Pus  as  indication  of  gastric  carcinoma,  96. 
Pus  in  esophagus,  11. 

in  gastric  contents,  231,  233. 

in  stomach,  87. 
Pyelitis,  286. 

slow  recovery  from,  287. 

treatment  of,  287. 
Pyemia,  cryptogenetic,  235. 
Pylephlebitis,  183,  480. 
Pylethrombosis,  480. 
Pylorectomy,  195. 
Pyloric  stenoses,  benign,   142. 

congenital,  131. 

organic,  145,  146. 

without  hemorrhage,  180. 
Pyloric  ulcer,  190. 
Pyloroplasty,  157,  195. 
Pylorospasm,  107,  169,  194,  195,  215. 
Pylorus,  benign  and  malignant  tumors  of, 
147. 

benign  constriction  of,  35. 

cancer  of,  35. 

carcinoma  of,  95,  197,  227,  256. 

carcinomatous  tumor  of,  197. 

cicatricial  and  hypertrophic  stenosis  of, 
224. 

cicatricial  narrowing  of,  45. 

cicatricial  thickening  of,  194. 

cicatrix  of,  35,  143. 

closure  of,  from  mechanical  causes,  35. 

constriction  of,  33,  34. 

contraction  of,  131. 

digital  divulsion  of,  157. 

flaccidity  of,  73,  142. 

hypertrophy  of,  33,  35,  131,  132,  196. 

insufficiency  of,  74,  185. 

necrosis  of,  130. 

obstruction  of,  226. 

open,  213. 


Pylorus,  organic  stenosis  of,  128. 
resection  of,  142,  258. 
spasm  of,  60,  70,  112,  117,  118,  144. 

from  nervous  influence,  162. 
spastic  processes  of,  129. 
stenosis  of,  43,  45,  126,  127,  130,  137. 
142,  211. 
malignant,  157. 
surgical  treatment  of,  157. 
stricture  of,  surgical  dilatation  of,  45. 
temporary  closure  of,  128. 
tuberculous  stenosis  of,  131. 
tumor  of,  136,  144,  226. 
ulcer  of,  99,  107,  130,  164,  170,  172,  173. 
traumatic,  163. 
Pyopneumothorax  subphrenicus,   183. 
Pyosalpinx,  rupture  of,  191. 
Pyrosis,  77,  78,  81,  134. 
Pyrosis  hydrochlorica,  208. 

Quassia  amara  as  gastric  spray,  59. 

Rademann's  nutritive  toast,  110. 
Rectal  alimentation,  118. 

in  gastric  ulcer,  201. 
Rectal  carcinoma,  mortality  in,  261 

occurring  in  pregnancy,  247. 

operative  results  in,  261. 
Rectal  nutrition,  116. 
Rectum,  carcinoma  of,  245,  260. 

catarrh  of,  715. 

curetting  of,  261. 

diastasis  of,  243. 

digital  or  ocular  exploration  of,  246. 

stenosis  of,  760. 

tuberculosis  of,  702. 

tumors  of,  249. 
Refraction  difference,  93. 
Reichmann's  disease,  113. 
Renal  colic  combined  with  gastric  ulcer, 

192. 
Renal  disease,  gastric  lavage  in,  47. 
Renal  vein,  erosion  of,  177. 
Resorts  for  mineral  spring  treatment,  215, 

216. 
Respiratory  interchange  of  gases,  48. 
Rest  in  cure  of  nephroptosis,  289. 

in  treatment  of  esophagus,  26. 
Rest  cure,  in  gastric  ulcer,  199,  201,  205. 
Retching,  33,  57. 

cause  of  hemorrhage,  66. 

during  iirastric  lavage,  54. 

in  esophageal  disease,  14. 
Rheumatism,  acute  articular,  peritonitis 

in,  529. 
Rhubarb,  action  of,  206. 

for  gastric  ulcer,  209. 
Rigidity,  gastric,  225. 

intestinal,  242,  243. 
Rokitansky,  hemorrhagic  erosions  of,  160. 
Rumbling,  abdominal,  285,  292. 

intestinal,  241. 
Rumination,  73. 

Sacrum,  resection  of,  261. 

Sahli's  glutoid  test,  316. 

Sahli's  test  of  gastric  function,  93. 


820 


INDEX  OF  SUBJECTS 


Salivation  in  pancreatic  disease,  320. 
Salol  test  of  gastric  contents,  140. 
Sarcinae  in  gastric  contents,  140,  223., 
in  stomach,  38. 
in  vomit,  182. 
Sarcoma,  operations  for,  259. 
Satiety  as  a  symptom,  146. 
Saxony,  gastroptosis  in,  266. 
Schmidt's  tests  for  all  nuclei,  625. 
Schreiber's  rubber  balloon,  30. 
Sehreiber's  sound,  28. 
Schulze's  experiments   on   the   pancreas, 

308. 
Scirrhus,  238. 
Scotch  douche,  280. 
Scotoma,  flittering,  79. 
Sea  baths,  advantage  of,  in  gastroptosis, 

280. 
Secretion,  diluting,  95. 
neuroses  of,  76. 
of  hydrochloric  acid,  93. 
Secretory    apparatus  of  stomach,   irrita- 
bility of,  110. 
Secretory     disturbances,     diagnosis    and 

therapy  of,  87. 
Secretory  insufficiency,  extreme,  121. 
Senator  method  of  dilating  esophagus,  29. 
Sepsis,  peritoneal,  523,  535. 
Sexual  excess  as  cause  of  atony,  127. 
Shield  to  support  abdomen,  292. 
Shock  as  cause  of  wandering  spleen,  293. 
Shock,  "reflex"  or  "nervous,"  521. 
Shoulder,   right,  pain  in,   170. 
Shredded  wheat  biscuit,  value  of,  66. 
Sigmoiditis,  249. 
Silver  nitrate  for  gastric  ulcer,  60,  206. 

in  hypersecretion,   118. 
Simon's  test  for  dissolved  albumin,  626. 
Singultus  in  cholelithiasis,  494. 
Sippy  dilator,  25. 
Sitz  baths,  280. 
Skeatol,  636. 
Skin,  dryness  of,  114. 
Skirts,  suspension  of,  from  shoulders,  276. 
Skolikoiditis,  541. 

Sleep  on  left  side,  impossibility  of,  298. 
Soaps,  amount  of,  in  pancreatic  disease, 

314. 
Sodium  chlorid  for  subacidity,  101. 
Sodium  hyposulphite,  irrigations  with,  38. 
Solar  plexus,  sensitiveness  of,  171. 
Sound,  esophageal,  6,  27. 
introduction  of,  30. 
passage  of,  3,  4. 
resistance  to,  19. 
use  of,  22,  23. 
varieties  of,  12. 
gastric,  dangers  in  use  of,  42. 
rubber  l)all,  26. 
splashing,  146. 

in  stomach,  133,  137,  270,  275. 
succussion,  122,  147. 
Sounds,  director,  28. 

esophageal,  English  and  French,  28. 
for  stomach,  double,  40. 
soft-rul>l)er,  39. 
Soups  in  the  dietary,  110 


Spasm,  esophageal,  14. 
causes  of,  14. 
diagnosis  of,  15. 
therapy  of,  31. 
gastric,  192. 
of  stomach,  43. 
pyloric,  193. 

pyloric  circumscribed,  195. 
rectal,  186. 
Spasm  as  a  neurosis,  14. 
Spasms,  esophageal,  3. 
reflex,  14. 
from  poisoning,  14. 
of  the  extremities,  177. 
tonic  muscular,  141. 
Sphincter,  new,  formation  of,  213. 
Sphincter  muscle,  contraction  of,  144. 
Spine,  pain  in,  from  gastric  ulcer,  170. 
Splanchnoptosis,  264,  294. 
Spleen,  displacement  of,  265,  292;  see  also 
Gastroptosis. 
drug  treatment  of,  293. 
enlargement  of,  178. 

in  cholelithiasis,  496. 
extirpation  of,  294. 
fixation  of,  293. 
hemolysis  of,  in  jaundice,  330. 
rupture  of,  191. 
wandering,  292. 
diagnosis  of,  293. 
symptoms  of,  293. 
treatment  of,  293. 
Splenopexy,  293. 
Sputum,  deglutition  of,  167. 

swallowing  of,  as  cause  of  tuberculosis, 
187. 
Stagnation  of  gastric  contents,  256. 
Starch,  saccharifi  cation  of,  78. 
Starches  in  food,  78. 

in  the  diet,  110. 
Starvation  cure,  82. 
Stasis,  gastric,  128. 

of  portal  vein  system,  66. 
Stasis  icterus,  330. 
Steapsin,  88,  305. 

tests  for,  93. 
Steatorrhea,  652. 
true,  312,  315. 
Stenosis,  cardiac,  126. 
chronic  intestinal,  242. 
compression,  of  esophagus,  30. 
differentiation  of  various  forms  of,  19. 
infrapapillary  duodenal,  140. 
intestinal,  feces  of,  752. 
malignant,  of  pylorus,  45. 
obstruction,  31. 
occlusion,  of  esophagus,  16. 
of  esophagus,  1,  6. 

acute  appearance  of,  17. 
congenital,  16. 
from  caustics,  11. 
from  compression,  2. 
symptoms  of,  2,  14. 
treatment  of,  19. 
pyloric,  107,  116,  136. 
spastic,  1. 
syphilitic,  249. 


INDEX  OF  SUBJECTS 


821 


stenosis,  value  of  history  in,  12. 

varieties  of,  2. 
Stomach,  abnormal  acidity  of,  129. 
abnormal  fermentation  in,  155. 
abnormal  formation  of,  55. 
abscess  of,  233. 
absence  of  secretion  in,  87. 
absorbent  function  of,  64. 
absorption  of,  151. 
acidity  of,  34,  83,  88,  123. 
activity  of,  44. 

test  of,  145. 
acute  atony  of,  127. 
adhesion  of,  to  neighboring  organs,  165. 
anatomical  changes  in,  87. 
anomalous  activity  of,  79. 
atony  of,  4.5,  73,  124,  169. 
autodistention  of,  137. 
boundaries  of,  136. 
cancer  of,  163. 
carcinoma  of,  191. 
carcinomatous  neoplasm  of,  194. 
carcinomatous  ulcer  of,  196. 
catarrh  of,  34,  57,  70. 
chemism  of,  185,  194,  197,  213. 
chemistry  of,  172. 
conservation  of  motility  of,  103. 
constrictions  in,  165. 
continuous  secretion  of  fluid  in,  35. 
corrosion  of,  59. 

decrease  in  motor  power  of,  123. 
descent  of  pyloric  portion  of,  35. 
diagnostic  evacuation  of,  138. 
digestive  stimulation  of,  129. 
dilatation  of,  32,  33,  55,  73,  122,  129. 

cure  of,  45. 
dilated,  adherent  to  liver,  185. 
diseases  of,  laboratory  investigation  of, 
36. 

nutrition  in,  61. 
displacement  of,  263,  265. 
distention  of,  as  cause  of  gastroptosis, 
267. 

by  gas,  169. 

with  water,  228. 
distortion  of,  182. 
douching  of,  40,  154. 
drawing  sensation  in,  83. 
electric  illumination  of,  136. 
electricity  to,  101. 
enlargement  of,  268. 
erosion  of,  98. 
evacuation  of,  129,  138. 
extirpation  of,  257. 
fermentative  decomposition  in,  59. 
fetal,  position  of,  35. 
flaccidity  of,  55,  162. 
flaccidity  of  muscularis  of,  126. 
functional  diagnosis  of,  87. 
functional  diseases  of,  63. 
functional  disturbances  of,  32,  88. 
functions  of,  63. 
habitual  overloading  of,  117. 
hemorrhage  from,  49,  64,  165,  175. 

treatment  of,  60. 
hour-glass,  56,  165.  185,  211. 
hypermotility  of,  643. 
53 


Stomach,  illiunination  of,  228,  277. 
implication  of,  in  nephroptosis,  285. 
increased  size  of,  122,  139. 
inflation  of,  270,  276. 

with  air,  227. 

with  air  or  carbonic  acid,  137. 
insufficiency  of,  64,  65,  270. 
irrigation  of,  38. 

with  drugs,  59. 
irritable,  57. 
massage  of,  153. 

mechanical  insufficiency  of,  61,  122. 
microbes  and  ferments  in,  55. 
motility  of,  72. 

diagnostic  determination  of,  44. 
motor  activity  of,  123,  128. 
motor  function  of,  84. 
motor  insufficiency  of,  45,  76,  116,  122, 

124,  125,  138,  154. 
motor  irritative  phenomena  in,  60. 
motor  power  of,  125. 
necrosis  in,  162. 
nervous  apparatus  of,  63. 
neuroses  of,  70,  206. 
normal  motility  of,  64. 
normal  position  of,  267. 
organic  acids  in,  61. 
organic  disease  of,  82,  83. 
over-distention  of,  45. 

during  gastric  lavage,  54. 
overfilling  of,  with  fluid,  42. 
over-loading  of,  34. 
palpation  of,  81,  83,  136. 
paralysis  of  muscular  wall  of,  126. 
peptic  labor  of,  90. 
percussion  of,  137. 
perforation  of,  165,  182. 
peristalsis  of,  126,  130,  137. 
permanent  secretion  of,  103. 
perverted  secretion  of,  89. 
position  of,  147. 
production  of  gas  in,  61. 
progressive  corrosive  necrosis  of,  165. 
prolapse  of,  273. 
prolapsed,  dilatation  of,  272. 
rapid  emptying  of,  71,  106. 
relative  dilatation  of,  125. 
retention  of  ingesta  in,  84. 
rigidity  of,  131. 
sarcoma  of,  235. 
secretory  activity  of,  76. 
secretory  and  fermentative  processes  in, 

47. 
secretory  disturbances  of,  53,  87. 
secretory  function  of,  64. 
size  of,  133,  137. 
sour,  81. 

spasmodic  contractions  of,  184. 
structure  substances  in,  89. 
subacidity  of,  92. 
syphilis  of,  187. 
test  of  function  of,  46,  83. 
tissue  necrosis  in,  163. 
transudation  of  fluids  into,  36. 
trial  lavage  of,  47. 
tuberculous  ulcers  of,  187. 
tumors  of,  191. 


822 


INDEX  OF  SUBJECTS 


Stomach,  tympany  of,  75,  138. 

ulcer  of,  107,  117,  533. 

vertical  position  of,  266,  269. 

washing  of,  34. 
Stomach-pump,  34. 

origin  of,  33. 

use  of,  36,  37. 

various  forms  of,  37. 
Stomach-sound,  rules  for  introduction  of, 

42. 
Stomach-tube,  clogging  of,  52. 

dangers  of  use  of,  42. 

defective  varieties  of,  49. 

different  forms  of,  41. 

injury  to  mucous  membrane  by,  52. 

introduction  of,  115,  124,  193. 
in  gastric  ulcer,  171. 
into  medical  practice,  119. 

method  of  using,  50. 

modern  form  of,  41. 

preparation  of,  for  use,  51, 

use  of,  by  patient,  61. 

with  ring  on  which  to  bite,  54. 
Stomach-tubes,  soft,  41,  49. 
Stomachs  of  dogs,  experiments  in,  108, 161, 

162. 
Stools,  fatty,  312. 
Strangury,  286. 
Strauss'  currant  test,  140. 
Stricture,  annular,  of  esophagus,  12. 

corrosive,  of  esophagus,  13. 

from  caustics,  8. 

internal  cicatricial,  756. 

of  esophagus,  treatment  of,  27- 

ring  form  of,  12. 

syphilitic,  249. 

tuberculous  cicatricial,  756,  762. 
Strychnin,  for  dilatation  of  stomach,  156. 
Stylet  in  stomach-tube,  40. 
Stylets,  introduction  of,  29. 
Subacidity,  94. 

as  symptom  in  various  diseases,  96. 

diagnosis  of,  96. 

diet  in,  100. 

drug  treatment  of,  102. 

extreme,  121. 

relative,  94. 

specific  gravity  of,  105. 

symptoms  of,  95. 

treatment  of,  99. 
Substances,  bactericidal,  639. 
Substitution  therapy,  102. 
Subsultus  tendinum,  177. 
Sugar,  by  rectum,  153. 

decreased  consumption  of,  308. 

formation  of,  308. 
in  liver,  308. 

in  the  diet,  111,  117. 

transformation  of,  305. 

use  of,  in  hyperacidity,  110. 
Superacidity,  104. 
Supersecretion,  104. 

Supraclavicular  region,  palpation  of,  228. 
Surgery,  advance  in,  221. 

gastric,  45. 

in  esophageal  disease.  26. 

in  gastric  diseases,  157. 


Suture  anastomosis    in    pyloric    stenosis, 

212. 
Swallowing  in  esophageal  disease,  18. 
Sweating,  accompanying  bulimia,  71. 

influence  of,  upon  gastric  juice,  111, 
Syncytiolysins,  348. 
Syplulis  of  stomach,  187. 
Syringe,  esophageal,  22. 

Tabes  dorsalis,  197. 

gastralgia  in,  72. 
Tabes  mesenterica,  673. 
Takadiastase,  78,  112. 
Taste,  sense  of,  perversion  of,  81. 
Teeth,  correction  of  defects  inr,  99. 

false,  arrested  in  esophagus,  16. 
Tenesmus,  rectal  and  vesical,  245. 
Tenesmus  in  hemorrhoids,  712. 
Tension,  gastric,  after  meals,  133. 
Test,  corrosive  sublimate,  of  the  feces,  626. 

fermentation,  of  feces,  618,  620. 

Gmelin's  in  the  feces,  628. 

of  gastric  function,  88. 

Teichmann's  hemin,  633. 

Weber-van  Deen,  633. 
Test  breakfast,  83,  89,  99,  138,  140. 

Ewald-Boas,  606. 

in  hypersecretion,  115. 
Test-diet,  in  examination  of  feces,  607. 
Test-meal,  61,  138. 

best  time  for,  65. 

of  Ewald-Boas,  64,  66. 

of  Leube-Riegel,  64,  65,  606. 
Tetanus,  esophagismus  in,  14. 
Tetany,  170,  239. 

as  sequel  of  dilatation,  142. 

cause  of,  156. 

from  gastric  disease,  33,  36,  141,  142. 
Thirst,  accompanying  gastric  disease,  134. 

artificial  relief  of,  26. 

in  esophageal  diseases,  5. 

in  gastric  neuroses,  77. 

in  hypersecretion,  114. 
Thorax,  examination  of,  18. 
Thrombosis  of  splenic  vein,  178. 

venous,  239. 
Thrombi,  displaced,  180. 
Thrombus  formation  in  stomach,  165. 

of  gastric  ulcer,  177. 
Thrush,  31. 

Tincture  of  iodin  test  for  bile  in  urine,  326. 
Tinnitus  aurium,  177. 

accompanying  bulimia,  71. 
Tissue,  dryness  of,  87,  118,  141. 

esophageal,  examination  of,  6. 
microscopic  examination  of,  9. 
shreds  of,  11. 
Tobacco,  effect  of,  on  stomach,  130. 
Toes,  drumstick  changes  in,  142. 
Tongue,  coated,  significance  of,  84,  171. 

in  gastric  disease,  134. 

in  gastric  ulcer,  198. 

in  visceral  carcinomata,  224. 

leukoplakia  of,  7. 
Tormina  ventriculi,  75. 
Tormina  ventriculi  nervosa,  243. 
Torsion  of  abdominal  organs,  211. 


INDEX  OF  SUBJECTS 


823 


Tonus,  gastric,  increased,  155. 
Toxins,  bacterial,  643. 
Trachitis,  8. 

Transudation  of  fluids  into  stomach,  36. 
Trauma,  a  cause  of  gastric  ulcer,  162. 
as  cause  of  spasm,  14. 
of  stomach,  130. 
Triferrin  in  gastric  ulcer,  204. 
Trypsin,  305. 
Tubercle  bacilli  in  the  feces,  248. 

in  stomach   166. 
Tubercular  ulcer  of  stomach,  166. 
Tuberculin,  193. 
Tuberculoma  of  intestinal  walls,  755. 

of  intestine,  762. 
Tuberculosis,  cecal,  590. 
gastric,  in  children,  166. 
intestinal,  635,  687. 

chronic  intestinal  catarrh  in,  691. 
constriction  of  intestine  in,  690. 
diagnosis  of,  697. 
diagnosis  injestion  of  tuberculin  in, 

697. 
diarrhea  in,  692. 

ethyl  sulphuric  acid  in  urine  in,  698. 
etiology  of,  687. 
general  clinical  picture  in,  695. 
hemorrhage  in,  693. 
offensive  odor  of  feces  in,  697. 
pathology  of,  689. 
prophylaxis  in,  698. 
rigidity  in.  695. 
symptoms  of,  691. 
symptoms  in  ulcerative,  691. 
treatment  of,  698. 
adrenalin  in,  701. 
bismuth  in,  701. 
food  in,  703. 
opium  in,  701. 
surgical,  702. 
symptomatic,  700. 
tuberculin  in,  699. 
miliary,  696. 
of  stomach,  187. 
pharyngeal,  166. 
pulmonary,  276. 
Tumor  in  greater  curvature  of  stomach, 
173. 
in  disease  of  the  pancreas,  317,  319. 
of  esophagus,  6. 
of  gall-bladder,  487. 
of  greater  curvature,  196. 
of  intestines,  241. 
pyloric,  194,  226. 
Tumors,  benign,  131. 
benign  intestinal,  756. 
from  hair,  196. 
from  trichobezoar,  196. 
spastic,  196. 
Tussis  hepatica,  483. 
Typhlon,   inflammatory    processes    from, 

248. 
Typhlophobia,  594. 
Typhoid,  bilious,  347. 

Ulcer,  carcinomatous,  196. 
corrosive,  166. 


Ulcer,  diphtheritic,  13. 
gastric,  528. 

cicatrices  of,  131. 
bismuth  treatment  of,  43. 
hyperacidity  in,  76. 
florid,  201. 
intestinal,  528. 

perforation  of,  191. 
of  cardia,  75. 

diagnosis  of,  75. 
of   stomach,    159.      See    also    Gastric 

Ulcer, 
peptic,  13,  162. 
pyloric,  33,  35. 
round,  159. 
syphilitic,  13,  187. 
in  stomach,  167. 
tuberculous,  13,  193. 

in  stomach,  166. 
as  cause  of  cancer,  10. 
of  esophagus,  5,  7,  8. 
Uremia,  gastric  lavage  in,  47. 
Ureter,  hemorrhage  from,  58. 
Ureters,  measurements  of,  288. 
torsion  and  kinking  of,  286. 
torsion  of,  in  movable  kidney,  192. 
Urinary  tract,  sepsis  in,  181. 
Urine,  alkalinity  of,  141. 
diminution  of,  141. 
in  gastric  disease,  36. 
in  pyelitis,  286. 
suppression  of,  142. 
Urobilin,  increase  of,  in  jaimdice,  331. 
Urobilin  icterus,  341. 
Urobilinuria,  340. 
Uterus,  septic  infections  of,  528. 


Vagotomia  subdiaphragmatica  in  rabbits, 

162. 
Valve  formation  in  esophagus,  13. 
Varices,  esophageal,  58. 

hemorrhages  from,  42. 
Vegetables  in  the  diet,  110. 
Vein,  golden,  of  hemorrhoids,  246,  712. 
Veins,  hemorrhoidal,  246. 

varicose,  in  esophagus,  178. 
Venous  stasis,  179. 
Vertebral  column,  carcinoma  of,  17. 

kyphoscoliosis  of,  265,  273. 

lordosis  of,  277. 

scoliosis  of,  283. 

tumor  of,  2. 
Vertigo,  82. 

in  ectasis,  135. 

in  gastric  dilatation,  142. 
Vessels,  erosion  of,  5. 
of  stomach,  165. 
Vicious  circle,  formation  of,  127. 
Vitellius,  mode  of,  for  emptying  stomach, 

38. 
Vocal  cords,  destruction  of,  5. 

unilateral  paralysis  of,  4. 
Voice  production,  4. 
Volvulus,  762,  771. 

of  intestines,  211. 
Vomit,  coffee-ground,  147. 


824 


INDEX  OF  SUBJECTS 


Vomiting,  acid,  77. 

as  symptom    of    visceral    carcinomata, 
222,  223. 

bilious,  127. 

expulsive,  57. 

fecal,  767,  775. 

in  dilatation  with  hypersecretion,  134. 

in  gall-stone  disease,  490. 

in  gastric  dilatation,  122. 

in  gastric  disease,  134. 

in  gastric  ulcer,  181. 

in  pancreatic  disease,  320. 

nervous,  74. 

of  blood-stained  mucus,  5. 

of  gastric  ulcer,  209. 

periodical,  74. 

spontaneous,  182. 
Vomito  negro  in  residual  perityphlitis,  579. 
Vomitus,  containing  three  layers,  134. 

in  hypersecretion,  114. 
Vomitus  maturitus,  182. 


Waist,  change  in  circumference  of,  271, 
272. 
compression  of,  a  cause  of  gastroptosis, 
266,  270,  273,  276. 
Water,  deficiency  of,  in  organism,  170. 

insufficient  absorption  of,  141. 
Weight,  increase  of,  after  gastric  lavage, 
35. 
of  body,  84. 
Weil's  disease,  338,  339. 

symptoms  of,  339. 
Weiss'  stomach-pump,  37. 
Wines  tolerated  in  hyperacidity.  111. 
Woulff's  bottle,  employment  of,  for  lavage, 
39. 

X-rays,  examination  of  heart  by,  296. 
Xeroform,  208. 

Yeast  fermentation,  140. 


(8> 


THE  END 


Date  Due 

PRINTED    IN 

U.S.*.             CAT     NO    24    161               ^ 

,UC  SOUTHERN  REGIONAL  LIBRARY  FACIUTY 


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A    000  51 1  633     0 


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WI  100 

B598d 

1910 
Billings,  Frank. 

Diseases  of  the  digestive  system, 


COLLEGE 
AND  SURG 


WI  100 
B598d 
1910 
Billings,  Frank. 

Diseases  of  the  digestive  system. 


MEDICAL  SCIENCES  LIBRARY 

UNIVERSITY  OF  CALIFORNIA,  IRVINE 

IRVINE,  CALIFORNIA  92664 


